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Racial disparities in cardiotoxicity after chemotherapy
a research review indicates.
“It’s important that both patients and clinicians be aware of these disparities so that more meaningful conversations around long-term cardiac health and cancer treatment can take place,” lead investigator Wondewossen Gebeyehu, with the University of Toronto, said in an interview.
However, patients “should not avoid chemotherapy, as the most important thing is making sure they get the best cancer treatment possible, and studies already show Black patients may get less optimal cancer treatments,” Mr. Gebeyehu added in a statement.
Ana Barac, MD, PHD, chair of cardio-oncology at Inova Schar Cancer Institute and Inova Heart and Vascular Institute, Fairfax, Va., who wasn’t involved in the study, agreed.
“The most important message is to look at preexisting cardiovascular disease, oncology diagnosis, and be aware of existing disparities in a specific cancer and CVD,” Barac said in an interview.
“What should NOT happen is to overinterpret this report of cardiotoxicity as an indication to modify/avoid planned cancer treatment to decrease cardiotoxicity. This approach could worsen oncology outcomes and lead to undertreatment of cancer, therefore posing real danger,” said Dr. Barac.
The study was presented at the American College of Cardiology Advancing the Cardiovascular Care of the Oncology Patient 2023 conference.
Causes unclear
Chemotherapy is known to increase the risk of cardiovascular heart failure and other forms of CVD, but less is known about racial disparities in the incidence of chemotherapy-induced cardiotoxicity.
Mr. Gebeyehu and colleagues conducted a systematic review and meta-analysis of the available literature to assess racial disparities in CV adverse effects among cancer patients who were treated with chemotherapeutic agents. They screened 7,057 studies, fully reviewed 57, and included 24 studies, representing 683,749 participants, in their analysis.
Breast cancer was the most commonly reported malignancy. Other common malignancies were prostate, kidney, and hematologic malignancies such as leukemia and lymphoma.
Chemotherapeutic agents included anthracyclines (doxorubicin, daunorubicin), trastuzumab, and hormonal therapies.
Black race or African ancestry was associated with increased odds of chemotherapy-associated cardiotoxicity (odds ratio, 1.71; 95% confidence interval, 1.40-2.10), as well as congestive heart failure (OR, 1.92; 95% CI, 1.68-2.19).
Mr. Gebeyehu said in an interview that it’s hard to speculate on causation with an analysis of preexisting data such as this. “Our initial analysis that we’ve reported on so far are unadjusted values, meaning they don’t adjust for those potential underlying factors,” he noted.
“However, some of the studies individually controlled for socioeconomic factors and still found increased vulnerability to chemotherapy-associated cardiotoxicity in patients of Black race or African ancestry,” Mr. Gebeyehu said.
“It’s certainly possible that a mix of both biological and socioeconomic factors are interacting to lead to these disparities. One example could be the underrepresentation of Black patients in clinical trials to develop drugs. These could lead to chemotherapeutic agents being poorly optimized in this population relative to other racial/ethnic groups,” he added.
Dr. Barac said this study adds to the growing body of evidence about the importance of racial disparities in CVD and cancer outcomes.
“It is important to note that only the unadjusted odds ratio was reported and that much more detail is needed to understand what may be underlying the disparities. It is critically important to await the adjusted analysis, as well as details of the type of cancers and treatment used, before clinical implications can be discussed,” said Dr. Barac, who served as codirector of the conference.
“The risk of cardiotoxicity needs to be presented in the context of the oncology and CV disease burden, as both can influence the risk, and there could be a synergistic effect of disparities,” Dr. Barac added.
The study had no specific funding. Mr. Gebeyehu and Dr. Barac disclosed no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
a research review indicates.
“It’s important that both patients and clinicians be aware of these disparities so that more meaningful conversations around long-term cardiac health and cancer treatment can take place,” lead investigator Wondewossen Gebeyehu, with the University of Toronto, said in an interview.
However, patients “should not avoid chemotherapy, as the most important thing is making sure they get the best cancer treatment possible, and studies already show Black patients may get less optimal cancer treatments,” Mr. Gebeyehu added in a statement.
Ana Barac, MD, PHD, chair of cardio-oncology at Inova Schar Cancer Institute and Inova Heart and Vascular Institute, Fairfax, Va., who wasn’t involved in the study, agreed.
“The most important message is to look at preexisting cardiovascular disease, oncology diagnosis, and be aware of existing disparities in a specific cancer and CVD,” Barac said in an interview.
“What should NOT happen is to overinterpret this report of cardiotoxicity as an indication to modify/avoid planned cancer treatment to decrease cardiotoxicity. This approach could worsen oncology outcomes and lead to undertreatment of cancer, therefore posing real danger,” said Dr. Barac.
The study was presented at the American College of Cardiology Advancing the Cardiovascular Care of the Oncology Patient 2023 conference.
Causes unclear
Chemotherapy is known to increase the risk of cardiovascular heart failure and other forms of CVD, but less is known about racial disparities in the incidence of chemotherapy-induced cardiotoxicity.
Mr. Gebeyehu and colleagues conducted a systematic review and meta-analysis of the available literature to assess racial disparities in CV adverse effects among cancer patients who were treated with chemotherapeutic agents. They screened 7,057 studies, fully reviewed 57, and included 24 studies, representing 683,749 participants, in their analysis.
Breast cancer was the most commonly reported malignancy. Other common malignancies were prostate, kidney, and hematologic malignancies such as leukemia and lymphoma.
Chemotherapeutic agents included anthracyclines (doxorubicin, daunorubicin), trastuzumab, and hormonal therapies.
Black race or African ancestry was associated with increased odds of chemotherapy-associated cardiotoxicity (odds ratio, 1.71; 95% confidence interval, 1.40-2.10), as well as congestive heart failure (OR, 1.92; 95% CI, 1.68-2.19).
Mr. Gebeyehu said in an interview that it’s hard to speculate on causation with an analysis of preexisting data such as this. “Our initial analysis that we’ve reported on so far are unadjusted values, meaning they don’t adjust for those potential underlying factors,” he noted.
“However, some of the studies individually controlled for socioeconomic factors and still found increased vulnerability to chemotherapy-associated cardiotoxicity in patients of Black race or African ancestry,” Mr. Gebeyehu said.
“It’s certainly possible that a mix of both biological and socioeconomic factors are interacting to lead to these disparities. One example could be the underrepresentation of Black patients in clinical trials to develop drugs. These could lead to chemotherapeutic agents being poorly optimized in this population relative to other racial/ethnic groups,” he added.
Dr. Barac said this study adds to the growing body of evidence about the importance of racial disparities in CVD and cancer outcomes.
“It is important to note that only the unadjusted odds ratio was reported and that much more detail is needed to understand what may be underlying the disparities. It is critically important to await the adjusted analysis, as well as details of the type of cancers and treatment used, before clinical implications can be discussed,” said Dr. Barac, who served as codirector of the conference.
“The risk of cardiotoxicity needs to be presented in the context of the oncology and CV disease burden, as both can influence the risk, and there could be a synergistic effect of disparities,” Dr. Barac added.
The study had no specific funding. Mr. Gebeyehu and Dr. Barac disclosed no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
a research review indicates.
“It’s important that both patients and clinicians be aware of these disparities so that more meaningful conversations around long-term cardiac health and cancer treatment can take place,” lead investigator Wondewossen Gebeyehu, with the University of Toronto, said in an interview.
However, patients “should not avoid chemotherapy, as the most important thing is making sure they get the best cancer treatment possible, and studies already show Black patients may get less optimal cancer treatments,” Mr. Gebeyehu added in a statement.
Ana Barac, MD, PHD, chair of cardio-oncology at Inova Schar Cancer Institute and Inova Heart and Vascular Institute, Fairfax, Va., who wasn’t involved in the study, agreed.
“The most important message is to look at preexisting cardiovascular disease, oncology diagnosis, and be aware of existing disparities in a specific cancer and CVD,” Barac said in an interview.
“What should NOT happen is to overinterpret this report of cardiotoxicity as an indication to modify/avoid planned cancer treatment to decrease cardiotoxicity. This approach could worsen oncology outcomes and lead to undertreatment of cancer, therefore posing real danger,” said Dr. Barac.
The study was presented at the American College of Cardiology Advancing the Cardiovascular Care of the Oncology Patient 2023 conference.
Causes unclear
Chemotherapy is known to increase the risk of cardiovascular heart failure and other forms of CVD, but less is known about racial disparities in the incidence of chemotherapy-induced cardiotoxicity.
Mr. Gebeyehu and colleagues conducted a systematic review and meta-analysis of the available literature to assess racial disparities in CV adverse effects among cancer patients who were treated with chemotherapeutic agents. They screened 7,057 studies, fully reviewed 57, and included 24 studies, representing 683,749 participants, in their analysis.
Breast cancer was the most commonly reported malignancy. Other common malignancies were prostate, kidney, and hematologic malignancies such as leukemia and lymphoma.
Chemotherapeutic agents included anthracyclines (doxorubicin, daunorubicin), trastuzumab, and hormonal therapies.
Black race or African ancestry was associated with increased odds of chemotherapy-associated cardiotoxicity (odds ratio, 1.71; 95% confidence interval, 1.40-2.10), as well as congestive heart failure (OR, 1.92; 95% CI, 1.68-2.19).
Mr. Gebeyehu said in an interview that it’s hard to speculate on causation with an analysis of preexisting data such as this. “Our initial analysis that we’ve reported on so far are unadjusted values, meaning they don’t adjust for those potential underlying factors,” he noted.
“However, some of the studies individually controlled for socioeconomic factors and still found increased vulnerability to chemotherapy-associated cardiotoxicity in patients of Black race or African ancestry,” Mr. Gebeyehu said.
“It’s certainly possible that a mix of both biological and socioeconomic factors are interacting to lead to these disparities. One example could be the underrepresentation of Black patients in clinical trials to develop drugs. These could lead to chemotherapeutic agents being poorly optimized in this population relative to other racial/ethnic groups,” he added.
Dr. Barac said this study adds to the growing body of evidence about the importance of racial disparities in CVD and cancer outcomes.
“It is important to note that only the unadjusted odds ratio was reported and that much more detail is needed to understand what may be underlying the disparities. It is critically important to await the adjusted analysis, as well as details of the type of cancers and treatment used, before clinical implications can be discussed,” said Dr. Barac, who served as codirector of the conference.
“The risk of cardiotoxicity needs to be presented in the context of the oncology and CV disease burden, as both can influence the risk, and there could be a synergistic effect of disparities,” Dr. Barac added.
The study had no specific funding. Mr. Gebeyehu and Dr. Barac disclosed no relevant conflicts of interest.
A version of this article originally appeared on Medscape.com.
Breast cancer screening advice ‘dangerous’ for black women
The U.S. Preventive Services Task Force currently recommends that breast cancer screening start at age 50 years, regardless of race or ethnicity.
But
The current “one-size-fits-all” policy to screen the entire female population from a certain age may be “neither fair and equitable nor optimal,” noted the authors, led by Tianhui Chen, PhD, with Zhejiang Cancer Hospital, Hangzhou, China.
The study was published online in JAMA Network Open.
Laurie R. Margolies, MD, chief of breast imaging at the Dubin Breast Center of the Mount Sinai Tisch Cancer Center in New York City, agreed.
Black women get breast cancer at a much younger age, are less likely to be diagnosed with early breast cancer, and are more likely to die of breast cancer, explained Dr. Margolies, who was not involved in the study.
“That’s why the guidelines that say begin at age 50 are flawed and so dangerous,” she said in an interview with this news organization. “This study is really important to highlight that we’re missing an opportunity to detect and treat breast cancer early in the Black population.”
The current study explored the optimal race- and ethnicity-specific ages to initiate breast cancer screening to address racial disparities in breast cancer mortality.
Using a nationwide population-based cross-sectional study design, the team analyzed data on 415,277 women who died of breast cancer in the United States from 2011 to 2020.
The cohort was 75% White, 15% Black, 7% Hispanic, 3% Asian or Pacific Islander, and < 1% Native American or Alaska Native. A total of 115,214 women (28%) died before age 60. The team calculated the 10-year cumulative risk of breast cancer–specific death by age and by race and ethnicity.
For those aged 40-49, breast cancer mortality was highest among Black women (27 deaths per 100,000 person-years), followed by White women (15 deaths per 100,000 person-years) and American Indian/Alaska Native, Hispanic, and Asian/Pacific Islander women (11 deaths per 100,000 person-years).
If breast screening started at age 50 for the entire population, the mean 10-year cumulative risk of dying from breast cancer would be 0.329%. Black women reached this risk threshold level at age 42, whereas non-Hispanic White women reached the threshold at age 51, American Indian/Alaska Native and Hispanic women at age 57, and Asian/Pacific Islander women at age 61.
If screening started at age 45 for all women, the mean 10-year cumulative risk of breast cancer death would be 0.235%. Black women reached this risk threshold level at age 38, non-Hispanic White women at age 46, Hispanic women at age 49, Asian/Pacific Islander women at age 50, and American Indian/Alaska Native women at age 51.
If screening started at age 40 for all women, with a mean 10-year cumulative risk of 0.154%, Black women would reach this risk threshold at age 34, White women at age 41, Hispanic women at age 43, and American Indian/Alaska Native and Asian/Pacific Islander women at age 43.
Dr. Chen and colleagues concluded that failure to consider race and ethnicity in breast cancer screening guidelines “may pose a significant risk for greater harm to a group already at increased risk.
“Changing guidelines based on readily available risk factors, such as race and ethnicity, is possible and may be the first, yet important step toward a personalized and fair screening program,” the team explained.
Dr. Margolies said she believes individualized screening recommendations will likely come, but first, all women should start screening at age 40 instead of age 50.
“Most American women are starting in their 40s, or starting at 40, because we know what the current guidelines are,” she said. “The question that this study doesn’t answer is, is age 40 young enough for the Black population? Maybe it should be 35.”
The study was supported by grants from the National Key Research-Development Program of China and from the Ten-Thousand Talents Plan of Zhejiang Province and by Start-Up Funds for Recruited Talents in Zhejiang Cancer Hospital. Dr. Chen and Dr. Margolies have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The U.S. Preventive Services Task Force currently recommends that breast cancer screening start at age 50 years, regardless of race or ethnicity.
But
The current “one-size-fits-all” policy to screen the entire female population from a certain age may be “neither fair and equitable nor optimal,” noted the authors, led by Tianhui Chen, PhD, with Zhejiang Cancer Hospital, Hangzhou, China.
The study was published online in JAMA Network Open.
Laurie R. Margolies, MD, chief of breast imaging at the Dubin Breast Center of the Mount Sinai Tisch Cancer Center in New York City, agreed.
Black women get breast cancer at a much younger age, are less likely to be diagnosed with early breast cancer, and are more likely to die of breast cancer, explained Dr. Margolies, who was not involved in the study.
“That’s why the guidelines that say begin at age 50 are flawed and so dangerous,” she said in an interview with this news organization. “This study is really important to highlight that we’re missing an opportunity to detect and treat breast cancer early in the Black population.”
The current study explored the optimal race- and ethnicity-specific ages to initiate breast cancer screening to address racial disparities in breast cancer mortality.
Using a nationwide population-based cross-sectional study design, the team analyzed data on 415,277 women who died of breast cancer in the United States from 2011 to 2020.
The cohort was 75% White, 15% Black, 7% Hispanic, 3% Asian or Pacific Islander, and < 1% Native American or Alaska Native. A total of 115,214 women (28%) died before age 60. The team calculated the 10-year cumulative risk of breast cancer–specific death by age and by race and ethnicity.
For those aged 40-49, breast cancer mortality was highest among Black women (27 deaths per 100,000 person-years), followed by White women (15 deaths per 100,000 person-years) and American Indian/Alaska Native, Hispanic, and Asian/Pacific Islander women (11 deaths per 100,000 person-years).
If breast screening started at age 50 for the entire population, the mean 10-year cumulative risk of dying from breast cancer would be 0.329%. Black women reached this risk threshold level at age 42, whereas non-Hispanic White women reached the threshold at age 51, American Indian/Alaska Native and Hispanic women at age 57, and Asian/Pacific Islander women at age 61.
If screening started at age 45 for all women, the mean 10-year cumulative risk of breast cancer death would be 0.235%. Black women reached this risk threshold level at age 38, non-Hispanic White women at age 46, Hispanic women at age 49, Asian/Pacific Islander women at age 50, and American Indian/Alaska Native women at age 51.
If screening started at age 40 for all women, with a mean 10-year cumulative risk of 0.154%, Black women would reach this risk threshold at age 34, White women at age 41, Hispanic women at age 43, and American Indian/Alaska Native and Asian/Pacific Islander women at age 43.
Dr. Chen and colleagues concluded that failure to consider race and ethnicity in breast cancer screening guidelines “may pose a significant risk for greater harm to a group already at increased risk.
“Changing guidelines based on readily available risk factors, such as race and ethnicity, is possible and may be the first, yet important step toward a personalized and fair screening program,” the team explained.
Dr. Margolies said she believes individualized screening recommendations will likely come, but first, all women should start screening at age 40 instead of age 50.
“Most American women are starting in their 40s, or starting at 40, because we know what the current guidelines are,” she said. “The question that this study doesn’t answer is, is age 40 young enough for the Black population? Maybe it should be 35.”
The study was supported by grants from the National Key Research-Development Program of China and from the Ten-Thousand Talents Plan of Zhejiang Province and by Start-Up Funds for Recruited Talents in Zhejiang Cancer Hospital. Dr. Chen and Dr. Margolies have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
The U.S. Preventive Services Task Force currently recommends that breast cancer screening start at age 50 years, regardless of race or ethnicity.
But
The current “one-size-fits-all” policy to screen the entire female population from a certain age may be “neither fair and equitable nor optimal,” noted the authors, led by Tianhui Chen, PhD, with Zhejiang Cancer Hospital, Hangzhou, China.
The study was published online in JAMA Network Open.
Laurie R. Margolies, MD, chief of breast imaging at the Dubin Breast Center of the Mount Sinai Tisch Cancer Center in New York City, agreed.
Black women get breast cancer at a much younger age, are less likely to be diagnosed with early breast cancer, and are more likely to die of breast cancer, explained Dr. Margolies, who was not involved in the study.
“That’s why the guidelines that say begin at age 50 are flawed and so dangerous,” she said in an interview with this news organization. “This study is really important to highlight that we’re missing an opportunity to detect and treat breast cancer early in the Black population.”
The current study explored the optimal race- and ethnicity-specific ages to initiate breast cancer screening to address racial disparities in breast cancer mortality.
Using a nationwide population-based cross-sectional study design, the team analyzed data on 415,277 women who died of breast cancer in the United States from 2011 to 2020.
The cohort was 75% White, 15% Black, 7% Hispanic, 3% Asian or Pacific Islander, and < 1% Native American or Alaska Native. A total of 115,214 women (28%) died before age 60. The team calculated the 10-year cumulative risk of breast cancer–specific death by age and by race and ethnicity.
For those aged 40-49, breast cancer mortality was highest among Black women (27 deaths per 100,000 person-years), followed by White women (15 deaths per 100,000 person-years) and American Indian/Alaska Native, Hispanic, and Asian/Pacific Islander women (11 deaths per 100,000 person-years).
If breast screening started at age 50 for the entire population, the mean 10-year cumulative risk of dying from breast cancer would be 0.329%. Black women reached this risk threshold level at age 42, whereas non-Hispanic White women reached the threshold at age 51, American Indian/Alaska Native and Hispanic women at age 57, and Asian/Pacific Islander women at age 61.
If screening started at age 45 for all women, the mean 10-year cumulative risk of breast cancer death would be 0.235%. Black women reached this risk threshold level at age 38, non-Hispanic White women at age 46, Hispanic women at age 49, Asian/Pacific Islander women at age 50, and American Indian/Alaska Native women at age 51.
If screening started at age 40 for all women, with a mean 10-year cumulative risk of 0.154%, Black women would reach this risk threshold at age 34, White women at age 41, Hispanic women at age 43, and American Indian/Alaska Native and Asian/Pacific Islander women at age 43.
Dr. Chen and colleagues concluded that failure to consider race and ethnicity in breast cancer screening guidelines “may pose a significant risk for greater harm to a group already at increased risk.
“Changing guidelines based on readily available risk factors, such as race and ethnicity, is possible and may be the first, yet important step toward a personalized and fair screening program,” the team explained.
Dr. Margolies said she believes individualized screening recommendations will likely come, but first, all women should start screening at age 40 instead of age 50.
“Most American women are starting in their 40s, or starting at 40, because we know what the current guidelines are,” she said. “The question that this study doesn’t answer is, is age 40 young enough for the Black population? Maybe it should be 35.”
The study was supported by grants from the National Key Research-Development Program of China and from the Ten-Thousand Talents Plan of Zhejiang Province and by Start-Up Funds for Recruited Talents in Zhejiang Cancer Hospital. Dr. Chen and Dr. Margolies have disclosed no relevant financial relationships.
A version of this article originally appeared on Medscape.com.
African ancestry genetically linked to worse CRC outcomes
, a disparity attributed to many factors, including socioeconomic, environmental, and genetic influences, as well as less access to care.
Results from a new genomic study provide greater clarity regarding the genetic piece of the puzzle: Persons of African background tend to have fewer targetable alterations, compared with patients of other races.
The findings were presented in a briefing and scientific poster session at the annual meeting of the American Association for Cancer Research.
Overall, the numbers to date show a clear trend: The incidence of and mortality from CRC are higher among Black patients than other populations. However, the extent to which genetic difference plays a role in these disparities remains unclear.
In the current study, researchers from Memorial Sloan Kettering (MSK) Cancer Center in New York explored how germline and somatic genomic alterations differ among patients of African ancestry, in comparison with those of European and other heritage, and how those differences might influence CRC outcomes.
Lead author Henry Walch, MS, a computational biologist at MSK, and colleagues compared genomic profiles among nearly 3,800 patients with CRC who were treated at MSK from 2014 to 2022. Patients in the study were classified by genetic ancestry as European (3,201 patients), African (236 patients), East Asian (253 patients), and South Asian (89 patients).
Tumor and normal tissues from the patients underwent next-generation DNA sequencing with a panel that covers 505 cancer-associated genes.
An analysis of overall survival by genetic ancestry confirmed findings from other studies: Overall survival was significantly worse among patients of African ancestry than among those of other groups (median 45.7 vs. 67.1 months).
The investigators used a precision oncology knowledge base (OncoKB) to assign levels of therapeutic actionability for each genomic alteration that was identified. The highest assigned value was for drugs that have been approved by the U.S. Food and Drug Administration and that target FDA-recognized biomarkers. The lowest value was assigned to biomarkers for which there was “compelling biological evidence” that the particular biomarker predicted response to a drug.
The team found that the percentage of patients who qualified for immunotherapy on the basis of microsatellite instability or high tumor mutational burden was significantly lower among patients of African heritage, compared with those of European heritage (13.5% vs. 20.4%; P = .008).
Compared with those of European ancestry, patients of African ancestry had significantly fewer actionable alterations (5.6% vs. 11.2%; P = .01). This difference was largely driven by the lack of targetable BRAF mutations (1.8% vs. 5.0%).
Mutations in APC, the most frequently altered gene in CRC, are typically associated with cancer outcomes, but the authors found that overall survival was similar for patients of African heritage regardless of whether they had altered or wild-type APC (median overall survival, 45.0 months for altered APC vs. 45.9 months for wild-type APC; P = .91). However, a significant association between APC status and overall survival was observed for patients of European ancestry (median, 64.6 months for altered APC vs. 45.6 months for wild-type APC; P < .0001).
Analyses that accounted for sex, age, primary tumor location, and stage at diagnosis also showed an association between APC status and overall survival for patients of European heritage (hazard ratio, 0.64), but not for patients of African heritage (HR, 0.74, P = .492).
Mr. Walch noted that a limitation of the study is that information regarding comprehensive treatment, environmental exposures, lifestyle, and socioeconomic factors was not available for the analysis but that these elements likely play an important role in patient outcomes.
“This is a complex problem involving many unseen factors, and the genomic landscape is a piece of a much larger puzzle,” said Mr. Walch. He noted that future studies will incorporate these factors into the models “with the ultimate goal of identifying opportunities to intervene and improve outcomes.”
Briefing moderator Lisa Newman, MD, MPH, of Weill Cornell Medicine and New York–Presbyterian, in New York, commented that Mr. Walch presented “some very compelling data that demonstrate the importance of including individuals from diverse backgrounds into [cancer] research.”
The study was funded in part by a Chris4Life Early Career Investigator Award Grant from the Colorectal Cancer Alliance for Francisco Sanchez-Vega, PhD, senior author of the study. Dr. Sanchez-Vega was also supported by an AACR-Minority and Minority-serving Institution Faculty Scholar in Cancer Research Award. Mr. Walch and Dr. Newman have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, a disparity attributed to many factors, including socioeconomic, environmental, and genetic influences, as well as less access to care.
Results from a new genomic study provide greater clarity regarding the genetic piece of the puzzle: Persons of African background tend to have fewer targetable alterations, compared with patients of other races.
The findings were presented in a briefing and scientific poster session at the annual meeting of the American Association for Cancer Research.
Overall, the numbers to date show a clear trend: The incidence of and mortality from CRC are higher among Black patients than other populations. However, the extent to which genetic difference plays a role in these disparities remains unclear.
In the current study, researchers from Memorial Sloan Kettering (MSK) Cancer Center in New York explored how germline and somatic genomic alterations differ among patients of African ancestry, in comparison with those of European and other heritage, and how those differences might influence CRC outcomes.
Lead author Henry Walch, MS, a computational biologist at MSK, and colleagues compared genomic profiles among nearly 3,800 patients with CRC who were treated at MSK from 2014 to 2022. Patients in the study were classified by genetic ancestry as European (3,201 patients), African (236 patients), East Asian (253 patients), and South Asian (89 patients).
Tumor and normal tissues from the patients underwent next-generation DNA sequencing with a panel that covers 505 cancer-associated genes.
An analysis of overall survival by genetic ancestry confirmed findings from other studies: Overall survival was significantly worse among patients of African ancestry than among those of other groups (median 45.7 vs. 67.1 months).
The investigators used a precision oncology knowledge base (OncoKB) to assign levels of therapeutic actionability for each genomic alteration that was identified. The highest assigned value was for drugs that have been approved by the U.S. Food and Drug Administration and that target FDA-recognized biomarkers. The lowest value was assigned to biomarkers for which there was “compelling biological evidence” that the particular biomarker predicted response to a drug.
The team found that the percentage of patients who qualified for immunotherapy on the basis of microsatellite instability or high tumor mutational burden was significantly lower among patients of African heritage, compared with those of European heritage (13.5% vs. 20.4%; P = .008).
Compared with those of European ancestry, patients of African ancestry had significantly fewer actionable alterations (5.6% vs. 11.2%; P = .01). This difference was largely driven by the lack of targetable BRAF mutations (1.8% vs. 5.0%).
Mutations in APC, the most frequently altered gene in CRC, are typically associated with cancer outcomes, but the authors found that overall survival was similar for patients of African heritage regardless of whether they had altered or wild-type APC (median overall survival, 45.0 months for altered APC vs. 45.9 months for wild-type APC; P = .91). However, a significant association between APC status and overall survival was observed for patients of European ancestry (median, 64.6 months for altered APC vs. 45.6 months for wild-type APC; P < .0001).
Analyses that accounted for sex, age, primary tumor location, and stage at diagnosis also showed an association between APC status and overall survival for patients of European heritage (hazard ratio, 0.64), but not for patients of African heritage (HR, 0.74, P = .492).
Mr. Walch noted that a limitation of the study is that information regarding comprehensive treatment, environmental exposures, lifestyle, and socioeconomic factors was not available for the analysis but that these elements likely play an important role in patient outcomes.
“This is a complex problem involving many unseen factors, and the genomic landscape is a piece of a much larger puzzle,” said Mr. Walch. He noted that future studies will incorporate these factors into the models “with the ultimate goal of identifying opportunities to intervene and improve outcomes.”
Briefing moderator Lisa Newman, MD, MPH, of Weill Cornell Medicine and New York–Presbyterian, in New York, commented that Mr. Walch presented “some very compelling data that demonstrate the importance of including individuals from diverse backgrounds into [cancer] research.”
The study was funded in part by a Chris4Life Early Career Investigator Award Grant from the Colorectal Cancer Alliance for Francisco Sanchez-Vega, PhD, senior author of the study. Dr. Sanchez-Vega was also supported by an AACR-Minority and Minority-serving Institution Faculty Scholar in Cancer Research Award. Mr. Walch and Dr. Newman have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
, a disparity attributed to many factors, including socioeconomic, environmental, and genetic influences, as well as less access to care.
Results from a new genomic study provide greater clarity regarding the genetic piece of the puzzle: Persons of African background tend to have fewer targetable alterations, compared with patients of other races.
The findings were presented in a briefing and scientific poster session at the annual meeting of the American Association for Cancer Research.
Overall, the numbers to date show a clear trend: The incidence of and mortality from CRC are higher among Black patients than other populations. However, the extent to which genetic difference plays a role in these disparities remains unclear.
In the current study, researchers from Memorial Sloan Kettering (MSK) Cancer Center in New York explored how germline and somatic genomic alterations differ among patients of African ancestry, in comparison with those of European and other heritage, and how those differences might influence CRC outcomes.
Lead author Henry Walch, MS, a computational biologist at MSK, and colleagues compared genomic profiles among nearly 3,800 patients with CRC who were treated at MSK from 2014 to 2022. Patients in the study were classified by genetic ancestry as European (3,201 patients), African (236 patients), East Asian (253 patients), and South Asian (89 patients).
Tumor and normal tissues from the patients underwent next-generation DNA sequencing with a panel that covers 505 cancer-associated genes.
An analysis of overall survival by genetic ancestry confirmed findings from other studies: Overall survival was significantly worse among patients of African ancestry than among those of other groups (median 45.7 vs. 67.1 months).
The investigators used a precision oncology knowledge base (OncoKB) to assign levels of therapeutic actionability for each genomic alteration that was identified. The highest assigned value was for drugs that have been approved by the U.S. Food and Drug Administration and that target FDA-recognized biomarkers. The lowest value was assigned to biomarkers for which there was “compelling biological evidence” that the particular biomarker predicted response to a drug.
The team found that the percentage of patients who qualified for immunotherapy on the basis of microsatellite instability or high tumor mutational burden was significantly lower among patients of African heritage, compared with those of European heritage (13.5% vs. 20.4%; P = .008).
Compared with those of European ancestry, patients of African ancestry had significantly fewer actionable alterations (5.6% vs. 11.2%; P = .01). This difference was largely driven by the lack of targetable BRAF mutations (1.8% vs. 5.0%).
Mutations in APC, the most frequently altered gene in CRC, are typically associated with cancer outcomes, but the authors found that overall survival was similar for patients of African heritage regardless of whether they had altered or wild-type APC (median overall survival, 45.0 months for altered APC vs. 45.9 months for wild-type APC; P = .91). However, a significant association between APC status and overall survival was observed for patients of European ancestry (median, 64.6 months for altered APC vs. 45.6 months for wild-type APC; P < .0001).
Analyses that accounted for sex, age, primary tumor location, and stage at diagnosis also showed an association between APC status and overall survival for patients of European heritage (hazard ratio, 0.64), but not for patients of African heritage (HR, 0.74, P = .492).
Mr. Walch noted that a limitation of the study is that information regarding comprehensive treatment, environmental exposures, lifestyle, and socioeconomic factors was not available for the analysis but that these elements likely play an important role in patient outcomes.
“This is a complex problem involving many unseen factors, and the genomic landscape is a piece of a much larger puzzle,” said Mr. Walch. He noted that future studies will incorporate these factors into the models “with the ultimate goal of identifying opportunities to intervene and improve outcomes.”
Briefing moderator Lisa Newman, MD, MPH, of Weill Cornell Medicine and New York–Presbyterian, in New York, commented that Mr. Walch presented “some very compelling data that demonstrate the importance of including individuals from diverse backgrounds into [cancer] research.”
The study was funded in part by a Chris4Life Early Career Investigator Award Grant from the Colorectal Cancer Alliance for Francisco Sanchez-Vega, PhD, senior author of the study. Dr. Sanchez-Vega was also supported by an AACR-Minority and Minority-serving Institution Faculty Scholar in Cancer Research Award. Mr. Walch and Dr. Newman have disclosed no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM AACR 2023
Circulating DNA has promise for cancer detection, but faces challenges
Cancer screening remains challenging. There are screens available for a handful of solid tumors, but uptake is low caused in part by health care access barriers as well as the potential for unnecessary follow-up procedures, according to Phillip Febbo, MD.
These issues could threaten efforts like that of President Joe Biden’s Cancer Moonshot initiative, which aims to reduce cancer mortality by 50%. Advances in circulating tumor (ct) DNA analysis could help address these problems, but a lack of diversity among study participants needs to be addressed to ensure it has broad utility, continued Dr. Febbo, during his presentation at the annual meeting of the American Association for Cancer Research.
The problem is particularly acute among African American, Hispanic, and other underserved populations who often face health care barriers that can exacerbate the issue, said Dr. Febbo, who is chief medical officer for Illumina. The lack of access is compounded by the fact that there are only currently screens for lung, breast, colorectal, cervical, and prostate cancer, leaving a vast unmet need.
“We still do not have screening tests for 70% of the deaths that are due to cancer,” he said.
ctDNA released from dying cancer cells has the potential to reveal a wide range of cancer types and reduce barriers to access, because it is based on a blood test. It can be analyzed for various factors, including mutations, chromosomal rearrangements, methylation patterns, and other characteristics that hint at the presence of cancer. However, it can’t be successful without sufficient inclusion in research studies, Dr. Febbo explained.
“We have to ensure we have the right representation [of] populations when we develop these tests, when we go through the clinical trials, and as we bring these into communities,” he said.
During his presentation, Dr. Febbo shared a slide showing that about 78% of participants in published gene-association studies were White.
ctDNA showed promise in at least on recent study. Dr. Febbo discussed the ECLIPSE trial, which used the Guardant Health SHIELD assay for colorectal cancer (CRC). About 13% of its approximately 20,000 participants were Black or African American, 15% were Hispanic, and 7% were Asian Americans. It also included both urban and rural individuals. In results announced in December 2022, the researchers found a sensitivity of 83%, which was lower than the 92.3% found in standard CRC screening, but above the 74% threshold set by the Food and Drug Administration. The specificity was 90%.
One approach that could dramatically change the landscape of cancer screening is a multicancer early detection (MCED) test, according to Dr. Febbo. The CancerSeek MCED test, developed by Johns Hopkins Kimmel Cancer Center researchers, uses a series of genetic and protein biomarkers to detect all cancers, with the exception of leukemia, skin cancer, and central nervous system tumors. Among 10,006 women aged between 65 and 75 years with no history of cancer, it had a sensitivity of 27.1% and a specificity of 98.9%, with a positive predictive value of 19.4%. The study’s population was 95% non-Hispanic White.
He also discussed the Pathfinder study, sponsored by the Illumina subsidiary Grail, which included 6,662 individuals age 50 and over from seven sites in the United States, and grouped them into normal and increased risk; 92% were non-Hispanic White. It used the Galleri MCED test, which performed with a sensitivity of 29%, specificity of 99.1%, and a positive predictive value of 38.0%. False positives produced to limited burden, with 93% undergoing imaging, 28% nonsurgical invasive procedures, and 2% undergoing fruitless invasive surgical procedures.
Dr. Febbo touted the potential for such tests to greatly reduce cancer mortality, but only if there is adequate uptake of screening procedures, particularly in underserved groups. He put up a slide of a model showing that MCED has the potential to reduce cancer mortality by 20%, but only if the screen is widely accepted among all groups. “I’ve had my team model this. If we accept the current use of screening tests, and we don’t address disparities, and we don’t ensure everybody feels included and participates actively – not only in the research, but also in the testing and adoption, you would cut that potential benefit in half. That would be hundreds of thousands of lives lost because we didn’t address disparities.”
Successful recruiting of African Americans for research
Following Dr. Febbo’s talk, Karriem Watson, MS, spoke about some potential solutions to the issue, including his own experiences and success stories in recruiting African Americans to play active roles in research. He is chief engagement officer for the National Institute of Health’s All of Us Research Program, which aims to gather health data on at least 1 million residents of the United States. Mr. Watson has spent time reaching out to people living in communities in the Chicago area to encourage participation in breast cancer screening. An event at his church inspired his own sister to get a mammogram, and she was diagnosed with early-stage breast cancer.
“I’m a living witness that early engagement can lead to early detection,” said Mr. Watson during his talk.
He reported that the All of Us research program has succeeded in creating diversity within its data collection, as 46.7% of participants identify as racial and ethnic minorities.
Mr. Watson took issue with the common perception that underrepresented communities may be hard to reach.
“I want to challenge us to think outside the box and really ask ourselves: Are populations hard to reach, or are there opportunities for us to do better and more intentional engagement?” He went on to describe a program to recruit African American men as citizen scientists. He and his colleagues developed a network that included barbers, faith leaders, and fraternity and civic organization members to help recruit participants for a prostate cancer screening project. They exceeded their initial recruitment goal.
They went on to develop a network of barbers in the south and west sides of Chicago to recruit individuals to participate in studies of protein methylation and lung cancer screening, as well as a project that investigated associations between neighborhood of residence and lung cancer. The results of those efforts have also informed other projects, including a smoking cessation study. “We’ve not only included African American men in our research, but we’ve included them as part of our research team,” said Mr. Watson.
Dr. Febbo is also a stockholder of Illumina. Mr. Watson has no relevant financial disclosures.
From American Association for Cancer Research (AACR) Annual Meeting 2023: Improving cancer outcomes through equitable access to cfDNA tests. Presented Monday, April 17, 2023.
Cancer screening remains challenging. There are screens available for a handful of solid tumors, but uptake is low caused in part by health care access barriers as well as the potential for unnecessary follow-up procedures, according to Phillip Febbo, MD.
These issues could threaten efforts like that of President Joe Biden’s Cancer Moonshot initiative, which aims to reduce cancer mortality by 50%. Advances in circulating tumor (ct) DNA analysis could help address these problems, but a lack of diversity among study participants needs to be addressed to ensure it has broad utility, continued Dr. Febbo, during his presentation at the annual meeting of the American Association for Cancer Research.
The problem is particularly acute among African American, Hispanic, and other underserved populations who often face health care barriers that can exacerbate the issue, said Dr. Febbo, who is chief medical officer for Illumina. The lack of access is compounded by the fact that there are only currently screens for lung, breast, colorectal, cervical, and prostate cancer, leaving a vast unmet need.
“We still do not have screening tests for 70% of the deaths that are due to cancer,” he said.
ctDNA released from dying cancer cells has the potential to reveal a wide range of cancer types and reduce barriers to access, because it is based on a blood test. It can be analyzed for various factors, including mutations, chromosomal rearrangements, methylation patterns, and other characteristics that hint at the presence of cancer. However, it can’t be successful without sufficient inclusion in research studies, Dr. Febbo explained.
“We have to ensure we have the right representation [of] populations when we develop these tests, when we go through the clinical trials, and as we bring these into communities,” he said.
During his presentation, Dr. Febbo shared a slide showing that about 78% of participants in published gene-association studies were White.
ctDNA showed promise in at least on recent study. Dr. Febbo discussed the ECLIPSE trial, which used the Guardant Health SHIELD assay for colorectal cancer (CRC). About 13% of its approximately 20,000 participants were Black or African American, 15% were Hispanic, and 7% were Asian Americans. It also included both urban and rural individuals. In results announced in December 2022, the researchers found a sensitivity of 83%, which was lower than the 92.3% found in standard CRC screening, but above the 74% threshold set by the Food and Drug Administration. The specificity was 90%.
One approach that could dramatically change the landscape of cancer screening is a multicancer early detection (MCED) test, according to Dr. Febbo. The CancerSeek MCED test, developed by Johns Hopkins Kimmel Cancer Center researchers, uses a series of genetic and protein biomarkers to detect all cancers, with the exception of leukemia, skin cancer, and central nervous system tumors. Among 10,006 women aged between 65 and 75 years with no history of cancer, it had a sensitivity of 27.1% and a specificity of 98.9%, with a positive predictive value of 19.4%. The study’s population was 95% non-Hispanic White.
He also discussed the Pathfinder study, sponsored by the Illumina subsidiary Grail, which included 6,662 individuals age 50 and over from seven sites in the United States, and grouped them into normal and increased risk; 92% were non-Hispanic White. It used the Galleri MCED test, which performed with a sensitivity of 29%, specificity of 99.1%, and a positive predictive value of 38.0%. False positives produced to limited burden, with 93% undergoing imaging, 28% nonsurgical invasive procedures, and 2% undergoing fruitless invasive surgical procedures.
Dr. Febbo touted the potential for such tests to greatly reduce cancer mortality, but only if there is adequate uptake of screening procedures, particularly in underserved groups. He put up a slide of a model showing that MCED has the potential to reduce cancer mortality by 20%, but only if the screen is widely accepted among all groups. “I’ve had my team model this. If we accept the current use of screening tests, and we don’t address disparities, and we don’t ensure everybody feels included and participates actively – not only in the research, but also in the testing and adoption, you would cut that potential benefit in half. That would be hundreds of thousands of lives lost because we didn’t address disparities.”
Successful recruiting of African Americans for research
Following Dr. Febbo’s talk, Karriem Watson, MS, spoke about some potential solutions to the issue, including his own experiences and success stories in recruiting African Americans to play active roles in research. He is chief engagement officer for the National Institute of Health’s All of Us Research Program, which aims to gather health data on at least 1 million residents of the United States. Mr. Watson has spent time reaching out to people living in communities in the Chicago area to encourage participation in breast cancer screening. An event at his church inspired his own sister to get a mammogram, and she was diagnosed with early-stage breast cancer.
“I’m a living witness that early engagement can lead to early detection,” said Mr. Watson during his talk.
He reported that the All of Us research program has succeeded in creating diversity within its data collection, as 46.7% of participants identify as racial and ethnic minorities.
Mr. Watson took issue with the common perception that underrepresented communities may be hard to reach.
“I want to challenge us to think outside the box and really ask ourselves: Are populations hard to reach, or are there opportunities for us to do better and more intentional engagement?” He went on to describe a program to recruit African American men as citizen scientists. He and his colleagues developed a network that included barbers, faith leaders, and fraternity and civic organization members to help recruit participants for a prostate cancer screening project. They exceeded their initial recruitment goal.
They went on to develop a network of barbers in the south and west sides of Chicago to recruit individuals to participate in studies of protein methylation and lung cancer screening, as well as a project that investigated associations between neighborhood of residence and lung cancer. The results of those efforts have also informed other projects, including a smoking cessation study. “We’ve not only included African American men in our research, but we’ve included them as part of our research team,” said Mr. Watson.
Dr. Febbo is also a stockholder of Illumina. Mr. Watson has no relevant financial disclosures.
From American Association for Cancer Research (AACR) Annual Meeting 2023: Improving cancer outcomes through equitable access to cfDNA tests. Presented Monday, April 17, 2023.
Cancer screening remains challenging. There are screens available for a handful of solid tumors, but uptake is low caused in part by health care access barriers as well as the potential for unnecessary follow-up procedures, according to Phillip Febbo, MD.
These issues could threaten efforts like that of President Joe Biden’s Cancer Moonshot initiative, which aims to reduce cancer mortality by 50%. Advances in circulating tumor (ct) DNA analysis could help address these problems, but a lack of diversity among study participants needs to be addressed to ensure it has broad utility, continued Dr. Febbo, during his presentation at the annual meeting of the American Association for Cancer Research.
The problem is particularly acute among African American, Hispanic, and other underserved populations who often face health care barriers that can exacerbate the issue, said Dr. Febbo, who is chief medical officer for Illumina. The lack of access is compounded by the fact that there are only currently screens for lung, breast, colorectal, cervical, and prostate cancer, leaving a vast unmet need.
“We still do not have screening tests for 70% of the deaths that are due to cancer,” he said.
ctDNA released from dying cancer cells has the potential to reveal a wide range of cancer types and reduce barriers to access, because it is based on a blood test. It can be analyzed for various factors, including mutations, chromosomal rearrangements, methylation patterns, and other characteristics that hint at the presence of cancer. However, it can’t be successful without sufficient inclusion in research studies, Dr. Febbo explained.
“We have to ensure we have the right representation [of] populations when we develop these tests, when we go through the clinical trials, and as we bring these into communities,” he said.
During his presentation, Dr. Febbo shared a slide showing that about 78% of participants in published gene-association studies were White.
ctDNA showed promise in at least on recent study. Dr. Febbo discussed the ECLIPSE trial, which used the Guardant Health SHIELD assay for colorectal cancer (CRC). About 13% of its approximately 20,000 participants were Black or African American, 15% were Hispanic, and 7% were Asian Americans. It also included both urban and rural individuals. In results announced in December 2022, the researchers found a sensitivity of 83%, which was lower than the 92.3% found in standard CRC screening, but above the 74% threshold set by the Food and Drug Administration. The specificity was 90%.
One approach that could dramatically change the landscape of cancer screening is a multicancer early detection (MCED) test, according to Dr. Febbo. The CancerSeek MCED test, developed by Johns Hopkins Kimmel Cancer Center researchers, uses a series of genetic and protein biomarkers to detect all cancers, with the exception of leukemia, skin cancer, and central nervous system tumors. Among 10,006 women aged between 65 and 75 years with no history of cancer, it had a sensitivity of 27.1% and a specificity of 98.9%, with a positive predictive value of 19.4%. The study’s population was 95% non-Hispanic White.
He also discussed the Pathfinder study, sponsored by the Illumina subsidiary Grail, which included 6,662 individuals age 50 and over from seven sites in the United States, and grouped them into normal and increased risk; 92% were non-Hispanic White. It used the Galleri MCED test, which performed with a sensitivity of 29%, specificity of 99.1%, and a positive predictive value of 38.0%. False positives produced to limited burden, with 93% undergoing imaging, 28% nonsurgical invasive procedures, and 2% undergoing fruitless invasive surgical procedures.
Dr. Febbo touted the potential for such tests to greatly reduce cancer mortality, but only if there is adequate uptake of screening procedures, particularly in underserved groups. He put up a slide of a model showing that MCED has the potential to reduce cancer mortality by 20%, but only if the screen is widely accepted among all groups. “I’ve had my team model this. If we accept the current use of screening tests, and we don’t address disparities, and we don’t ensure everybody feels included and participates actively – not only in the research, but also in the testing and adoption, you would cut that potential benefit in half. That would be hundreds of thousands of lives lost because we didn’t address disparities.”
Successful recruiting of African Americans for research
Following Dr. Febbo’s talk, Karriem Watson, MS, spoke about some potential solutions to the issue, including his own experiences and success stories in recruiting African Americans to play active roles in research. He is chief engagement officer for the National Institute of Health’s All of Us Research Program, which aims to gather health data on at least 1 million residents of the United States. Mr. Watson has spent time reaching out to people living in communities in the Chicago area to encourage participation in breast cancer screening. An event at his church inspired his own sister to get a mammogram, and she was diagnosed with early-stage breast cancer.
“I’m a living witness that early engagement can lead to early detection,” said Mr. Watson during his talk.
He reported that the All of Us research program has succeeded in creating diversity within its data collection, as 46.7% of participants identify as racial and ethnic minorities.
Mr. Watson took issue with the common perception that underrepresented communities may be hard to reach.
“I want to challenge us to think outside the box and really ask ourselves: Are populations hard to reach, or are there opportunities for us to do better and more intentional engagement?” He went on to describe a program to recruit African American men as citizen scientists. He and his colleagues developed a network that included barbers, faith leaders, and fraternity and civic organization members to help recruit participants for a prostate cancer screening project. They exceeded their initial recruitment goal.
They went on to develop a network of barbers in the south and west sides of Chicago to recruit individuals to participate in studies of protein methylation and lung cancer screening, as well as a project that investigated associations between neighborhood of residence and lung cancer. The results of those efforts have also informed other projects, including a smoking cessation study. “We’ve not only included African American men in our research, but we’ve included them as part of our research team,” said Mr. Watson.
Dr. Febbo is also a stockholder of Illumina. Mr. Watson has no relevant financial disclosures.
From American Association for Cancer Research (AACR) Annual Meeting 2023: Improving cancer outcomes through equitable access to cfDNA tests. Presented Monday, April 17, 2023.
FROM AACR 2023
Use age, not weight, to screen for diabetes; assess over 35s
Universal screening of all U.S. adults aged 35-70 years for prediabetes and type 2 diabetes, regardless of body mass index, would provide the fairest means of detection, according to a new analysis.
This would better detect prediabetes and diabetes in ethnic groups that have a higher risk of diabetes at lower cutoffs. Compared with White individuals, Black or Hispanic adults have a higher risk of developing type 2 diabetes at a younger age, and Asian, Hispanic, and Black Americans all have a higher risk of developing it at a lower BMI.
In the new study, researchers examined six different screening scenarios in a nationally representative sample without diabetes.
They compared screening for prediabetes and type 2 diabetes using criteria from the 2021 U.S. Preventive Services Task Force (USPSTF) recommendations with the 2015 USPSTF recommendations, as well as four other screening thresholds with lower age or weight.
Universal screening for prediabetes and diabetes at age 35-70, regardless of BMI – which appears to be the sweet spot for most equitable detection in different races – may be easier to put into practice because it will mean clinicians don’t have to remember alternate cutoffs for different patient groups, the researchers suggested.
“All major racial and ethnic minority groups develop diabetes at lower weights than White adults, and it’s most pronounced for Asian Americans,” lead author Matthew J. O’Brien, MD, explained in a press release.
“If we make decisions about diabetes testing based on weight we will miss some people from racial and ethnic minority groups who are developing prediabetes and diabetes at lower weights,” said Dr. O’Brien, of Northwestern University, Chicago.
Going forward, to achieve equity in diagnosing prediabetes and diabetes “also requires addressing structural barriers [facing racial and ethnic minorities], which include not having a usual source of primary care, lacking health insurance, or having copays for screening tests based on insurance coverage,” the authors noted in their paper, published online in the American Journal of Preventive Medicine.
There is also a need for further study to examine the cost-effectiveness of any approach, and to study the impact of screening criteria on diagnosis, treatment, and outcomes in diverse populations.
Nationally representative sample, six screening scenarios
In the overall U.S. population, 81% of adults with prediabetes are unaware they have it, said Dr. O’Brien and colleagues, and 23% of diabetes cases are undiagnosed.
And Black, Hispanic, or Asian individuals have a nearly twofold higher prevalence of diabetes compared with White individuals.
The 2021 USPSTF recommendations state that clinicians should screen asymptomatic adults aged 35-70 years with overweight/obesity (BMI ≥ 25 kg/m2) and “should consider screening at an earlier age in persons from groups with disproportionately high incidence and prevalence (American Indian/Alaska Native, Asian American, Black, Hispanic/Latino, or Native Hawaiian/Pacific Islander persons) or in persons who have a family history of diabetes, a history of gestational diabetes, or a history of polycystic ovarian syndrome, and at a lower BMI in Asian American persons. Data suggest that a BMI of 23 or greater may be an appropriate cut point in Asian American persons.”
Dr. O’Brien and colleagues identified 3,243 nonpregnant adults without diagnosed diabetes who participated in the National Health and Nutrition Examination Survey (NHANES) in 2017-2020 and had an A1c blood test. (Half also had a fasting plasma glucose test.)
First, they compared screening using the more recent and earlier USPSTF criteria: BMI of at least 25 kg/m2 and age 35-70 (2021 criteria) and BMI of at least 25 kg/m2 and age 40-70 (2015 criteria).
They estimated that 13.9 million more adults would be eligible for screening using the 2021 versus the 2015 screening criteria.
The increases in screening eligibility were highest in Hispanic individuals (30.6%), followed by Asian individuals (17.9%), White individuals (14.0%), and Black individuals (13.9%).
Using the USPSTF 2021 versus 2015 screening criteria resulted in marginally higher sensitivity (58.6% vs. 52.9%) but lower specificity (69.3% vs. 76.4%) overall, as well as within each racial group.
Next, the researchers examined screening at two lower age cutoffs and two lower BMI cutoffs: BMI of at least 25 kg/m2 and age 30-70, BMI of at least 25 kg/m2 and age 18-70, age 35-70 and BMI of at least 23 kg/m2, and age 35-70 and any BMI.
Screening at these lower age and weight thresholds resulted in even greater sensitivity and lower specificity than using the 2021 USPSTF criteria, especially among Hispanic, non-Hispanic Black, and Asian adults.
However, screening all adults aged 35-70 years regardless of BMI yielded the most equitable detection of prediabetes and diabetes – with a sensitivity of 67.8% and a specificity of 52.1% in the overall population, and a sensitivity of 70.1%, 70.4%, 68.4%, and 67.6%, and a specificity of 53.8%, 59.9%, 56.2%, and 48.9%, in the Asian, Black, Hispanic, and White subgroups, respectively.
The American Diabetes Association currently recommends screening all adults aged ≥ 35 years, or at any age if they have overweight/obesity and an additional diabetes risk factor, the researchers noted.
The study was partly funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Universal screening of all U.S. adults aged 35-70 years for prediabetes and type 2 diabetes, regardless of body mass index, would provide the fairest means of detection, according to a new analysis.
This would better detect prediabetes and diabetes in ethnic groups that have a higher risk of diabetes at lower cutoffs. Compared with White individuals, Black or Hispanic adults have a higher risk of developing type 2 diabetes at a younger age, and Asian, Hispanic, and Black Americans all have a higher risk of developing it at a lower BMI.
In the new study, researchers examined six different screening scenarios in a nationally representative sample without diabetes.
They compared screening for prediabetes and type 2 diabetes using criteria from the 2021 U.S. Preventive Services Task Force (USPSTF) recommendations with the 2015 USPSTF recommendations, as well as four other screening thresholds with lower age or weight.
Universal screening for prediabetes and diabetes at age 35-70, regardless of BMI – which appears to be the sweet spot for most equitable detection in different races – may be easier to put into practice because it will mean clinicians don’t have to remember alternate cutoffs for different patient groups, the researchers suggested.
“All major racial and ethnic minority groups develop diabetes at lower weights than White adults, and it’s most pronounced for Asian Americans,” lead author Matthew J. O’Brien, MD, explained in a press release.
“If we make decisions about diabetes testing based on weight we will miss some people from racial and ethnic minority groups who are developing prediabetes and diabetes at lower weights,” said Dr. O’Brien, of Northwestern University, Chicago.
Going forward, to achieve equity in diagnosing prediabetes and diabetes “also requires addressing structural barriers [facing racial and ethnic minorities], which include not having a usual source of primary care, lacking health insurance, or having copays for screening tests based on insurance coverage,” the authors noted in their paper, published online in the American Journal of Preventive Medicine.
There is also a need for further study to examine the cost-effectiveness of any approach, and to study the impact of screening criteria on diagnosis, treatment, and outcomes in diverse populations.
Nationally representative sample, six screening scenarios
In the overall U.S. population, 81% of adults with prediabetes are unaware they have it, said Dr. O’Brien and colleagues, and 23% of diabetes cases are undiagnosed.
And Black, Hispanic, or Asian individuals have a nearly twofold higher prevalence of diabetes compared with White individuals.
The 2021 USPSTF recommendations state that clinicians should screen asymptomatic adults aged 35-70 years with overweight/obesity (BMI ≥ 25 kg/m2) and “should consider screening at an earlier age in persons from groups with disproportionately high incidence and prevalence (American Indian/Alaska Native, Asian American, Black, Hispanic/Latino, or Native Hawaiian/Pacific Islander persons) or in persons who have a family history of diabetes, a history of gestational diabetes, or a history of polycystic ovarian syndrome, and at a lower BMI in Asian American persons. Data suggest that a BMI of 23 or greater may be an appropriate cut point in Asian American persons.”
Dr. O’Brien and colleagues identified 3,243 nonpregnant adults without diagnosed diabetes who participated in the National Health and Nutrition Examination Survey (NHANES) in 2017-2020 and had an A1c blood test. (Half also had a fasting plasma glucose test.)
First, they compared screening using the more recent and earlier USPSTF criteria: BMI of at least 25 kg/m2 and age 35-70 (2021 criteria) and BMI of at least 25 kg/m2 and age 40-70 (2015 criteria).
They estimated that 13.9 million more adults would be eligible for screening using the 2021 versus the 2015 screening criteria.
The increases in screening eligibility were highest in Hispanic individuals (30.6%), followed by Asian individuals (17.9%), White individuals (14.0%), and Black individuals (13.9%).
Using the USPSTF 2021 versus 2015 screening criteria resulted in marginally higher sensitivity (58.6% vs. 52.9%) but lower specificity (69.3% vs. 76.4%) overall, as well as within each racial group.
Next, the researchers examined screening at two lower age cutoffs and two lower BMI cutoffs: BMI of at least 25 kg/m2 and age 30-70, BMI of at least 25 kg/m2 and age 18-70, age 35-70 and BMI of at least 23 kg/m2, and age 35-70 and any BMI.
Screening at these lower age and weight thresholds resulted in even greater sensitivity and lower specificity than using the 2021 USPSTF criteria, especially among Hispanic, non-Hispanic Black, and Asian adults.
However, screening all adults aged 35-70 years regardless of BMI yielded the most equitable detection of prediabetes and diabetes – with a sensitivity of 67.8% and a specificity of 52.1% in the overall population, and a sensitivity of 70.1%, 70.4%, 68.4%, and 67.6%, and a specificity of 53.8%, 59.9%, 56.2%, and 48.9%, in the Asian, Black, Hispanic, and White subgroups, respectively.
The American Diabetes Association currently recommends screening all adults aged ≥ 35 years, or at any age if they have overweight/obesity and an additional diabetes risk factor, the researchers noted.
The study was partly funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
Universal screening of all U.S. adults aged 35-70 years for prediabetes and type 2 diabetes, regardless of body mass index, would provide the fairest means of detection, according to a new analysis.
This would better detect prediabetes and diabetes in ethnic groups that have a higher risk of diabetes at lower cutoffs. Compared with White individuals, Black or Hispanic adults have a higher risk of developing type 2 diabetes at a younger age, and Asian, Hispanic, and Black Americans all have a higher risk of developing it at a lower BMI.
In the new study, researchers examined six different screening scenarios in a nationally representative sample without diabetes.
They compared screening for prediabetes and type 2 diabetes using criteria from the 2021 U.S. Preventive Services Task Force (USPSTF) recommendations with the 2015 USPSTF recommendations, as well as four other screening thresholds with lower age or weight.
Universal screening for prediabetes and diabetes at age 35-70, regardless of BMI – which appears to be the sweet spot for most equitable detection in different races – may be easier to put into practice because it will mean clinicians don’t have to remember alternate cutoffs for different patient groups, the researchers suggested.
“All major racial and ethnic minority groups develop diabetes at lower weights than White adults, and it’s most pronounced for Asian Americans,” lead author Matthew J. O’Brien, MD, explained in a press release.
“If we make decisions about diabetes testing based on weight we will miss some people from racial and ethnic minority groups who are developing prediabetes and diabetes at lower weights,” said Dr. O’Brien, of Northwestern University, Chicago.
Going forward, to achieve equity in diagnosing prediabetes and diabetes “also requires addressing structural barriers [facing racial and ethnic minorities], which include not having a usual source of primary care, lacking health insurance, or having copays for screening tests based on insurance coverage,” the authors noted in their paper, published online in the American Journal of Preventive Medicine.
There is also a need for further study to examine the cost-effectiveness of any approach, and to study the impact of screening criteria on diagnosis, treatment, and outcomes in diverse populations.
Nationally representative sample, six screening scenarios
In the overall U.S. population, 81% of adults with prediabetes are unaware they have it, said Dr. O’Brien and colleagues, and 23% of diabetes cases are undiagnosed.
And Black, Hispanic, or Asian individuals have a nearly twofold higher prevalence of diabetes compared with White individuals.
The 2021 USPSTF recommendations state that clinicians should screen asymptomatic adults aged 35-70 years with overweight/obesity (BMI ≥ 25 kg/m2) and “should consider screening at an earlier age in persons from groups with disproportionately high incidence and prevalence (American Indian/Alaska Native, Asian American, Black, Hispanic/Latino, or Native Hawaiian/Pacific Islander persons) or in persons who have a family history of diabetes, a history of gestational diabetes, or a history of polycystic ovarian syndrome, and at a lower BMI in Asian American persons. Data suggest that a BMI of 23 or greater may be an appropriate cut point in Asian American persons.”
Dr. O’Brien and colleagues identified 3,243 nonpregnant adults without diagnosed diabetes who participated in the National Health and Nutrition Examination Survey (NHANES) in 2017-2020 and had an A1c blood test. (Half also had a fasting plasma glucose test.)
First, they compared screening using the more recent and earlier USPSTF criteria: BMI of at least 25 kg/m2 and age 35-70 (2021 criteria) and BMI of at least 25 kg/m2 and age 40-70 (2015 criteria).
They estimated that 13.9 million more adults would be eligible for screening using the 2021 versus the 2015 screening criteria.
The increases in screening eligibility were highest in Hispanic individuals (30.6%), followed by Asian individuals (17.9%), White individuals (14.0%), and Black individuals (13.9%).
Using the USPSTF 2021 versus 2015 screening criteria resulted in marginally higher sensitivity (58.6% vs. 52.9%) but lower specificity (69.3% vs. 76.4%) overall, as well as within each racial group.
Next, the researchers examined screening at two lower age cutoffs and two lower BMI cutoffs: BMI of at least 25 kg/m2 and age 30-70, BMI of at least 25 kg/m2 and age 18-70, age 35-70 and BMI of at least 23 kg/m2, and age 35-70 and any BMI.
Screening at these lower age and weight thresholds resulted in even greater sensitivity and lower specificity than using the 2021 USPSTF criteria, especially among Hispanic, non-Hispanic Black, and Asian adults.
However, screening all adults aged 35-70 years regardless of BMI yielded the most equitable detection of prediabetes and diabetes – with a sensitivity of 67.8% and a specificity of 52.1% in the overall population, and a sensitivity of 70.1%, 70.4%, 68.4%, and 67.6%, and a specificity of 53.8%, 59.9%, 56.2%, and 48.9%, in the Asian, Black, Hispanic, and White subgroups, respectively.
The American Diabetes Association currently recommends screening all adults aged ≥ 35 years, or at any age if they have overweight/obesity and an additional diabetes risk factor, the researchers noted.
The study was partly funded by the National Institute of Diabetes and Digestive and Kidney Diseases of the National Institutes of Health. The authors have reported no relevant financial relationships.
A version of this article first appeared on Medscape.com.
FROM THE AMERICAN JOURNAL OF PREVENTIVE MEDICINE
AHA statement targets nuance in CVD risk assessment of women
In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.
They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.
The scientific statement was published online in Circulation.
Look beyond traditional risk factors
“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release.
“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.
Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.
Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.
The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.
“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.
“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
No one-size-fits-all approach
The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.
It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.
“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.
“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.
Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.
They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.
A version of this article first appeared on Medscape.com.
In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.
They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.
The scientific statement was published online in Circulation.
Look beyond traditional risk factors
“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release.
“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.
Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.
Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.
The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.
“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.
“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
No one-size-fits-all approach
The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.
It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.
“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.
“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.
Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.
They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.
A version of this article first appeared on Medscape.com.
In a new scientific statement, the American Heart Association highlighted the importance of incorporating nonbiological risk factors and social determinants of health in cardiovascular disease (CVD) risk assessment for women, particularly women from different racial and ethnic backgrounds.
CVD risk assessment in women is multifaceted and goes well beyond traditional risk factors to include sex-specific biological risk factors, as well as social, behavioral, and environmental factors, the writing group noted.
They said a greater focus on addressing all CVD risk factors among women from underrepresented races and ethnicities is warranted to avert future CVD.
The scientific statement was published online in Circulation.
Look beyond traditional risk factors
“Risk assessment is the first step in preventing heart disease, yet there are many limitations to traditional risk factors and their ability to comprehensively estimate a woman’s risk for cardiovascular disease,” Jennifer H. Mieres, MD, vice chair of the writing group and professor of cardiology at Hofstra University, Hempstead, N.Y., said in a news release.
“The delivery of equitable cardiovascular health care for women depends on improving the knowledge and awareness of all members of the healthcare team about the full spectrum of cardiovascular risk factors for women, including female-specific and female-predominant risk factors,” Dr. Mieres added.
Female-specific factors that should be included in CVD risk assessment include pregnancy-related conditions such as preeclampsia, preterm delivery, and gestational diabetes, the writing group said.
Other factors include menstrual cycle history; types of birth control and/or hormone replacement therapy used; polycystic ovarian syndrome (PCOS), which affects 10% of women of reproductive age and is associated with increased CVD risk; and autoimmune disorders, depression, and PTSD, all of which are more common in women and are also associated with higher risk for CVD.
The statement also highlights the key role that social determinants of health (SDOH) play in the development of CVD in women, particularly women from diverse racial and ethnic backgrounds. SDOH include education level, economic stability, neighborhood safety, working conditions, environmental hazards, and access to quality health care.
“It is critical that risk assessment be expanded to include [SDOH] as risk factors if we are to improve health outcomes in all women,” Laxmi Mehta, MD, chair of the writing group and director of preventative cardiology and women’s cardiovascular health at Ohio State University Wexner Medical Center, Columbus, said in the news release.
“It is also important for the health care team to consider [SDOH] when working with women on shared decisions about cardiovascular disease prevention and treatment,” Dr. Mehta noted.
No one-size-fits-all approach
The statement highlighted significant differences in CVD risk among women of different racial and ethnic backgrounds and provides detailed CV risk factor profiles for non-Hispanic Black, Hispanic/Latinx, Asian and American Indian/Alaska Native women.
It noted that language barriers, discrimination, acculturation, and health care access disproportionately affect women of underrepresented racial and ethnic groups. These factors result in a higher prevalence of CVD and significant challenges in CVD diagnosis and treatment.
“When customizing CVD prevention and treatment strategies to improve cardiovascular health for women, a one-size-fits-all approach is unlikely to be successful,” Dr. Mieres said.
“We must be cognizant of the complex interplay of sex, race and ethnicity, as well as social determinants of health, and how they impact the risk of cardiovascular disease and adverse outcomes in order to avert future CVD morbidity and mortality,” Dr. Mieres added.
Looking ahead, the writing group said future CVD prevention guidelines could be strengthened by including culturally-specific lifestyle recommendations.
They also said community-based approaches, faith-based community partnerships, and peer support to encourage a healthy lifestyle could play a key role in preventing CVD among all women.
This scientific statement was prepared by the volunteer writing group on behalf of the AHA’s Cardiovascular Disease and Stroke in Women and Underrepresented Populations Committee of the Council on Clinical Cardiology, the Council on Cardiovascular and Stroke Nursing, the Council on Hypertension, the Council on Lifelong Congenital Heart Disease and Heart Health in the Young, the Council on Lifestyle and Cardiometabolic Health, the Council on Peripheral Vascular Disease, and the Stroke Council.
A version of this article first appeared on Medscape.com.
FROM CIRCULATION
Melasma
THE COMPARISON
A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.
B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.
C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.
Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.
Epidemiology
Melasma commonly affects women ages 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2
Key clinical features in people with darker skin tones
Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5
Worth noting
Prevention
- Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
- Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
- Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.
Treatment
- First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
- Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or a-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
- Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or secondline topical therapy.
- Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots, and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
- Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
- Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.
Health disparity highlight
Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and self-esteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out of pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.
1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies. Dermatol Ther. 2017;30(3). doi:10.1111/dth.12465
8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone/tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
THE COMPARISON
A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.
B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.
C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.
Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.
Epidemiology
Melasma commonly affects women ages 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2
Key clinical features in people with darker skin tones
Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5
Worth noting
Prevention
- Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
- Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
- Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.
Treatment
- First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
- Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or a-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
- Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or secondline topical therapy.
- Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots, and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
- Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
- Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.
Health disparity highlight
Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and self-esteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out of pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.
THE COMPARISON
A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.
B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.
C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.
Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.
Epidemiology
Melasma commonly affects women ages 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2
Key clinical features in people with darker skin tones
Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5
Worth noting
Prevention
- Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
- Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
- Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.
Treatment
- First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
- Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or a-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
- Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or secondline topical therapy.
- Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots, and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
- Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
- Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.
Health disparity highlight
Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and self-esteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out of pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.
1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies. Dermatol Ther. 2017;30(3). doi:10.1111/dth.12465
8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone/tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
1. Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
2. Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
3. Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
4. Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
5. Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
6. Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
7. Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies. Dermatol Ther. 2017;30(3). doi:10.1111/dth.12465
8. Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
9. Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
10. Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
11. Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
12. Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
13. Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone/tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
Type of insurance linked to length of survival after lung surgery
The study used public insurance status as a marker for low socioeconomic status (SES) and suggests that patients with combined insurance may constitute a separate population that deserves more attention.
Lower SES has been linked to later stage diagnoses and worse outcomes in NSCLC. Private insurance is a generally-accepted indicator of higher SES, while public insurance like Medicare or Medicaid, alone or in combination with private supplementary insurance, is an indicator of lower SES.
Although previous studies have found associations between patients having public health insurance and experiencing later-stage diagnoses and worse overall survival, there have been few studies of surgical outcomes, and almost no research has examined combination health insurance, according to Allison O. Dumitriu Carcoana, who presented the research during a poster session at the European Lung Cancer Congress 2023.
“This is an important insurance subgroup for us because the majority of our patients fall into this subgroup by being over 65 years old and thus qualifying for Medicare while also paying for a private supplement,” said Ms. Dumitriu Carcoana, who is a medical student at University of South Florida Health Morsani College of Medicine, Tampa.
A previous analysis by the group found an association between private insurance status and better discharge status, as well as higher 5-year overall survival. After accumulating an additional 278 patients, the researchers examined 10-year survival outcomes.
In the new analysis, 52% of 711 participants had combination insurance, while 28% had private insurance, and 20% had public insurance. The subgroups all had similar demographic and histological characteristics. The study was unique in that it found no between-group differences in higher stage at diagnosis, whereas previous studies have found a greater risk of higher stage diagnosis among individuals with public insurance. As expected, patients in the combined insurance group had a higher mean age (P less than .0001) and higher Charlson comorbidity index scores (P = .0014), which in turn was associated with lower 10-year survival. The group also had the highest percentage of former smokers, while the public insurance group had the highest percentage of current smokers (P = .0003).
At both 5 and 10 years, the private insurance group had better OS than the group with public (P less than .001) and the combination insurance group (P = .08). Public health insurance was associated with worse OS at 5 years (hazard ratio, 1.83; P less than .005) but not at 10 years (HR, 1.18; P = .51), while combination insurance was associated with worse OS at 10 years (HR, 1.72; P = .02).
“We think that patients with public health insurance having the worst 5-year overall survival, despite their lower ages and fewer comorbid conditions, compared with patients with combination insurance, highlights the impact of lower socioeconomic status on health outcomes. These patients had the same tumor characteristics, BMI, sex, and race as our patients in the other two insurance groups. The only other significant risk factor [the group had besides having a higher proportion of patients with lower socioeconomic status was that it had a higher proportion of current smokers]. But the multivariate analyses showed that insurance status was an independent predictor of survival, regardless of smoking status or other comorbidities,” said Ms. Dumitriu Carcoana.
“At 10 years post-operatively, the survival curves have shifted and the combination patients had the worst 10-year overall survival. We attribute this to their higher number of comorbid conditions and increased age. In practice, [this means that] the group of patients with public insurance type, but no supplement, should be identified clinically, and the clinical team can initiate a discussion,” Ms. Dumitriu Carcoana said.
“Do these patients feel that they can make follow-up appointments, keep up with medication costs, and make the right lifestyle decisions postoperatively on their current insurance plan? If not, can they afford a private supplement? In our cohort specifically, it may also be important to do more preoperative counseling on the importance of smoking cessation,” she added.
The study is interesting, but it has some important limitations, according to Raja Flores, MD, who was not involved with the study. The authors stated that there was no difference between the insurance groups with respect to mortality or cancer stage, which is the most important predictor of survival. However, the poster didn't include details of the authors' analysis, making it difficult to interpret, Dr. Flores said.
The fact that the study includes a single surgeon has some disadvantages in terms of broader applicability, but it also controls for surgical technique. “Different surgeons have different ways of doing things, so if you had the same surgeon doing it the same way every time, you can look at other variables like insurance (status) and stage,” said Dr. Flores.
The results may also provide an argument against using robotic surgery in patients who do not have insurance, especially since they have not been proven to be better than standard minimally invasive surgery with no robotic assistance. With uninsured patients, “you’re using taxpayer money for a more expensive procedure that isn’t proving to be any better,” Dr. Flores explained.
The study was performed at a single center and cannot prove causation due to its retrospective nature.
Ms. Dumitriu Carcoana and Dr. Flores have no relevant financial disclosures.
*This article was updated on 4/13/2023.
The study used public insurance status as a marker for low socioeconomic status (SES) and suggests that patients with combined insurance may constitute a separate population that deserves more attention.
Lower SES has been linked to later stage diagnoses and worse outcomes in NSCLC. Private insurance is a generally-accepted indicator of higher SES, while public insurance like Medicare or Medicaid, alone or in combination with private supplementary insurance, is an indicator of lower SES.
Although previous studies have found associations between patients having public health insurance and experiencing later-stage diagnoses and worse overall survival, there have been few studies of surgical outcomes, and almost no research has examined combination health insurance, according to Allison O. Dumitriu Carcoana, who presented the research during a poster session at the European Lung Cancer Congress 2023.
“This is an important insurance subgroup for us because the majority of our patients fall into this subgroup by being over 65 years old and thus qualifying for Medicare while also paying for a private supplement,” said Ms. Dumitriu Carcoana, who is a medical student at University of South Florida Health Morsani College of Medicine, Tampa.
A previous analysis by the group found an association between private insurance status and better discharge status, as well as higher 5-year overall survival. After accumulating an additional 278 patients, the researchers examined 10-year survival outcomes.
In the new analysis, 52% of 711 participants had combination insurance, while 28% had private insurance, and 20% had public insurance. The subgroups all had similar demographic and histological characteristics. The study was unique in that it found no between-group differences in higher stage at diagnosis, whereas previous studies have found a greater risk of higher stage diagnosis among individuals with public insurance. As expected, patients in the combined insurance group had a higher mean age (P less than .0001) and higher Charlson comorbidity index scores (P = .0014), which in turn was associated with lower 10-year survival. The group also had the highest percentage of former smokers, while the public insurance group had the highest percentage of current smokers (P = .0003).
At both 5 and 10 years, the private insurance group had better OS than the group with public (P less than .001) and the combination insurance group (P = .08). Public health insurance was associated with worse OS at 5 years (hazard ratio, 1.83; P less than .005) but not at 10 years (HR, 1.18; P = .51), while combination insurance was associated with worse OS at 10 years (HR, 1.72; P = .02).
“We think that patients with public health insurance having the worst 5-year overall survival, despite their lower ages and fewer comorbid conditions, compared with patients with combination insurance, highlights the impact of lower socioeconomic status on health outcomes. These patients had the same tumor characteristics, BMI, sex, and race as our patients in the other two insurance groups. The only other significant risk factor [the group had besides having a higher proportion of patients with lower socioeconomic status was that it had a higher proportion of current smokers]. But the multivariate analyses showed that insurance status was an independent predictor of survival, regardless of smoking status or other comorbidities,” said Ms. Dumitriu Carcoana.
“At 10 years post-operatively, the survival curves have shifted and the combination patients had the worst 10-year overall survival. We attribute this to their higher number of comorbid conditions and increased age. In practice, [this means that] the group of patients with public insurance type, but no supplement, should be identified clinically, and the clinical team can initiate a discussion,” Ms. Dumitriu Carcoana said.
“Do these patients feel that they can make follow-up appointments, keep up with medication costs, and make the right lifestyle decisions postoperatively on their current insurance plan? If not, can they afford a private supplement? In our cohort specifically, it may also be important to do more preoperative counseling on the importance of smoking cessation,” she added.
The study is interesting, but it has some important limitations, according to Raja Flores, MD, who was not involved with the study. The authors stated that there was no difference between the insurance groups with respect to mortality or cancer stage, which is the most important predictor of survival. However, the poster didn't include details of the authors' analysis, making it difficult to interpret, Dr. Flores said.
The fact that the study includes a single surgeon has some disadvantages in terms of broader applicability, but it also controls for surgical technique. “Different surgeons have different ways of doing things, so if you had the same surgeon doing it the same way every time, you can look at other variables like insurance (status) and stage,” said Dr. Flores.
The results may also provide an argument against using robotic surgery in patients who do not have insurance, especially since they have not been proven to be better than standard minimally invasive surgery with no robotic assistance. With uninsured patients, “you’re using taxpayer money for a more expensive procedure that isn’t proving to be any better,” Dr. Flores explained.
The study was performed at a single center and cannot prove causation due to its retrospective nature.
Ms. Dumitriu Carcoana and Dr. Flores have no relevant financial disclosures.
*This article was updated on 4/13/2023.
The study used public insurance status as a marker for low socioeconomic status (SES) and suggests that patients with combined insurance may constitute a separate population that deserves more attention.
Lower SES has been linked to later stage diagnoses and worse outcomes in NSCLC. Private insurance is a generally-accepted indicator of higher SES, while public insurance like Medicare or Medicaid, alone or in combination with private supplementary insurance, is an indicator of lower SES.
Although previous studies have found associations between patients having public health insurance and experiencing later-stage diagnoses and worse overall survival, there have been few studies of surgical outcomes, and almost no research has examined combination health insurance, according to Allison O. Dumitriu Carcoana, who presented the research during a poster session at the European Lung Cancer Congress 2023.
“This is an important insurance subgroup for us because the majority of our patients fall into this subgroup by being over 65 years old and thus qualifying for Medicare while also paying for a private supplement,” said Ms. Dumitriu Carcoana, who is a medical student at University of South Florida Health Morsani College of Medicine, Tampa.
A previous analysis by the group found an association between private insurance status and better discharge status, as well as higher 5-year overall survival. After accumulating an additional 278 patients, the researchers examined 10-year survival outcomes.
In the new analysis, 52% of 711 participants had combination insurance, while 28% had private insurance, and 20% had public insurance. The subgroups all had similar demographic and histological characteristics. The study was unique in that it found no between-group differences in higher stage at diagnosis, whereas previous studies have found a greater risk of higher stage diagnosis among individuals with public insurance. As expected, patients in the combined insurance group had a higher mean age (P less than .0001) and higher Charlson comorbidity index scores (P = .0014), which in turn was associated with lower 10-year survival. The group also had the highest percentage of former smokers, while the public insurance group had the highest percentage of current smokers (P = .0003).
At both 5 and 10 years, the private insurance group had better OS than the group with public (P less than .001) and the combination insurance group (P = .08). Public health insurance was associated with worse OS at 5 years (hazard ratio, 1.83; P less than .005) but not at 10 years (HR, 1.18; P = .51), while combination insurance was associated with worse OS at 10 years (HR, 1.72; P = .02).
“We think that patients with public health insurance having the worst 5-year overall survival, despite their lower ages and fewer comorbid conditions, compared with patients with combination insurance, highlights the impact of lower socioeconomic status on health outcomes. These patients had the same tumor characteristics, BMI, sex, and race as our patients in the other two insurance groups. The only other significant risk factor [the group had besides having a higher proportion of patients with lower socioeconomic status was that it had a higher proportion of current smokers]. But the multivariate analyses showed that insurance status was an independent predictor of survival, regardless of smoking status or other comorbidities,” said Ms. Dumitriu Carcoana.
“At 10 years post-operatively, the survival curves have shifted and the combination patients had the worst 10-year overall survival. We attribute this to their higher number of comorbid conditions and increased age. In practice, [this means that] the group of patients with public insurance type, but no supplement, should be identified clinically, and the clinical team can initiate a discussion,” Ms. Dumitriu Carcoana said.
“Do these patients feel that they can make follow-up appointments, keep up with medication costs, and make the right lifestyle decisions postoperatively on their current insurance plan? If not, can they afford a private supplement? In our cohort specifically, it may also be important to do more preoperative counseling on the importance of smoking cessation,” she added.
The study is interesting, but it has some important limitations, according to Raja Flores, MD, who was not involved with the study. The authors stated that there was no difference between the insurance groups with respect to mortality or cancer stage, which is the most important predictor of survival. However, the poster didn't include details of the authors' analysis, making it difficult to interpret, Dr. Flores said.
The fact that the study includes a single surgeon has some disadvantages in terms of broader applicability, but it also controls for surgical technique. “Different surgeons have different ways of doing things, so if you had the same surgeon doing it the same way every time, you can look at other variables like insurance (status) and stage,” said Dr. Flores.
The results may also provide an argument against using robotic surgery in patients who do not have insurance, especially since they have not been proven to be better than standard minimally invasive surgery with no robotic assistance. With uninsured patients, “you’re using taxpayer money for a more expensive procedure that isn’t proving to be any better,” Dr. Flores explained.
The study was performed at a single center and cannot prove causation due to its retrospective nature.
Ms. Dumitriu Carcoana and Dr. Flores have no relevant financial disclosures.
*This article was updated on 4/13/2023.
FROM ELCC 2023
Melasma
THE COMPARISON
A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.
B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.
C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.
Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.
Epidemiology
Melasma commonly affects women aged 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2
Key clinical features in people with darker skin tones
Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5
Worth noting
Prevention
• Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
• Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
• Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.
Treatment
• First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
• Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or α-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
• Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or second-line topical therapy.
• Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
• Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
• Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.
Health disparity highlight
Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and selfesteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out-of-pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.
- Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
- Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
- Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
- Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
- Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
- Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
- Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies [published online January 30, 2017]. Dermatol Ther. doi:10.1111/dth.12465
- Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
- Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
- Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
- Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
- Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
- Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone /tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
THE COMPARISON
A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.
B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.
C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.
Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.
Epidemiology
Melasma commonly affects women aged 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2
Key clinical features in people with darker skin tones
Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5
Worth noting
Prevention
• Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
• Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
• Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.
Treatment
• First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
• Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or α-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
• Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or second-line topical therapy.
• Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
• Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
• Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.
Health disparity highlight
Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and selfesteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out-of-pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.
THE COMPARISON
A Melasma on the face of a Hispanic woman, with hyperpigmentation on the cheeks, bridge of the nose, and upper lip.
B Melasma on the face of a Malaysian woman, with hyperpigmentation on the upper cheeks and bridge of the nose.
C Melasma on the face of an African woman, with hyperpigmentation on the upper cheeks and lateral to the eyes.
Melasma (also known as chloasma) is a pigmentary disorder that causes chronic symmetric hyperpigmentation on the face. In patients with darker skin tones, centrofacial areas are affected.1 Increased deposition of melanin distributed in the dermis leads to dermal melanosis. Newer research suggests that mast cell and keratinocyte interactions, altered gene regulation, neovascularization, and disruptions in the basement membrane cause melasma.2 Patients present with epidermal or dermal melasma or a combination of both (mixed melasma).3 Wood lamp examination is helpful to distinguish between epidermal and dermal melasma. Dermal and mixed melasma can be difficult to treat and require multimodal treatments.
Epidemiology
Melasma commonly affects women aged 20 to 40 years,4 with a female to male ratio of 9:1.5 Potential triggers of melasma include hormones (eg, pregnancy, oral contraceptives, hormone replacement therapy) and exposure to UV light.2,5 Melasma occurs in patients of all racial and ethnic backgrounds; however, the prevalence is higher in patients with darker skin tones.2
Key clinical features in people with darker skin tones
Melasma commonly manifests as symmetrically distributed, reticulated (lacy), dark brown to grayish brown patches on the cheeks, nose, forehead, upper lip, and chin in patients with darker skin tones.5 The pigment can be tan brown in patients with lighter skin tones. Given that postinflammatory hyperpigmentation and other pigmentary disorders can cause a similar appearance, a biopsy sometimes is needed to confirm the diagnosis, but melasma is diagnosed via physical examination in most patients. Melasma can be misdiagnosed as postinflammatory hyperpigmentation, solar lentigines, exogenous ochronosis, and Hori nevus.5
Worth noting
Prevention
• Daily sunscreen use is critical to prevent worsening of melasma. Sunscreen may not appear cosmetically elegant on darker skin tones, which creates a barrier to its use.6 Protection from both sunlight and visible light is necessary. Visible light, including light from light bulbs and device-emitted blue light, can worsen melasma. Iron oxides in tinted sunscreen offer protection from visible light.
• Physicians can recommend sunscreens that are more transparent or tinted for a better cosmetic match.
• Severe flares of melasma can occur with sun exposure despite good control with medications and laser modalities.
Treatment
• First-line therapies include topical hydroquinone 2% to 4%, tretinoin, azelaic acid, kojic acid, or ascorbic acid (vitamin C). A popular topical compound is a steroid, tretinoin, and hydroquinone.1,5 Over-the-counter hydroquinone has been removed from the market due to safety concerns; however, it is still first line in the treatment of melasma. If hydroquinone is prescribed, treatment intervals of 6 to 8 weeks followed by a hydroquinone-free period is advised to reduce the risk for exogenous ochronosis (a paradoxical darkening of the skin).
• Chemical peels are second-line treatments that are effective for melasma. Improvement in epidermal melasma has been shown with chemical peels containing Jessner solution, salicylic acid, or α-hydroxy acid. Patients with dermal and mixed melasma have seen improvement with trichloroacetic acid 25% to 35% with or without Jessner solution.1
• Cysteamine is a topical treatment created from the degradation of coenzyme A. It disrupts the synthesis of melanin to create a more even skin tone. It may be recommended in combination with sunscreen as a first-line or second-line topical therapy.
• Oral tranexamic acid is a third-line treatment that is an analogue for lysine. It decreases prostaglandin production, which leads to a lower number of tyrosine precursors available for the creation of melanin. Tranexamic acid has been shown to lighten the appearance of melasma.7 The most common and dangerous adverse effect of tranexamic acid is blood clots and this treatment should be avoided in those on combination (estrogen and progestin) contraceptives or those with a personal or family history of clotting disorders.8
• Fourth-line treatments such as lasers (performed by dermatologists) can destroy the deposition of pigment while avoiding destruction of epidermal keratinocytes.1,9,10 They also are commonly employed in refractive melasma. The most common lasers are nonablative fractionated lasers and low-fluence Q-switched lasers. The Q-switched Nd:YAG and picosecond lasers are safe for treating melasma in darker skin tones. Ablative fractionated lasers such as CO2 lasers and erbium:YAG lasers also have been used in the treatment of melasma; however, there is still an extremely high risk for postinflammatory dyspigmentation 1 to 2 months after the procedure.10
• Although there is still a risk for rebound hyperpigmentation after laser treatment, use of topical hydroquinone pretreatment may help decrease postoperative hyperpigmentation.1,5 Patients who are treated with the incorrect laser or overtreated may develop postinflammatory hyperpigmentation, rebound hyperpigmentation, or hypopigmentation.
Health disparity highlight
Melasma, most common in patients with skin of color, is a common chronic pigmentation disorder that is cosmetically and psychologically burdensome,11 leading to decreased quality of life, emotional functioning, and selfesteem.12 Clinicians should counsel patients and work closely on long-term management. The treatment options for melasma are considered cosmetic and may be cost prohibitive for many to cover out-of-pocket. Topical treatments have been found to be the most cost-effective.13 Some compounding pharmacies and drug discount programs provide more affordable treatment pricing; however, some patients are still unable to afford these options.
- Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
- Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
- Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
- Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
- Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
- Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
- Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies [published online January 30, 2017]. Dermatol Ther. doi:10.1111/dth.12465
- Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
- Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
- Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
- Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
- Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
- Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone /tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
- Cunha PR, Kroumpouzos G. Melasma and vitiligo: novel and experimental therapies. J Clin Exp Derm Res. 2016;7:2. doi:10.4172/2155-9554.1000e106
- Rajanala S, Maymone MBC, Vashi NA. Melasma pathogenesis: a review of the latest research, pathological findings, and investigational therapies. Dermatol Online J. 2019;25:13030/qt47b7r28c.
- Grimes PE, Yamada N, Bhawan J. Light microscopic, immunohistochemical, and ultrastructural alterations in patients with melasma. Am J Dermatopathol. 2005;27:96-101.
- Achar A, Rathi SK. Melasma: a clinico-epidemiological study of 312 cases. Indian J Dermatol. 2011;56:380-382.
- Ogbechie-Godec OA, Elbuluk N. Melasma: an up-to-date comprehensive review. Dermatol Ther. 2017;7:305-318.
- Morquette AJ, Waples ER, Heath CR. The importance of cosmetically elegant sunscreen in skin of color populations. J Cosmet Dermatol. 2022;21:1337-1338.
- Taraz M, Nikham S, Ehsani AH. Tranexamic acid in treatment of melasma: a comprehensive review of clinical studies [published online January 30, 2017]. Dermatol Ther. doi:10.1111/dth.12465
- Bala HR, Lee S, Wong C, et al. Oral tranexamic acid for the treatment of melasma: a review. Dermatol Surg. 2018;44:814-825.
- Castanedo-Cazares JP, Hernandez-Blanco D, Carlos-Ortega B, et al. Near-visible light and UV photoprotection in the treatment of melasma: a double-blind randomized trial. Photodermatol Photoimmunol Photomed. 2014;30:35-42.
- Trivedi MK, Yang FC, Cho BK. A review of laser and light therapy in melasma. Int J Womens Dermatol. 2017;3:11-20.
- Dodmani PN, Deshmukh AR. Assessment of quality of life of melasma patients as per melasma quality of life scale (MELASQoL). Pigment Int. 2020;7:75-79.
- Balkrishnan R, McMichael A, Camacho FT, et al. Development and validation of a health‐related quality of life instrument for women with melasma. Br J Dermatol. 2003;149:572-577.
- Alikhan A, Daly M, Wu J, et al. Cost-effectiveness of a hydroquinone /tretinoin/fluocinolone acetonide cream combination in treating melasma in the United States. J Dermatolog Treat. 2010;21:276-281.
Treatment of Frontal Fibrosing Alopecia in Black Patients: A Systematic Review
Frontal fibrosing alopecia (FFA) is a lymphocytic cicatricial alopecia that primarily affects postmenopausal women. Considered a subtype of lichen planopilaris (LPP), FFA is histologically identical but presents as symmetric frontotemporal hairline recession rather than the multifocal distribution typical of LPP (Figure 1). Patients also may experience symptoms such as itching, facial papules, and eyebrow loss. As a progressive and scarring alopecia, early management of FFA is necessary to prevent permanent hair loss; however, there still are no clear guidelines regarding the efficacy of different treatment options for FFA due to a lack of randomized controlled studies in the literature. Patients with skin of color (SOC) also may have varying responses to treatment, further complicating the establishment of any treatment algorithm. Furthermore, symptoms, clinical findings, and demographics of FFA have been observed to vary across different ethnicities, especially among Black individuals. We conducted a systematic review of the literature on FFA in Black patients, with an analysis of demographics, clinical findings, concomitant skin conditions, treatments given, and treatment responses.
Methods
A PubMed search of articles indexed for MEDLINE was conducted of studies investigating FFA in patients with SOC from January 1, 2000, through November 30, 2020, using the terms frontal fibrosing alopecia, ethnicity, African, Black, Asian, Indian, Hispanic, and Latino. Articles were included if they were available in English and discussed treatment and clinical outcomes of FFA in Black individuals. The reference lists of included studies also were reviewed. Articles were assessed for quality of evidence using a 4-point scale (1=well-designed randomized controlled trials; 2=controlled trials with limitations or well-designed cohort or case-control studies; 3=case series with or without intervention; 4=case reports). Variables related to study type, patient demographics, treatments, and clinical outcomes were recorded.
Results
Of the 69 search results, 8 studies—2 retrospective cohort studies, 3 case series, and 3 case reports—describing 51 Black individuals with FFA were included in our review (eTable). Of these, 49 (96.1%) were female and 2 (3.9%) were male. Of the 45 females with data available for menopausal status, 24 (53.3%) were premenopausal and 21 (46.7%) were postmenopausal; data were not available for 4 females. Patients identified as African or African American in 27 (52.9%) cases, South African in 19 (37.3%), Black in 3 (5.9%), Indian in 1 (2.0%), and Afro-Caribbean in 1 (2.0%). The average age of FFA onset was 43.8 years in females (raw data available in 24 patients) and 35 years in males (raw data available in 2 patients). A family history of hair loss was reported in 15.7% (8/51) of patients.
Involved areas of hair loss included the frontotemporal hairline (51/51 [100%]), eyebrows (32/51 [62.7%]), limbs (4/51 [7.8%]), occiput (4/51 [7.8%]), facial hair (2/51 [3.9%]), vertex scalp (1/51 [2.0%]), and eyelashes (1/51 [2.0%]). Patchy alopecia suggestive of LPP was reported in 2 (3.9%) patients.
Patients frequently presented with scalp pruritus (26/51 [51.0%]), perifollicular papules or pustules (9/51 [17.6%]), and perifollicular hyperpigmentation (9/51 [17.6%]). Other associated symptoms included perifollicular erythema (6/51 [11.8%]), scalp pain (5/51 [9.8%]), hyperkeratosis or flaking (3/51 [5.9%]), and facial papules (2/51 [3.9%]). Loss of follicular ostia, prominent follicular ostia, and the lonely hair sign (Figure 2) was described in 21 (41.2%), 5 (9.8%), and 15 (29.4%) of patients, respectively. Hairstyles that involve scalp traction (19/51 [37.3%]) and/or chemicals (28/51 [54.9%]), such as hair dye or chemical relaxers, commonly were reported in patients prior to the onset of FFA.
The most commonly reported dermatologic comorbidities included traction alopecia (17/51 [33.3%]), followed by lichen planus pigmentosus (LLPigm)(7/51 [13.7%]), LPP (2/51 [3.9%]), psoriasis (1/51 [2.0%]), and morphea (1/51 [2.0%]). Reported comorbid diseases included Sjögren syndrome (2/51 [3.9%]), hypothyroidism (2/51 [3.9%]), HIV (1/51 [2.0%]), and diabetes mellitus (1/51 [2.0%]).
Of available reports (n=32), the most common histologic findings included perifollicular fibrosis (23/32 [71.9%]), lichenoid lymphocytic inflammation (22/23 [95.7%]) primarily affecting the isthmus and infundibular areas of the follicles, and decreased follicular density (21/23 [91.3%]).
The average time interval from treatment initiation to treatment assessment in available reports (n=25) was 1.8 years (range, 0.5–2 years). Response to treatment included regrowth of hair in 5.9% (3/51) of patients, FFA stabilization in 39.2% (20/51), FFA progression in 51.0% (26/51), and not reported in 3.9% (2/51). Combination therapy was used in 84.3% (43/51) of patients, while monotherapy was used in 11.8% (6/51), and 3.9% (2/51) did not have any treatment reported. Response to treatment was highly variable among patients, as were the combinations of therapeutic agents used (Table). Regrowth of hair was rare, occurring in only 2 (100%) patients treated with oral prednisone plus hydroxychloroquine (HCQ) or chloroquine (CHQ), and in 1 (50.0%) patient treated with topical corticosteroids plus antifungal shampoo, while there was no response in the other patient treated with this combination.
Improvement in hair loss, defined as having at least slowed progression of FFA, was observed in 100% (2/2) of patients who had oral steroids as part of their treatment regimen, followed by 5-alpha-reductase inhibitors (5-ARIs)(finasteride and dutasteride; 62.5% [5/8]), intralesional steroids (57.1% [8/14]), HCQ/CHQ (42.9% [15/35]), topical steroids (41.5% [17/41]), antifungal shampoo (40.0% [2/5]), topical/oral minoxidil (36.0% [9/25]), and tacrolimus (33.3% [7/21]).
Comment
Frontal fibrosing alopecia is a progressive scarring alopecia and a clinical variant of LPP. First described in 1994 by Kossard,1 it initially was thought to be a disease of postmenopausal White women. Although still most prevalent in White individuals, there has been a growing number of reports describing FFA in patients with SOC, including Black individuals.10 Despite the increasing number of cases over the years, studies on the treatment of FFA remain sparse. Without expert guidelines, treatments usually are chosen based on clinician preferences. Few observational studies on these treatment modalities and their clinical outcomes exist, and the cohorts largely are composed of White patients.10-12 However, Black individuals may respond differently to these treatments, just as they have been shown to exhibit unique features of FFA.3
Demographics of Patients With FFA—Consistent with our findings, prior studies have found that Black patients are more likely to be younger and premenopausal at FFA onset than their White counterparts.13-15 Among the Black individuals included in our review, the majority were premenopausal (53%) with an average age of FFA onset of 46.7 years. Conversely, only 5% of 60 White females with FFA reported in a retrospective review were premenopausal and had an older mean age of FFA onset of 64 years,1 substantiating prior reports.
Clinical Findings in Patients With FFA—The clinical findings observed in our cohort were consistent with what has previously been described in Black patients, including loss of follicular ostia (41.2%), lonely hair sign (29.4%), perifollicular erythema (11.8%), perifollicular papules (17.6%), and hyperkeratosis or flaking (5.9%). In comparing these findings with a review of 932 patients, 86% of whom were White, the observed frequencies of follicular ostia loss (38.3%) and lonely hair sign (26.7%) were similar; however, perifollicular erythema (44.2%), and hyperkeratosis (44.4%) were more prevalent in this group, while perifollicular papules (6.2%) were less common compared to our Black cohort.16 An explanation for this discrepancy in perifollicular erythema may be the increased skin pigmentation diminishing the appearance of erythema in Black individuals. Our cohort of Black individuals noted the presence of follicular hyperpigmentation (17.6%) and a high prevalence of scalp pruritus (51.0%), which appear to be more common in Black patients.3,17 Although it is unclear why these differences in FFA presentation exist, it may be helpful for clinicians to be aware of these unique features when examining Black patients with suspected FFA.
Concomitant Cutaneous Disorders—A notable proportion of our cohort also had concomitant traction alopecia, which presents with frontotemporal alopecia, similar to FFA, making the diagnosis more challenging; however, the presence of perifollicular hyperpigmentation and facial hyperpigmentation in FFA may aid in differentiating these 2 entities.3 Other concomitant conditions noted in our review included androgenic alopecia, Sjögren syndrome, psoriasis, hypothyroidism, morphea, and HIV, suggesting a potential interplay between autoimmune, genetic, hormonal, and environmental components in the etiology of FFA. In fact, a recent study found that a persistent inflammatory response, loss of immune privilege, and a genetic susceptibility are some of the key processes in the pathogenesis of FFA.18 Although the authors speculated that there may be other triggers in initiating the onset of FFA, such as steroid hormones, sun exposure, and topical allergens, more evidence and controlled studies are needed
Additionally, concomitant LPPigm occurred in 13.7% of our FFA cohort, which appears to be more common in patients with darker skin types.5,19-21 Lichen planus pigmentosus is a rare variant of LPP, and previous reports suggest that it may be associated with FFA.5 Similar to FFA, the pathogenesis of LPPigm also is unclear, and its treatment may be just as difficult.22 Because LPPigm may occur before, during, or after onset of FFA,23 it may be helpful for clinicians to search for the signs of LPPigm in patients with darker skin types patients presenting with hair loss both as a diagnostic clue and so that treatment may be tailored to both conditions.
Response to Treatment—Similar to the varying clinical pictures, the response to treatment also can vary between patients of different ethnicities. For Black patients, treatment outcomes did not seem as successful as they did for other patients with SOC described in the literature. A retrospective cohort of 58 Asian individuals with FFA found that up to 90% had improvement or stabilization of FFA after treatment,23 while only 45.1% (23/51) of the Black patients included in our study had improvement or stabilization. One reason may be that a greater proportion of Black patients are premenopausal at FFA onset (53%) compared to what is reported in Asian patients (28%),23 and women who are premenopausal at FFA onset often face more severe disease.15 Although there may be additional explanations for these differences in treatment outcomes between ethnic groups, further investigation is needed.
All patients included in our study received either monotherapy or combination therapy of topical/intralesional/oral steroids, HCQ or CHQ, 5-ARIs, topical/oral minoxidil, antifungal shampoo, and/or a calcineurin inhibitor; however, most patients (51.0%) did not see a response to treatment, while only 45.1% showed slowed or halted progression of FFA. Hair regrowth was rare, occurring in only 3 (5.9%) patients; 2 of them were the only patients treated with oral prednisone, making for a potentially promising therapeutic for Black patients that should be further investigated in larger controlled cohort studies. In a prior study, intramuscular steroids (40 mg every 3 weeks) plus topical minoxidil were unsuccessful in slowing the progression of FFA in 3 postmenopausal women,24 which may be explained by the racial differences in the response to FFA treatments and perhaps also menopausal status. Although not included in any of the regimens in our review, isotretinoin was shown to be effective in an ethnically unspecified group of patients (n=16) and also may be efficacious in Black individuals.25 Although FFA may stabilize with time,26 this was not observed in any of the patients included in our study; however, we only included patients who were treated, making it impossible to discern whether resolution was idiopathic or due to treatment.
Future Research—Research on treatments for FFA is lacking, especially in patients with SOC. Although we observed that there may be differences in the treatment response among Black individuals compared to other patients with SOC, additional studies are needed to delineate these racial differences, which can help guide management. More randomized controlled trials evaluating the various treatment regimens also are required to establish treatment guidelines. Frontal fibrosing alopecia likely is underdiagnosed in Black individuals, contributing to the lack of research in this group. Darker skin can obscure some of the clinical and dermoscopic features that are more visible in fair skin. Furthermore, it may be challenging to distinguish clinical features of FFA in the setting of concomitant traction alopecia, which is more common in Black patients.27 Frontal fibrosing alopecia presenting in Black women also is less likely to be biopsied, contributing to the tendency to miss FFA in favor of traction or androgenic alopecia, which often are assumed to be more common in this population.2,27 Therefore, histologic evaluation through biopsy is paramount in securing an accurate diagnosis for Black patients with frontotemporal alopecia.
Study Limitations—The studies included in our review were limited by a lack of control comparison groups, especially among the retrospective cohort studies. Additionally, some of the studies included cases refractory to prior treatment modalities, possibly leading to a selection bias of more severe cases that were not representative of FFA in the general population. Thus, further studies involving larger populations of those with SOC are needed to fully evaluate the clinical utility of the current treatment modalities in this group.
- Kossard S. Postmenopausal frontal fibrosing alopecia. scarring alopecia in a pattern distribution. Arch Dermatol. 1994;130:770-774.
- Dlova NC, Jordaan HF, Skenjane A, et al. Frontal fibrosing alopecia: a clinical review of 20 black patients from South Africa. Br J Dermatol. 2013;169:939-941. doi:10.1111/bjd.12424
- Callender VD, Reid SD, Obayan O, et al. Diagnostic clues to frontal fibrosing alopecia in patients of African descent. J Clin Aesthet Dermatol. 2016;9:45-51.
- Donati A, Molina L, Doche I, et al. Facial papules in frontal fibrosing alopecia: evidence of vellus follicle involvement. Arch Dermatol. 2011;147:1424-1427. doi:10.1001/archdermatol.2011.321
- Uwakwe LN, Cardwell LA, Dothard EH, et al. Frontal fibrosing alopecia and concomitant lichen planus pigmentosus: a case series of seven African American women. J Drugs Dermatol. 2018;17:397-400.
- Naz E, Vidaurrázaga C, Hernández-Cano N, et al. Postmenopausal frontal fibrosing alopecia. Clin Exp Dermatol. 2003;28:25-27. doi:10.1046/j.1365-2230.2003.01131.x
- Dlova NC, Goh CL. Frontal fibrosing alopecia in an African man. Int J Dermatol. 2015;54:81-83. doi:10.1111/j.1365-4632.2012.05821.x
- Huerth K, Kindred C. Frontal fibrosing alopecia presenting as androgenetic alopecia in an African American woman. J Drugs Dermatol. 2020;19:794-795. doi:10.36849/jdd.2020.4682
- Furlan KC, Kakizaki P, Chartuni JC, et al. Frontal fibrosing alopecia in association with Sjögren’s syndrome: more than a simple coincidence. An Bras Dermatol. 2016;91(5 suppl 1):14-16. doi:10.1590/abd1806-4841.20164526
- Zhang M, Zhang L, Rosman IS, et al. Frontal fibrosing alopecia demographics: a survey of 29 patients. Cutis. 2019;103:E16-E22.
- MacDonald A, Clark C, Holmes S. Frontal fibrosing alopecia: a review of 60 cases. J Am Acad Dermatol. 2012;67:955-961. doi:10.1016/j.jaad.2011.12.038
- Starace M, Brandi N, Alessandrini A, et al. Frontal fibrosing alopecia: a case series of 65 patients seen in a single Italian centre. J Eur Acad Dermatol Venereol. 2019;33:433-438. doi:10.1111/jdv.15372
- Dlova NC. Frontal fibrosing alopecia and lichen planus pigmentosus: is there a link? Br J Dermatol. 2013;168:439-442. doi:10.1111/j.1365-2133.2012.11146.x
- Petrof G, Cuell A, Rajkomar VV, et al. Retrospective review of 18 British South Asian women with frontal fibrosing alopecia. Int J Dermatol. 2018;57:490-491. doi:10.1111/ijd.13929
- Mervis JS, Borda LJ, Miteva M. Facial and extrafacial lesions in an ethnically diverse series of 91 patients with frontal fibrosing alopecia followed at a single center. Dermatology. 2019;235:112-119. doi:10.1159/000494603
- Valesky EM, Maier MD, Kippenberger S, et al. Frontal fibrosing alopecia - review of recent case reports and case series in PubMed. J Dtsch Dermatol Ges. Aug 2018;16:992-999. doi:10.1111/ddg.13601
- Adotama P, Callender V, Kolla A, et al. Comparing the clinical differences in white and black women with frontal fibrosing alopecia. Br J Dermatol. 2021;185:1074-1076. doi:10.1111/bjd.20605
- Miao YJ, Jing J, Du XF, et al. Frontal fibrosing alopecia: a review of disease pathogenesis. Front Med (Lausanne). 2022;9:911944. doi:10.3389/fmed.2022.911944
- Pirmez R, Duque-Estrada B, Donati A, et al. Clinical and dermoscopic features of lichen planus pigmentosus in 37 patients with frontal fibrosing alopecia. Br J Dermatol. 2016;175:1387-1390. doi:10.1111/bjd.14722
- Berliner JG, McCalmont TH, Price VH, et al. Frontal fibrosing alopecia and lichen planus pigmentosus. J Am Acad Dermatol. 2014;71:E26-E27. doi:10.1016/j.jaad.2013.12.031
- Romiti R, Biancardi Gavioli CF, et al. Clinical and histopathological findings of frontal fibrosing alopecia-associated lichen planus pigmentosus. Skin Appendage Disord. 2017;3:59-63. doi:10.1159/000456038
- Mulinari-Brenner FA, Guilherme MR, Peretti MC, et al. Frontal fibrosing alopecia and lichen planus pigmentosus: diagnosis and therapeutic challenge. An Bras Dermatol. 2017;92(5 suppl 1):79-81. doi:10.1590/abd1806-4841.20175833
- Panchaprateep R, Ruxrungtham P, Chancheewa B, et al. Clinical characteristics, trichoscopy, histopathology and treatment outcomes of frontal fibrosing alopecia in an Asian population: a retro-prospective cohort study. J Dermatol. 2020;47:1301-1311. doi:10.1111/1346-8138.15517
- Tosti A, Piraccini BM, Iorizzo M, et al. Frontal fibrosing alopecia in postmenopausal women. J Am Acad Dermatol. 2005;52:55-60. doi:10.1016/j.jaad.2004.05.014
- Rokni GR, Emadi SN, Dabbaghzade A, et al. Evaluating the combined efficacy of oral isotretinoin and topical tacrolimus versus oral finasteride and topical tacrolimus in frontal fibrosing alopecia—a randomized controlled trial. J Cosmet Dermatol. 2023;22:613-619. doi:10.1111/jocd.15232
- Kossard S, Lee MS, Wilkinson B. Postmenopausal frontal fibrosing alopecia: a frontal variant of lichen planopilaris. J Am Acad Dermatol. 1997;36:59-66. doi:10.1016/s0190-9622(97)70326-8
- Miteva M, Whiting D, Harries M, et al. Frontal fibrosing alopecia in black patients. Br J Dermatol. 2012;167:208-210. doi:10.1111/j.1365-2133.2012.10809.x
Frontal fibrosing alopecia (FFA) is a lymphocytic cicatricial alopecia that primarily affects postmenopausal women. Considered a subtype of lichen planopilaris (LPP), FFA is histologically identical but presents as symmetric frontotemporal hairline recession rather than the multifocal distribution typical of LPP (Figure 1). Patients also may experience symptoms such as itching, facial papules, and eyebrow loss. As a progressive and scarring alopecia, early management of FFA is necessary to prevent permanent hair loss; however, there still are no clear guidelines regarding the efficacy of different treatment options for FFA due to a lack of randomized controlled studies in the literature. Patients with skin of color (SOC) also may have varying responses to treatment, further complicating the establishment of any treatment algorithm. Furthermore, symptoms, clinical findings, and demographics of FFA have been observed to vary across different ethnicities, especially among Black individuals. We conducted a systematic review of the literature on FFA in Black patients, with an analysis of demographics, clinical findings, concomitant skin conditions, treatments given, and treatment responses.
Methods
A PubMed search of articles indexed for MEDLINE was conducted of studies investigating FFA in patients with SOC from January 1, 2000, through November 30, 2020, using the terms frontal fibrosing alopecia, ethnicity, African, Black, Asian, Indian, Hispanic, and Latino. Articles were included if they were available in English and discussed treatment and clinical outcomes of FFA in Black individuals. The reference lists of included studies also were reviewed. Articles were assessed for quality of evidence using a 4-point scale (1=well-designed randomized controlled trials; 2=controlled trials with limitations or well-designed cohort or case-control studies; 3=case series with or without intervention; 4=case reports). Variables related to study type, patient demographics, treatments, and clinical outcomes were recorded.
Results
Of the 69 search results, 8 studies—2 retrospective cohort studies, 3 case series, and 3 case reports—describing 51 Black individuals with FFA were included in our review (eTable). Of these, 49 (96.1%) were female and 2 (3.9%) were male. Of the 45 females with data available for menopausal status, 24 (53.3%) were premenopausal and 21 (46.7%) were postmenopausal; data were not available for 4 females. Patients identified as African or African American in 27 (52.9%) cases, South African in 19 (37.3%), Black in 3 (5.9%), Indian in 1 (2.0%), and Afro-Caribbean in 1 (2.0%). The average age of FFA onset was 43.8 years in females (raw data available in 24 patients) and 35 years in males (raw data available in 2 patients). A family history of hair loss was reported in 15.7% (8/51) of patients.
Involved areas of hair loss included the frontotemporal hairline (51/51 [100%]), eyebrows (32/51 [62.7%]), limbs (4/51 [7.8%]), occiput (4/51 [7.8%]), facial hair (2/51 [3.9%]), vertex scalp (1/51 [2.0%]), and eyelashes (1/51 [2.0%]). Patchy alopecia suggestive of LPP was reported in 2 (3.9%) patients.
Patients frequently presented with scalp pruritus (26/51 [51.0%]), perifollicular papules or pustules (9/51 [17.6%]), and perifollicular hyperpigmentation (9/51 [17.6%]). Other associated symptoms included perifollicular erythema (6/51 [11.8%]), scalp pain (5/51 [9.8%]), hyperkeratosis or flaking (3/51 [5.9%]), and facial papules (2/51 [3.9%]). Loss of follicular ostia, prominent follicular ostia, and the lonely hair sign (Figure 2) was described in 21 (41.2%), 5 (9.8%), and 15 (29.4%) of patients, respectively. Hairstyles that involve scalp traction (19/51 [37.3%]) and/or chemicals (28/51 [54.9%]), such as hair dye or chemical relaxers, commonly were reported in patients prior to the onset of FFA.
The most commonly reported dermatologic comorbidities included traction alopecia (17/51 [33.3%]), followed by lichen planus pigmentosus (LLPigm)(7/51 [13.7%]), LPP (2/51 [3.9%]), psoriasis (1/51 [2.0%]), and morphea (1/51 [2.0%]). Reported comorbid diseases included Sjögren syndrome (2/51 [3.9%]), hypothyroidism (2/51 [3.9%]), HIV (1/51 [2.0%]), and diabetes mellitus (1/51 [2.0%]).
Of available reports (n=32), the most common histologic findings included perifollicular fibrosis (23/32 [71.9%]), lichenoid lymphocytic inflammation (22/23 [95.7%]) primarily affecting the isthmus and infundibular areas of the follicles, and decreased follicular density (21/23 [91.3%]).
The average time interval from treatment initiation to treatment assessment in available reports (n=25) was 1.8 years (range, 0.5–2 years). Response to treatment included regrowth of hair in 5.9% (3/51) of patients, FFA stabilization in 39.2% (20/51), FFA progression in 51.0% (26/51), and not reported in 3.9% (2/51). Combination therapy was used in 84.3% (43/51) of patients, while monotherapy was used in 11.8% (6/51), and 3.9% (2/51) did not have any treatment reported. Response to treatment was highly variable among patients, as were the combinations of therapeutic agents used (Table). Regrowth of hair was rare, occurring in only 2 (100%) patients treated with oral prednisone plus hydroxychloroquine (HCQ) or chloroquine (CHQ), and in 1 (50.0%) patient treated with topical corticosteroids plus antifungal shampoo, while there was no response in the other patient treated with this combination.
Improvement in hair loss, defined as having at least slowed progression of FFA, was observed in 100% (2/2) of patients who had oral steroids as part of their treatment regimen, followed by 5-alpha-reductase inhibitors (5-ARIs)(finasteride and dutasteride; 62.5% [5/8]), intralesional steroids (57.1% [8/14]), HCQ/CHQ (42.9% [15/35]), topical steroids (41.5% [17/41]), antifungal shampoo (40.0% [2/5]), topical/oral minoxidil (36.0% [9/25]), and tacrolimus (33.3% [7/21]).
Comment
Frontal fibrosing alopecia is a progressive scarring alopecia and a clinical variant of LPP. First described in 1994 by Kossard,1 it initially was thought to be a disease of postmenopausal White women. Although still most prevalent in White individuals, there has been a growing number of reports describing FFA in patients with SOC, including Black individuals.10 Despite the increasing number of cases over the years, studies on the treatment of FFA remain sparse. Without expert guidelines, treatments usually are chosen based on clinician preferences. Few observational studies on these treatment modalities and their clinical outcomes exist, and the cohorts largely are composed of White patients.10-12 However, Black individuals may respond differently to these treatments, just as they have been shown to exhibit unique features of FFA.3
Demographics of Patients With FFA—Consistent with our findings, prior studies have found that Black patients are more likely to be younger and premenopausal at FFA onset than their White counterparts.13-15 Among the Black individuals included in our review, the majority were premenopausal (53%) with an average age of FFA onset of 46.7 years. Conversely, only 5% of 60 White females with FFA reported in a retrospective review were premenopausal and had an older mean age of FFA onset of 64 years,1 substantiating prior reports.
Clinical Findings in Patients With FFA—The clinical findings observed in our cohort were consistent with what has previously been described in Black patients, including loss of follicular ostia (41.2%), lonely hair sign (29.4%), perifollicular erythema (11.8%), perifollicular papules (17.6%), and hyperkeratosis or flaking (5.9%). In comparing these findings with a review of 932 patients, 86% of whom were White, the observed frequencies of follicular ostia loss (38.3%) and lonely hair sign (26.7%) were similar; however, perifollicular erythema (44.2%), and hyperkeratosis (44.4%) were more prevalent in this group, while perifollicular papules (6.2%) were less common compared to our Black cohort.16 An explanation for this discrepancy in perifollicular erythema may be the increased skin pigmentation diminishing the appearance of erythema in Black individuals. Our cohort of Black individuals noted the presence of follicular hyperpigmentation (17.6%) and a high prevalence of scalp pruritus (51.0%), which appear to be more common in Black patients.3,17 Although it is unclear why these differences in FFA presentation exist, it may be helpful for clinicians to be aware of these unique features when examining Black patients with suspected FFA.
Concomitant Cutaneous Disorders—A notable proportion of our cohort also had concomitant traction alopecia, which presents with frontotemporal alopecia, similar to FFA, making the diagnosis more challenging; however, the presence of perifollicular hyperpigmentation and facial hyperpigmentation in FFA may aid in differentiating these 2 entities.3 Other concomitant conditions noted in our review included androgenic alopecia, Sjögren syndrome, psoriasis, hypothyroidism, morphea, and HIV, suggesting a potential interplay between autoimmune, genetic, hormonal, and environmental components in the etiology of FFA. In fact, a recent study found that a persistent inflammatory response, loss of immune privilege, and a genetic susceptibility are some of the key processes in the pathogenesis of FFA.18 Although the authors speculated that there may be other triggers in initiating the onset of FFA, such as steroid hormones, sun exposure, and topical allergens, more evidence and controlled studies are needed
Additionally, concomitant LPPigm occurred in 13.7% of our FFA cohort, which appears to be more common in patients with darker skin types.5,19-21 Lichen planus pigmentosus is a rare variant of LPP, and previous reports suggest that it may be associated with FFA.5 Similar to FFA, the pathogenesis of LPPigm also is unclear, and its treatment may be just as difficult.22 Because LPPigm may occur before, during, or after onset of FFA,23 it may be helpful for clinicians to search for the signs of LPPigm in patients with darker skin types patients presenting with hair loss both as a diagnostic clue and so that treatment may be tailored to both conditions.
Response to Treatment—Similar to the varying clinical pictures, the response to treatment also can vary between patients of different ethnicities. For Black patients, treatment outcomes did not seem as successful as they did for other patients with SOC described in the literature. A retrospective cohort of 58 Asian individuals with FFA found that up to 90% had improvement or stabilization of FFA after treatment,23 while only 45.1% (23/51) of the Black patients included in our study had improvement or stabilization. One reason may be that a greater proportion of Black patients are premenopausal at FFA onset (53%) compared to what is reported in Asian patients (28%),23 and women who are premenopausal at FFA onset often face more severe disease.15 Although there may be additional explanations for these differences in treatment outcomes between ethnic groups, further investigation is needed.
All patients included in our study received either monotherapy or combination therapy of topical/intralesional/oral steroids, HCQ or CHQ, 5-ARIs, topical/oral minoxidil, antifungal shampoo, and/or a calcineurin inhibitor; however, most patients (51.0%) did not see a response to treatment, while only 45.1% showed slowed or halted progression of FFA. Hair regrowth was rare, occurring in only 3 (5.9%) patients; 2 of them were the only patients treated with oral prednisone, making for a potentially promising therapeutic for Black patients that should be further investigated in larger controlled cohort studies. In a prior study, intramuscular steroids (40 mg every 3 weeks) plus topical minoxidil were unsuccessful in slowing the progression of FFA in 3 postmenopausal women,24 which may be explained by the racial differences in the response to FFA treatments and perhaps also menopausal status. Although not included in any of the regimens in our review, isotretinoin was shown to be effective in an ethnically unspecified group of patients (n=16) and also may be efficacious in Black individuals.25 Although FFA may stabilize with time,26 this was not observed in any of the patients included in our study; however, we only included patients who were treated, making it impossible to discern whether resolution was idiopathic or due to treatment.
Future Research—Research on treatments for FFA is lacking, especially in patients with SOC. Although we observed that there may be differences in the treatment response among Black individuals compared to other patients with SOC, additional studies are needed to delineate these racial differences, which can help guide management. More randomized controlled trials evaluating the various treatment regimens also are required to establish treatment guidelines. Frontal fibrosing alopecia likely is underdiagnosed in Black individuals, contributing to the lack of research in this group. Darker skin can obscure some of the clinical and dermoscopic features that are more visible in fair skin. Furthermore, it may be challenging to distinguish clinical features of FFA in the setting of concomitant traction alopecia, which is more common in Black patients.27 Frontal fibrosing alopecia presenting in Black women also is less likely to be biopsied, contributing to the tendency to miss FFA in favor of traction or androgenic alopecia, which often are assumed to be more common in this population.2,27 Therefore, histologic evaluation through biopsy is paramount in securing an accurate diagnosis for Black patients with frontotemporal alopecia.
Study Limitations—The studies included in our review were limited by a lack of control comparison groups, especially among the retrospective cohort studies. Additionally, some of the studies included cases refractory to prior treatment modalities, possibly leading to a selection bias of more severe cases that were not representative of FFA in the general population. Thus, further studies involving larger populations of those with SOC are needed to fully evaluate the clinical utility of the current treatment modalities in this group.
Frontal fibrosing alopecia (FFA) is a lymphocytic cicatricial alopecia that primarily affects postmenopausal women. Considered a subtype of lichen planopilaris (LPP), FFA is histologically identical but presents as symmetric frontotemporal hairline recession rather than the multifocal distribution typical of LPP (Figure 1). Patients also may experience symptoms such as itching, facial papules, and eyebrow loss. As a progressive and scarring alopecia, early management of FFA is necessary to prevent permanent hair loss; however, there still are no clear guidelines regarding the efficacy of different treatment options for FFA due to a lack of randomized controlled studies in the literature. Patients with skin of color (SOC) also may have varying responses to treatment, further complicating the establishment of any treatment algorithm. Furthermore, symptoms, clinical findings, and demographics of FFA have been observed to vary across different ethnicities, especially among Black individuals. We conducted a systematic review of the literature on FFA in Black patients, with an analysis of demographics, clinical findings, concomitant skin conditions, treatments given, and treatment responses.
Methods
A PubMed search of articles indexed for MEDLINE was conducted of studies investigating FFA in patients with SOC from January 1, 2000, through November 30, 2020, using the terms frontal fibrosing alopecia, ethnicity, African, Black, Asian, Indian, Hispanic, and Latino. Articles were included if they were available in English and discussed treatment and clinical outcomes of FFA in Black individuals. The reference lists of included studies also were reviewed. Articles were assessed for quality of evidence using a 4-point scale (1=well-designed randomized controlled trials; 2=controlled trials with limitations or well-designed cohort or case-control studies; 3=case series with or without intervention; 4=case reports). Variables related to study type, patient demographics, treatments, and clinical outcomes were recorded.
Results
Of the 69 search results, 8 studies—2 retrospective cohort studies, 3 case series, and 3 case reports—describing 51 Black individuals with FFA were included in our review (eTable). Of these, 49 (96.1%) were female and 2 (3.9%) were male. Of the 45 females with data available for menopausal status, 24 (53.3%) were premenopausal and 21 (46.7%) were postmenopausal; data were not available for 4 females. Patients identified as African or African American in 27 (52.9%) cases, South African in 19 (37.3%), Black in 3 (5.9%), Indian in 1 (2.0%), and Afro-Caribbean in 1 (2.0%). The average age of FFA onset was 43.8 years in females (raw data available in 24 patients) and 35 years in males (raw data available in 2 patients). A family history of hair loss was reported in 15.7% (8/51) of patients.
Involved areas of hair loss included the frontotemporal hairline (51/51 [100%]), eyebrows (32/51 [62.7%]), limbs (4/51 [7.8%]), occiput (4/51 [7.8%]), facial hair (2/51 [3.9%]), vertex scalp (1/51 [2.0%]), and eyelashes (1/51 [2.0%]). Patchy alopecia suggestive of LPP was reported in 2 (3.9%) patients.
Patients frequently presented with scalp pruritus (26/51 [51.0%]), perifollicular papules or pustules (9/51 [17.6%]), and perifollicular hyperpigmentation (9/51 [17.6%]). Other associated symptoms included perifollicular erythema (6/51 [11.8%]), scalp pain (5/51 [9.8%]), hyperkeratosis or flaking (3/51 [5.9%]), and facial papules (2/51 [3.9%]). Loss of follicular ostia, prominent follicular ostia, and the lonely hair sign (Figure 2) was described in 21 (41.2%), 5 (9.8%), and 15 (29.4%) of patients, respectively. Hairstyles that involve scalp traction (19/51 [37.3%]) and/or chemicals (28/51 [54.9%]), such as hair dye or chemical relaxers, commonly were reported in patients prior to the onset of FFA.
The most commonly reported dermatologic comorbidities included traction alopecia (17/51 [33.3%]), followed by lichen planus pigmentosus (LLPigm)(7/51 [13.7%]), LPP (2/51 [3.9%]), psoriasis (1/51 [2.0%]), and morphea (1/51 [2.0%]). Reported comorbid diseases included Sjögren syndrome (2/51 [3.9%]), hypothyroidism (2/51 [3.9%]), HIV (1/51 [2.0%]), and diabetes mellitus (1/51 [2.0%]).
Of available reports (n=32), the most common histologic findings included perifollicular fibrosis (23/32 [71.9%]), lichenoid lymphocytic inflammation (22/23 [95.7%]) primarily affecting the isthmus and infundibular areas of the follicles, and decreased follicular density (21/23 [91.3%]).
The average time interval from treatment initiation to treatment assessment in available reports (n=25) was 1.8 years (range, 0.5–2 years). Response to treatment included regrowth of hair in 5.9% (3/51) of patients, FFA stabilization in 39.2% (20/51), FFA progression in 51.0% (26/51), and not reported in 3.9% (2/51). Combination therapy was used in 84.3% (43/51) of patients, while monotherapy was used in 11.8% (6/51), and 3.9% (2/51) did not have any treatment reported. Response to treatment was highly variable among patients, as were the combinations of therapeutic agents used (Table). Regrowth of hair was rare, occurring in only 2 (100%) patients treated with oral prednisone plus hydroxychloroquine (HCQ) or chloroquine (CHQ), and in 1 (50.0%) patient treated with topical corticosteroids plus antifungal shampoo, while there was no response in the other patient treated with this combination.
Improvement in hair loss, defined as having at least slowed progression of FFA, was observed in 100% (2/2) of patients who had oral steroids as part of their treatment regimen, followed by 5-alpha-reductase inhibitors (5-ARIs)(finasteride and dutasteride; 62.5% [5/8]), intralesional steroids (57.1% [8/14]), HCQ/CHQ (42.9% [15/35]), topical steroids (41.5% [17/41]), antifungal shampoo (40.0% [2/5]), topical/oral minoxidil (36.0% [9/25]), and tacrolimus (33.3% [7/21]).
Comment
Frontal fibrosing alopecia is a progressive scarring alopecia and a clinical variant of LPP. First described in 1994 by Kossard,1 it initially was thought to be a disease of postmenopausal White women. Although still most prevalent in White individuals, there has been a growing number of reports describing FFA in patients with SOC, including Black individuals.10 Despite the increasing number of cases over the years, studies on the treatment of FFA remain sparse. Without expert guidelines, treatments usually are chosen based on clinician preferences. Few observational studies on these treatment modalities and their clinical outcomes exist, and the cohorts largely are composed of White patients.10-12 However, Black individuals may respond differently to these treatments, just as they have been shown to exhibit unique features of FFA.3
Demographics of Patients With FFA—Consistent with our findings, prior studies have found that Black patients are more likely to be younger and premenopausal at FFA onset than their White counterparts.13-15 Among the Black individuals included in our review, the majority were premenopausal (53%) with an average age of FFA onset of 46.7 years. Conversely, only 5% of 60 White females with FFA reported in a retrospective review were premenopausal and had an older mean age of FFA onset of 64 years,1 substantiating prior reports.
Clinical Findings in Patients With FFA—The clinical findings observed in our cohort were consistent with what has previously been described in Black patients, including loss of follicular ostia (41.2%), lonely hair sign (29.4%), perifollicular erythema (11.8%), perifollicular papules (17.6%), and hyperkeratosis or flaking (5.9%). In comparing these findings with a review of 932 patients, 86% of whom were White, the observed frequencies of follicular ostia loss (38.3%) and lonely hair sign (26.7%) were similar; however, perifollicular erythema (44.2%), and hyperkeratosis (44.4%) were more prevalent in this group, while perifollicular papules (6.2%) were less common compared to our Black cohort.16 An explanation for this discrepancy in perifollicular erythema may be the increased skin pigmentation diminishing the appearance of erythema in Black individuals. Our cohort of Black individuals noted the presence of follicular hyperpigmentation (17.6%) and a high prevalence of scalp pruritus (51.0%), which appear to be more common in Black patients.3,17 Although it is unclear why these differences in FFA presentation exist, it may be helpful for clinicians to be aware of these unique features when examining Black patients with suspected FFA.
Concomitant Cutaneous Disorders—A notable proportion of our cohort also had concomitant traction alopecia, which presents with frontotemporal alopecia, similar to FFA, making the diagnosis more challenging; however, the presence of perifollicular hyperpigmentation and facial hyperpigmentation in FFA may aid in differentiating these 2 entities.3 Other concomitant conditions noted in our review included androgenic alopecia, Sjögren syndrome, psoriasis, hypothyroidism, morphea, and HIV, suggesting a potential interplay between autoimmune, genetic, hormonal, and environmental components in the etiology of FFA. In fact, a recent study found that a persistent inflammatory response, loss of immune privilege, and a genetic susceptibility are some of the key processes in the pathogenesis of FFA.18 Although the authors speculated that there may be other triggers in initiating the onset of FFA, such as steroid hormones, sun exposure, and topical allergens, more evidence and controlled studies are needed
Additionally, concomitant LPPigm occurred in 13.7% of our FFA cohort, which appears to be more common in patients with darker skin types.5,19-21 Lichen planus pigmentosus is a rare variant of LPP, and previous reports suggest that it may be associated with FFA.5 Similar to FFA, the pathogenesis of LPPigm also is unclear, and its treatment may be just as difficult.22 Because LPPigm may occur before, during, or after onset of FFA,23 it may be helpful for clinicians to search for the signs of LPPigm in patients with darker skin types patients presenting with hair loss both as a diagnostic clue and so that treatment may be tailored to both conditions.
Response to Treatment—Similar to the varying clinical pictures, the response to treatment also can vary between patients of different ethnicities. For Black patients, treatment outcomes did not seem as successful as they did for other patients with SOC described in the literature. A retrospective cohort of 58 Asian individuals with FFA found that up to 90% had improvement or stabilization of FFA after treatment,23 while only 45.1% (23/51) of the Black patients included in our study had improvement or stabilization. One reason may be that a greater proportion of Black patients are premenopausal at FFA onset (53%) compared to what is reported in Asian patients (28%),23 and women who are premenopausal at FFA onset often face more severe disease.15 Although there may be additional explanations for these differences in treatment outcomes between ethnic groups, further investigation is needed.
All patients included in our study received either monotherapy or combination therapy of topical/intralesional/oral steroids, HCQ or CHQ, 5-ARIs, topical/oral minoxidil, antifungal shampoo, and/or a calcineurin inhibitor; however, most patients (51.0%) did not see a response to treatment, while only 45.1% showed slowed or halted progression of FFA. Hair regrowth was rare, occurring in only 3 (5.9%) patients; 2 of them were the only patients treated with oral prednisone, making for a potentially promising therapeutic for Black patients that should be further investigated in larger controlled cohort studies. In a prior study, intramuscular steroids (40 mg every 3 weeks) plus topical minoxidil were unsuccessful in slowing the progression of FFA in 3 postmenopausal women,24 which may be explained by the racial differences in the response to FFA treatments and perhaps also menopausal status. Although not included in any of the regimens in our review, isotretinoin was shown to be effective in an ethnically unspecified group of patients (n=16) and also may be efficacious in Black individuals.25 Although FFA may stabilize with time,26 this was not observed in any of the patients included in our study; however, we only included patients who were treated, making it impossible to discern whether resolution was idiopathic or due to treatment.
Future Research—Research on treatments for FFA is lacking, especially in patients with SOC. Although we observed that there may be differences in the treatment response among Black individuals compared to other patients with SOC, additional studies are needed to delineate these racial differences, which can help guide management. More randomized controlled trials evaluating the various treatment regimens also are required to establish treatment guidelines. Frontal fibrosing alopecia likely is underdiagnosed in Black individuals, contributing to the lack of research in this group. Darker skin can obscure some of the clinical and dermoscopic features that are more visible in fair skin. Furthermore, it may be challenging to distinguish clinical features of FFA in the setting of concomitant traction alopecia, which is more common in Black patients.27 Frontal fibrosing alopecia presenting in Black women also is less likely to be biopsied, contributing to the tendency to miss FFA in favor of traction or androgenic alopecia, which often are assumed to be more common in this population.2,27 Therefore, histologic evaluation through biopsy is paramount in securing an accurate diagnosis for Black patients with frontotemporal alopecia.
Study Limitations—The studies included in our review were limited by a lack of control comparison groups, especially among the retrospective cohort studies. Additionally, some of the studies included cases refractory to prior treatment modalities, possibly leading to a selection bias of more severe cases that were not representative of FFA in the general population. Thus, further studies involving larger populations of those with SOC are needed to fully evaluate the clinical utility of the current treatment modalities in this group.
- Kossard S. Postmenopausal frontal fibrosing alopecia. scarring alopecia in a pattern distribution. Arch Dermatol. 1994;130:770-774.
- Dlova NC, Jordaan HF, Skenjane A, et al. Frontal fibrosing alopecia: a clinical review of 20 black patients from South Africa. Br J Dermatol. 2013;169:939-941. doi:10.1111/bjd.12424
- Callender VD, Reid SD, Obayan O, et al. Diagnostic clues to frontal fibrosing alopecia in patients of African descent. J Clin Aesthet Dermatol. 2016;9:45-51.
- Donati A, Molina L, Doche I, et al. Facial papules in frontal fibrosing alopecia: evidence of vellus follicle involvement. Arch Dermatol. 2011;147:1424-1427. doi:10.1001/archdermatol.2011.321
- Uwakwe LN, Cardwell LA, Dothard EH, et al. Frontal fibrosing alopecia and concomitant lichen planus pigmentosus: a case series of seven African American women. J Drugs Dermatol. 2018;17:397-400.
- Naz E, Vidaurrázaga C, Hernández-Cano N, et al. Postmenopausal frontal fibrosing alopecia. Clin Exp Dermatol. 2003;28:25-27. doi:10.1046/j.1365-2230.2003.01131.x
- Dlova NC, Goh CL. Frontal fibrosing alopecia in an African man. Int J Dermatol. 2015;54:81-83. doi:10.1111/j.1365-4632.2012.05821.x
- Huerth K, Kindred C. Frontal fibrosing alopecia presenting as androgenetic alopecia in an African American woman. J Drugs Dermatol. 2020;19:794-795. doi:10.36849/jdd.2020.4682
- Furlan KC, Kakizaki P, Chartuni JC, et al. Frontal fibrosing alopecia in association with Sjögren’s syndrome: more than a simple coincidence. An Bras Dermatol. 2016;91(5 suppl 1):14-16. doi:10.1590/abd1806-4841.20164526
- Zhang M, Zhang L, Rosman IS, et al. Frontal fibrosing alopecia demographics: a survey of 29 patients. Cutis. 2019;103:E16-E22.
- MacDonald A, Clark C, Holmes S. Frontal fibrosing alopecia: a review of 60 cases. J Am Acad Dermatol. 2012;67:955-961. doi:10.1016/j.jaad.2011.12.038
- Starace M, Brandi N, Alessandrini A, et al. Frontal fibrosing alopecia: a case series of 65 patients seen in a single Italian centre. J Eur Acad Dermatol Venereol. 2019;33:433-438. doi:10.1111/jdv.15372
- Dlova NC. Frontal fibrosing alopecia and lichen planus pigmentosus: is there a link? Br J Dermatol. 2013;168:439-442. doi:10.1111/j.1365-2133.2012.11146.x
- Petrof G, Cuell A, Rajkomar VV, et al. Retrospective review of 18 British South Asian women with frontal fibrosing alopecia. Int J Dermatol. 2018;57:490-491. doi:10.1111/ijd.13929
- Mervis JS, Borda LJ, Miteva M. Facial and extrafacial lesions in an ethnically diverse series of 91 patients with frontal fibrosing alopecia followed at a single center. Dermatology. 2019;235:112-119. doi:10.1159/000494603
- Valesky EM, Maier MD, Kippenberger S, et al. Frontal fibrosing alopecia - review of recent case reports and case series in PubMed. J Dtsch Dermatol Ges. Aug 2018;16:992-999. doi:10.1111/ddg.13601
- Adotama P, Callender V, Kolla A, et al. Comparing the clinical differences in white and black women with frontal fibrosing alopecia. Br J Dermatol. 2021;185:1074-1076. doi:10.1111/bjd.20605
- Miao YJ, Jing J, Du XF, et al. Frontal fibrosing alopecia: a review of disease pathogenesis. Front Med (Lausanne). 2022;9:911944. doi:10.3389/fmed.2022.911944
- Pirmez R, Duque-Estrada B, Donati A, et al. Clinical and dermoscopic features of lichen planus pigmentosus in 37 patients with frontal fibrosing alopecia. Br J Dermatol. 2016;175:1387-1390. doi:10.1111/bjd.14722
- Berliner JG, McCalmont TH, Price VH, et al. Frontal fibrosing alopecia and lichen planus pigmentosus. J Am Acad Dermatol. 2014;71:E26-E27. doi:10.1016/j.jaad.2013.12.031
- Romiti R, Biancardi Gavioli CF, et al. Clinical and histopathological findings of frontal fibrosing alopecia-associated lichen planus pigmentosus. Skin Appendage Disord. 2017;3:59-63. doi:10.1159/000456038
- Mulinari-Brenner FA, Guilherme MR, Peretti MC, et al. Frontal fibrosing alopecia and lichen planus pigmentosus: diagnosis and therapeutic challenge. An Bras Dermatol. 2017;92(5 suppl 1):79-81. doi:10.1590/abd1806-4841.20175833
- Panchaprateep R, Ruxrungtham P, Chancheewa B, et al. Clinical characteristics, trichoscopy, histopathology and treatment outcomes of frontal fibrosing alopecia in an Asian population: a retro-prospective cohort study. J Dermatol. 2020;47:1301-1311. doi:10.1111/1346-8138.15517
- Tosti A, Piraccini BM, Iorizzo M, et al. Frontal fibrosing alopecia in postmenopausal women. J Am Acad Dermatol. 2005;52:55-60. doi:10.1016/j.jaad.2004.05.014
- Rokni GR, Emadi SN, Dabbaghzade A, et al. Evaluating the combined efficacy of oral isotretinoin and topical tacrolimus versus oral finasteride and topical tacrolimus in frontal fibrosing alopecia—a randomized controlled trial. J Cosmet Dermatol. 2023;22:613-619. doi:10.1111/jocd.15232
- Kossard S, Lee MS, Wilkinson B. Postmenopausal frontal fibrosing alopecia: a frontal variant of lichen planopilaris. J Am Acad Dermatol. 1997;36:59-66. doi:10.1016/s0190-9622(97)70326-8
- Miteva M, Whiting D, Harries M, et al. Frontal fibrosing alopecia in black patients. Br J Dermatol. 2012;167:208-210. doi:10.1111/j.1365-2133.2012.10809.x
- Kossard S. Postmenopausal frontal fibrosing alopecia. scarring alopecia in a pattern distribution. Arch Dermatol. 1994;130:770-774.
- Dlova NC, Jordaan HF, Skenjane A, et al. Frontal fibrosing alopecia: a clinical review of 20 black patients from South Africa. Br J Dermatol. 2013;169:939-941. doi:10.1111/bjd.12424
- Callender VD, Reid SD, Obayan O, et al. Diagnostic clues to frontal fibrosing alopecia in patients of African descent. J Clin Aesthet Dermatol. 2016;9:45-51.
- Donati A, Molina L, Doche I, et al. Facial papules in frontal fibrosing alopecia: evidence of vellus follicle involvement. Arch Dermatol. 2011;147:1424-1427. doi:10.1001/archdermatol.2011.321
- Uwakwe LN, Cardwell LA, Dothard EH, et al. Frontal fibrosing alopecia and concomitant lichen planus pigmentosus: a case series of seven African American women. J Drugs Dermatol. 2018;17:397-400.
- Naz E, Vidaurrázaga C, Hernández-Cano N, et al. Postmenopausal frontal fibrosing alopecia. Clin Exp Dermatol. 2003;28:25-27. doi:10.1046/j.1365-2230.2003.01131.x
- Dlova NC, Goh CL. Frontal fibrosing alopecia in an African man. Int J Dermatol. 2015;54:81-83. doi:10.1111/j.1365-4632.2012.05821.x
- Huerth K, Kindred C. Frontal fibrosing alopecia presenting as androgenetic alopecia in an African American woman. J Drugs Dermatol. 2020;19:794-795. doi:10.36849/jdd.2020.4682
- Furlan KC, Kakizaki P, Chartuni JC, et al. Frontal fibrosing alopecia in association with Sjögren’s syndrome: more than a simple coincidence. An Bras Dermatol. 2016;91(5 suppl 1):14-16. doi:10.1590/abd1806-4841.20164526
- Zhang M, Zhang L, Rosman IS, et al. Frontal fibrosing alopecia demographics: a survey of 29 patients. Cutis. 2019;103:E16-E22.
- MacDonald A, Clark C, Holmes S. Frontal fibrosing alopecia: a review of 60 cases. J Am Acad Dermatol. 2012;67:955-961. doi:10.1016/j.jaad.2011.12.038
- Starace M, Brandi N, Alessandrini A, et al. Frontal fibrosing alopecia: a case series of 65 patients seen in a single Italian centre. J Eur Acad Dermatol Venereol. 2019;33:433-438. doi:10.1111/jdv.15372
- Dlova NC. Frontal fibrosing alopecia and lichen planus pigmentosus: is there a link? Br J Dermatol. 2013;168:439-442. doi:10.1111/j.1365-2133.2012.11146.x
- Petrof G, Cuell A, Rajkomar VV, et al. Retrospective review of 18 British South Asian women with frontal fibrosing alopecia. Int J Dermatol. 2018;57:490-491. doi:10.1111/ijd.13929
- Mervis JS, Borda LJ, Miteva M. Facial and extrafacial lesions in an ethnically diverse series of 91 patients with frontal fibrosing alopecia followed at a single center. Dermatology. 2019;235:112-119. doi:10.1159/000494603
- Valesky EM, Maier MD, Kippenberger S, et al. Frontal fibrosing alopecia - review of recent case reports and case series in PubMed. J Dtsch Dermatol Ges. Aug 2018;16:992-999. doi:10.1111/ddg.13601
- Adotama P, Callender V, Kolla A, et al. Comparing the clinical differences in white and black women with frontal fibrosing alopecia. Br J Dermatol. 2021;185:1074-1076. doi:10.1111/bjd.20605
- Miao YJ, Jing J, Du XF, et al. Frontal fibrosing alopecia: a review of disease pathogenesis. Front Med (Lausanne). 2022;9:911944. doi:10.3389/fmed.2022.911944
- Pirmez R, Duque-Estrada B, Donati A, et al. Clinical and dermoscopic features of lichen planus pigmentosus in 37 patients with frontal fibrosing alopecia. Br J Dermatol. 2016;175:1387-1390. doi:10.1111/bjd.14722
- Berliner JG, McCalmont TH, Price VH, et al. Frontal fibrosing alopecia and lichen planus pigmentosus. J Am Acad Dermatol. 2014;71:E26-E27. doi:10.1016/j.jaad.2013.12.031
- Romiti R, Biancardi Gavioli CF, et al. Clinical and histopathological findings of frontal fibrosing alopecia-associated lichen planus pigmentosus. Skin Appendage Disord. 2017;3:59-63. doi:10.1159/000456038
- Mulinari-Brenner FA, Guilherme MR, Peretti MC, et al. Frontal fibrosing alopecia and lichen planus pigmentosus: diagnosis and therapeutic challenge. An Bras Dermatol. 2017;92(5 suppl 1):79-81. doi:10.1590/abd1806-4841.20175833
- Panchaprateep R, Ruxrungtham P, Chancheewa B, et al. Clinical characteristics, trichoscopy, histopathology and treatment outcomes of frontal fibrosing alopecia in an Asian population: a retro-prospective cohort study. J Dermatol. 2020;47:1301-1311. doi:10.1111/1346-8138.15517
- Tosti A, Piraccini BM, Iorizzo M, et al. Frontal fibrosing alopecia in postmenopausal women. J Am Acad Dermatol. 2005;52:55-60. doi:10.1016/j.jaad.2004.05.014
- Rokni GR, Emadi SN, Dabbaghzade A, et al. Evaluating the combined efficacy of oral isotretinoin and topical tacrolimus versus oral finasteride and topical tacrolimus in frontal fibrosing alopecia—a randomized controlled trial. J Cosmet Dermatol. 2023;22:613-619. doi:10.1111/jocd.15232
- Kossard S, Lee MS, Wilkinson B. Postmenopausal frontal fibrosing alopecia: a frontal variant of lichen planopilaris. J Am Acad Dermatol. 1997;36:59-66. doi:10.1016/s0190-9622(97)70326-8
- Miteva M, Whiting D, Harries M, et al. Frontal fibrosing alopecia in black patients. Br J Dermatol. 2012;167:208-210. doi:10.1111/j.1365-2133.2012.10809.x
Practice Points
- Treatment of frontal fibrosing alopecia (FFA) is challenging, and there are no evidence-based treatment guidelines available. Patients with skin of color (SOC) may have varying responses to treatment modalities.
- Special consideration should be taken when treating FFA in patients with SOC.
- Histologic evaluation through biopsy is paramount in securing an accurate diagnosis for Black patients with frontotemporal alopecia.