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Parental E-Cigarette Use Linked With Higher Risk for Pediatric Atopic Dermatitis
Key clinical point: Use of e-cigarettes by parents is associated with an increased risk for atopic dermatitis (AD) in children.
Major finding: The prevalence of parental e-cigarette use was 18.0% (95% CI 16.5%-19.0%) among children with AD and 14.4% (95% CI 13.9%-15.0%) among those without AD. The risk for AD was significantly higher in children whose parents used e-cigarettes (adjusted odds ratio 1.24; P = .002).
Study details: This retrospective, cross-sectional analysis of data from the US National Health Interview Survey (2014-2018) included 48,637,111 children (age < 18 years), of whom 6,354,515 had a history of AD.
Disclosures: This study did not receive specific funding from any sources. Albert S. Chiou declared receiving consultation fees from Corvus Therapeutics outside the submitted work.
Source: Youn GM, Sarin KY, Chiou AS, et al. Parental e-cigarette use and pediatric atopic dermatitis. JAMA Dermatol. 2024 (May 22). doi: 10.1001/jamadermatol.2024.1283 Source
Key clinical point: Use of e-cigarettes by parents is associated with an increased risk for atopic dermatitis (AD) in children.
Major finding: The prevalence of parental e-cigarette use was 18.0% (95% CI 16.5%-19.0%) among children with AD and 14.4% (95% CI 13.9%-15.0%) among those without AD. The risk for AD was significantly higher in children whose parents used e-cigarettes (adjusted odds ratio 1.24; P = .002).
Study details: This retrospective, cross-sectional analysis of data from the US National Health Interview Survey (2014-2018) included 48,637,111 children (age < 18 years), of whom 6,354,515 had a history of AD.
Disclosures: This study did not receive specific funding from any sources. Albert S. Chiou declared receiving consultation fees from Corvus Therapeutics outside the submitted work.
Source: Youn GM, Sarin KY, Chiou AS, et al. Parental e-cigarette use and pediatric atopic dermatitis. JAMA Dermatol. 2024 (May 22). doi: 10.1001/jamadermatol.2024.1283 Source
Key clinical point: Use of e-cigarettes by parents is associated with an increased risk for atopic dermatitis (AD) in children.
Major finding: The prevalence of parental e-cigarette use was 18.0% (95% CI 16.5%-19.0%) among children with AD and 14.4% (95% CI 13.9%-15.0%) among those without AD. The risk for AD was significantly higher in children whose parents used e-cigarettes (adjusted odds ratio 1.24; P = .002).
Study details: This retrospective, cross-sectional analysis of data from the US National Health Interview Survey (2014-2018) included 48,637,111 children (age < 18 years), of whom 6,354,515 had a history of AD.
Disclosures: This study did not receive specific funding from any sources. Albert S. Chiou declared receiving consultation fees from Corvus Therapeutics outside the submitted work.
Source: Youn GM, Sarin KY, Chiou AS, et al. Parental e-cigarette use and pediatric atopic dermatitis. JAMA Dermatol. 2024 (May 22). doi: 10.1001/jamadermatol.2024.1283 Source
High Sodium Intake Linked to Increased Atopic Dermatitis Risk
Key clinical point: High dietary intake of sodium, estimated according to 24-hour urinary sodium excretion, was associated with a greater likelihood of atopic dermatitis (AD) diagnosis, having active AD, and increasing severity of AD.
Major finding: A 1-g increase in estimated 24-hour urine sodium excretion was associated with an increased likelihood of AD (adjusted odds ratio [aOR] 1.11; 95% CI 1.07-1.14), active AD (aOR 1.16; 95% CI 1.05-1.28), and increasing AD severity (aOR 1.11; 95% CI 1.07-1.15).
Study details: This cross-sectional study evaluated the association between high levels of dietary sodium intake and AD prevalence, activity, and severity in 215,832 adults from the UK Biobank cohort, of whom 10,839 had AD.
Disclosures: This study was supported by grants from the Medical Student in Aging Research Program and US National Institute on Aging and by the National Eczema Association. One author declared receiving research funding to her institution and consulting fees from various sources.
Source: Chiang BM, Ye M, Chattopadhyay A, et al. Sodium intake and atopic dermatitis. JAMA Dermatol. 2024 (Jun 5). doi: 10.1001/jamadermatol.2024.1544 Source
Key clinical point: High dietary intake of sodium, estimated according to 24-hour urinary sodium excretion, was associated with a greater likelihood of atopic dermatitis (AD) diagnosis, having active AD, and increasing severity of AD.
Major finding: A 1-g increase in estimated 24-hour urine sodium excretion was associated with an increased likelihood of AD (adjusted odds ratio [aOR] 1.11; 95% CI 1.07-1.14), active AD (aOR 1.16; 95% CI 1.05-1.28), and increasing AD severity (aOR 1.11; 95% CI 1.07-1.15).
Study details: This cross-sectional study evaluated the association between high levels of dietary sodium intake and AD prevalence, activity, and severity in 215,832 adults from the UK Biobank cohort, of whom 10,839 had AD.
Disclosures: This study was supported by grants from the Medical Student in Aging Research Program and US National Institute on Aging and by the National Eczema Association. One author declared receiving research funding to her institution and consulting fees from various sources.
Source: Chiang BM, Ye M, Chattopadhyay A, et al. Sodium intake and atopic dermatitis. JAMA Dermatol. 2024 (Jun 5). doi: 10.1001/jamadermatol.2024.1544 Source
Key clinical point: High dietary intake of sodium, estimated according to 24-hour urinary sodium excretion, was associated with a greater likelihood of atopic dermatitis (AD) diagnosis, having active AD, and increasing severity of AD.
Major finding: A 1-g increase in estimated 24-hour urine sodium excretion was associated with an increased likelihood of AD (adjusted odds ratio [aOR] 1.11; 95% CI 1.07-1.14), active AD (aOR 1.16; 95% CI 1.05-1.28), and increasing AD severity (aOR 1.11; 95% CI 1.07-1.15).
Study details: This cross-sectional study evaluated the association between high levels of dietary sodium intake and AD prevalence, activity, and severity in 215,832 adults from the UK Biobank cohort, of whom 10,839 had AD.
Disclosures: This study was supported by grants from the Medical Student in Aging Research Program and US National Institute on Aging and by the National Eczema Association. One author declared receiving research funding to her institution and consulting fees from various sources.
Source: Chiang BM, Ye M, Chattopadhyay A, et al. Sodium intake and atopic dermatitis. JAMA Dermatol. 2024 (Jun 5). doi: 10.1001/jamadermatol.2024.1544 Source
How to Make Life Decisions
Halifax, Nova Scotia; American Samoa; Queens, New York; Lansing, Michigan; Gurugram, India. I often ask patients where they’re from. Practicing in San Diego, the answers are a geography lesson. People from around the world come here. I sometimes add the more interesting question: How’d you end up here? Many took the three highways to San Diego: the Navy, the defense industry (like General Dynamics), or followed a partner. My Queens patient had a better answer: Super Bowl XXII. On Sunday, Jan. 31st, 1988, the Redskins played the Broncos in San Diego. John Elway and the Broncos lost, but it didn’t matter. “I was scrapin’ the ice off my windshield that Monday morning when I thought, that’s it. I’m done! I drove to the garage where I worked and quit on the spot. Then I drove home and packed my bags.”
In a paper on how to make life decisions, this guy would be Exhibit A: “Don’t overthink it.” That approach might not be suitable for everyone, or for every decision. It might actually be an example of how not to make life decisions (more on that later). But,
The first treatise on this subject was a paper by one Franklin, Ben in 1772. Providing advice to a friend on how to make a career decision, Franklin argued: “My way is to divide half a sheet of paper by a line into two columns; writing over the one Pro and over the other Con.” This “moral algebra” as he called it was a framework to put rigor to a messy, organic problem.
The flaw in this method is that in the end you have two lists. Then what? Do the length of the lists decide? What if some factors are more important? Well, let’s add tools to help. You could use a spreadsheet and assign weights to each variable. Then sum the values and choose based on that. So if “not scraping ice off your windshield” is twice as important as “doubling your rent,” then you’ve got your answer. But what if you aren’t good at estimating how important things are? Actually, most of us are pretty awful at assigning weights to life variables – having bags of money is the consummate example. Seems important, but because of habituation, it turns out to not be sustainable. Note Exhibit B, our wealthy neighbor who owns a Lambo and G-Wagen (AMG squared, of course), who just parked a Cybertruck in his driveway. Realizing the risk of depending on peoples’ flawed judgment, companies instead use statistical modeling called bootstrap aggregating to “vote” on the weights for variables in a prediction. If you aren’t sure how important a new Rivian or walking to the beach would be, a model can answer that for you! It’s a bit disconcerting, I know. I mean, how can a model know what we’d like? Wait, isn’t that how Netflix picks stuff for you? Exactly.
Ok, so why don’t we just ask our friendly personal AI? “OK, ChatGPT, given what you know about me, where can I have it all?” Alas, here we slam into a glass wall. It seems the answer is out there but even our life-changing magical AI tools fail us. Mathematically, it is impossible to have it all. An illustrative example of this is called the economic “impossible trinity problem.” Even the most sophisticated algorithm cannot find an optional solution to some trinities such as fixed foreign exchange rate, free capital movement, and an independent monetary policy. Economists have concluded you must trade off one to have the other two. Impossible trinities are common in economics and in life. Armistead Maupin in his “Tales of the City” codifies it as Mona’s Law, the essence of which is: You cannot have the perfect job, the perfect partner, and the perfect house at the same time. (See Exhibit C, one Tom Brady).
This brings me to my final point, hard decisions are matters of the heart and experiencing life is the best way to understand its beautiful chaos. If making rash judgments is ill-advised and using technology cannot solve all problems (try asking your AI buddy for the square root of 2 as a fraction) what tools can we use? Maybe try reading more novels. They allow us to experience multiple lifetimes in a short time, which is what we need to learn what matters. Reading Dorothea’s choice at the end of “Middlemarch” is a nice example. Should she give up Lowick Manor and marry the penniless Ladislaw or keep it and use her wealth to help others? Seeing her struggle helps us understand how to answer questions like: Should I give up my academic practice or marry that guy or move to Texas? These cannot be reduced to arithmetic. The only way to know is to know as much of life as possible.
My last visit with my Queens patient was our last together. He’s divorced and moving from San Diego to Gallatin, Tennessee. “I’ve paid my last taxes to California, Doc. I decided that’s it, I’m done!” Perhaps he should have read “The Grapes of Wrath” before he set out for California in the first place.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.
Halifax, Nova Scotia; American Samoa; Queens, New York; Lansing, Michigan; Gurugram, India. I often ask patients where they’re from. Practicing in San Diego, the answers are a geography lesson. People from around the world come here. I sometimes add the more interesting question: How’d you end up here? Many took the three highways to San Diego: the Navy, the defense industry (like General Dynamics), or followed a partner. My Queens patient had a better answer: Super Bowl XXII. On Sunday, Jan. 31st, 1988, the Redskins played the Broncos in San Diego. John Elway and the Broncos lost, but it didn’t matter. “I was scrapin’ the ice off my windshield that Monday morning when I thought, that’s it. I’m done! I drove to the garage where I worked and quit on the spot. Then I drove home and packed my bags.”
In a paper on how to make life decisions, this guy would be Exhibit A: “Don’t overthink it.” That approach might not be suitable for everyone, or for every decision. It might actually be an example of how not to make life decisions (more on that later). But,
The first treatise on this subject was a paper by one Franklin, Ben in 1772. Providing advice to a friend on how to make a career decision, Franklin argued: “My way is to divide half a sheet of paper by a line into two columns; writing over the one Pro and over the other Con.” This “moral algebra” as he called it was a framework to put rigor to a messy, organic problem.
The flaw in this method is that in the end you have two lists. Then what? Do the length of the lists decide? What if some factors are more important? Well, let’s add tools to help. You could use a spreadsheet and assign weights to each variable. Then sum the values and choose based on that. So if “not scraping ice off your windshield” is twice as important as “doubling your rent,” then you’ve got your answer. But what if you aren’t good at estimating how important things are? Actually, most of us are pretty awful at assigning weights to life variables – having bags of money is the consummate example. Seems important, but because of habituation, it turns out to not be sustainable. Note Exhibit B, our wealthy neighbor who owns a Lambo and G-Wagen (AMG squared, of course), who just parked a Cybertruck in his driveway. Realizing the risk of depending on peoples’ flawed judgment, companies instead use statistical modeling called bootstrap aggregating to “vote” on the weights for variables in a prediction. If you aren’t sure how important a new Rivian or walking to the beach would be, a model can answer that for you! It’s a bit disconcerting, I know. I mean, how can a model know what we’d like? Wait, isn’t that how Netflix picks stuff for you? Exactly.
Ok, so why don’t we just ask our friendly personal AI? “OK, ChatGPT, given what you know about me, where can I have it all?” Alas, here we slam into a glass wall. It seems the answer is out there but even our life-changing magical AI tools fail us. Mathematically, it is impossible to have it all. An illustrative example of this is called the economic “impossible trinity problem.” Even the most sophisticated algorithm cannot find an optional solution to some trinities such as fixed foreign exchange rate, free capital movement, and an independent monetary policy. Economists have concluded you must trade off one to have the other two. Impossible trinities are common in economics and in life. Armistead Maupin in his “Tales of the City” codifies it as Mona’s Law, the essence of which is: You cannot have the perfect job, the perfect partner, and the perfect house at the same time. (See Exhibit C, one Tom Brady).
This brings me to my final point, hard decisions are matters of the heart and experiencing life is the best way to understand its beautiful chaos. If making rash judgments is ill-advised and using technology cannot solve all problems (try asking your AI buddy for the square root of 2 as a fraction) what tools can we use? Maybe try reading more novels. They allow us to experience multiple lifetimes in a short time, which is what we need to learn what matters. Reading Dorothea’s choice at the end of “Middlemarch” is a nice example. Should she give up Lowick Manor and marry the penniless Ladislaw or keep it and use her wealth to help others? Seeing her struggle helps us understand how to answer questions like: Should I give up my academic practice or marry that guy or move to Texas? These cannot be reduced to arithmetic. The only way to know is to know as much of life as possible.
My last visit with my Queens patient was our last together. He’s divorced and moving from San Diego to Gallatin, Tennessee. “I’ve paid my last taxes to California, Doc. I decided that’s it, I’m done!” Perhaps he should have read “The Grapes of Wrath” before he set out for California in the first place.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.
Halifax, Nova Scotia; American Samoa; Queens, New York; Lansing, Michigan; Gurugram, India. I often ask patients where they’re from. Practicing in San Diego, the answers are a geography lesson. People from around the world come here. I sometimes add the more interesting question: How’d you end up here? Many took the three highways to San Diego: the Navy, the defense industry (like General Dynamics), or followed a partner. My Queens patient had a better answer: Super Bowl XXII. On Sunday, Jan. 31st, 1988, the Redskins played the Broncos in San Diego. John Elway and the Broncos lost, but it didn’t matter. “I was scrapin’ the ice off my windshield that Monday morning when I thought, that’s it. I’m done! I drove to the garage where I worked and quit on the spot. Then I drove home and packed my bags.”
In a paper on how to make life decisions, this guy would be Exhibit A: “Don’t overthink it.” That approach might not be suitable for everyone, or for every decision. It might actually be an example of how not to make life decisions (more on that later). But,
The first treatise on this subject was a paper by one Franklin, Ben in 1772. Providing advice to a friend on how to make a career decision, Franklin argued: “My way is to divide half a sheet of paper by a line into two columns; writing over the one Pro and over the other Con.” This “moral algebra” as he called it was a framework to put rigor to a messy, organic problem.
The flaw in this method is that in the end you have two lists. Then what? Do the length of the lists decide? What if some factors are more important? Well, let’s add tools to help. You could use a spreadsheet and assign weights to each variable. Then sum the values and choose based on that. So if “not scraping ice off your windshield” is twice as important as “doubling your rent,” then you’ve got your answer. But what if you aren’t good at estimating how important things are? Actually, most of us are pretty awful at assigning weights to life variables – having bags of money is the consummate example. Seems important, but because of habituation, it turns out to not be sustainable. Note Exhibit B, our wealthy neighbor who owns a Lambo and G-Wagen (AMG squared, of course), who just parked a Cybertruck in his driveway. Realizing the risk of depending on peoples’ flawed judgment, companies instead use statistical modeling called bootstrap aggregating to “vote” on the weights for variables in a prediction. If you aren’t sure how important a new Rivian or walking to the beach would be, a model can answer that for you! It’s a bit disconcerting, I know. I mean, how can a model know what we’d like? Wait, isn’t that how Netflix picks stuff for you? Exactly.
Ok, so why don’t we just ask our friendly personal AI? “OK, ChatGPT, given what you know about me, where can I have it all?” Alas, here we slam into a glass wall. It seems the answer is out there but even our life-changing magical AI tools fail us. Mathematically, it is impossible to have it all. An illustrative example of this is called the economic “impossible trinity problem.” Even the most sophisticated algorithm cannot find an optional solution to some trinities such as fixed foreign exchange rate, free capital movement, and an independent monetary policy. Economists have concluded you must trade off one to have the other two. Impossible trinities are common in economics and in life. Armistead Maupin in his “Tales of the City” codifies it as Mona’s Law, the essence of which is: You cannot have the perfect job, the perfect partner, and the perfect house at the same time. (See Exhibit C, one Tom Brady).
This brings me to my final point, hard decisions are matters of the heart and experiencing life is the best way to understand its beautiful chaos. If making rash judgments is ill-advised and using technology cannot solve all problems (try asking your AI buddy for the square root of 2 as a fraction) what tools can we use? Maybe try reading more novels. They allow us to experience multiple lifetimes in a short time, which is what we need to learn what matters. Reading Dorothea’s choice at the end of “Middlemarch” is a nice example. Should she give up Lowick Manor and marry the penniless Ladislaw or keep it and use her wealth to help others? Seeing her struggle helps us understand how to answer questions like: Should I give up my academic practice or marry that guy or move to Texas? These cannot be reduced to arithmetic. The only way to know is to know as much of life as possible.
My last visit with my Queens patient was our last together. He’s divorced and moving from San Diego to Gallatin, Tennessee. “I’ve paid my last taxes to California, Doc. I decided that’s it, I’m done!” Perhaps he should have read “The Grapes of Wrath” before he set out for California in the first place.
Dr. Benabio is director of Healthcare Transformation and chief of dermatology at Kaiser Permanente San Diego. The opinions expressed in this column are his own and do not represent those of Kaiser Permanente. Dr. Benabio is @Dermdoc on Twitter. Write to him at dermnews@mdedge.com.
Neurofilament Light Chain Detects Early Chemotherapy-Related Neurotoxicity
Investigators found Nfl levels increased in cancer patients following a first infusion of the medication paclitaxel and corresponded to neuropathy severity 6-12 months post-treatment, suggesting the blood protein may provide an early CIPN biomarker.
“Nfl after a single cycle could detect axonal degeneration,” said lead investigator Masarra Joda, a researcher and PhD candidate at the University of Sydney in Australia. She added that “quantification of Nfl may provide a clinically useful marker of emerging neurotoxicity in patients vulnerable to CIPN.”
The findings were presented at the Peripheral Nerve Society (PNS) 2024 annual meeting.
Common, Burdensome Side Effect
A common side effect of chemotherapy, CIPN manifests as sensory neuropathy and causes degeneration of the peripheral axons. A protein biomarker of axonal degeneration, Nfl has previously been investigated as a way of identifying patients at risk of CIPN.
The goal of the current study was to identify the potential link between Nfl with neurophysiological markers of axon degeneration in patients receiving the neurotoxin chemotherapy paclitaxel.
The study included 93 cancer patients. All were assessed at the beginning, middle, and end of treatment. CIPN was assessed using blood samples of Nfl and the Total Neuropathy Score (TNS), the Common Terminology Criteria for Adverse Events (CTCAE) neuropathy scale, and patient-reported measures using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire–Chemotherapy-Induced Peripheral Neuropathy Module (EORTC-CIPN20).
Axonal degeneration was measured with neurophysiological tests including sural nerve compound sensory action potential (CSAP) for the lower limbs, and sensory median nerve CSAP, as well as stimulus threshold testing, for the upper limbs.
Almost all of study participants (97%) were female. The majority (66%) had breast cancer and 30% had gynecological cancer. Most (73%) were receiving a weekly regimen of paclitaxel, and the remainder were treated with taxanes plus platinum once every 3 weeks. By the end of treatment, 82% of the patients had developed CIPN, which was mild in 44% and moderate/severe in 38%.
Nfl levels increased significantly from baseline to after the first dose of chemotherapy (P < .001), “highlighting that nerve damage occurs from the very beginning of treatment,” senior investigator Susanna Park, PhD, told this news organization.
In addition, “patients with higher Nfl levels after a single paclitaxel treatment had greater neuropathy at the end of treatment (higher EORTC scores [P ≤ .026], and higher TNS scores [P ≤ .00]),” added Dr. Park, who is associate professor at the University of Sydney.
“Importantly, we also looked at long-term outcomes beyond the end of chemotherapy, because chronic neuropathy produces a significant burden in cancer survivors,” said Dr. Park.
“Among a total of 44 patients who completed the 6- to 12-month post-treatment follow-up, NfL levels after a single treatment were linked to severity of nerve damage quantified with neurophysiological tests, and greater Nfl levels at mid-treatment were correlated with worse patient and neurologically graded neuropathy at 6-12 months.”
Dr. Park said the results suggest that NfL may provide a biomarker of long-term axon damage and that Nfl assays “may enable clinicians to evaluate the risk of long-term toxicity early during paclitaxel treatment to hopefully provide clinically significant information to guide better treatment titration.”
Currently, she said, CIPN is a prominent cause of dose reduction and early chemotherapy cessation.
“For example, in early breast cancer around 25% of patients experience a dose reduction due to the severity of neuropathy symptoms.” But, she said, “there is no standardized way of identifying which patients are at risk of long-term neuropathy and therefore, may benefit more from dose reduction. In this setting, a biomarker such as Nfl could provide oncologists with more information about the risk of long-term toxicity and take that into account in dose decision-making.”
For some cancers, she added, there are multiple potential therapy options.
“A biomarker such as NfL could assist in determining risk-benefit profile in terms of switching to alternate therapies. However, further studies will be needed to fully define the utility of NfL as a biomarker of paclitaxel neuropathy.”
Promising Research
Commenting on the research for this news organization, Maryam Lustberg, MD, associate professor, director of the Center for Breast Cancer at Smilow Cancer Hospital and Yale Cancer Center, and chief of Breast Medical Oncology at Yale Cancer Center, in New Haven, Connecticut, said the study “builds on a body of work previously reported by others showing that neurofilament light chains as detected in the blood can be associated with early signs of neurotoxic injury.”
She added that the research “is promising, since existing clinical and patient-reported measures tend to under-detect chemotherapy-induced neuropathy until more permanent injury might have occurred.”
Dr. Lustberg, who is immediate past president of the Multinational Association of Supportive Care in Cancer, said future studies are needed before Nfl testing can be implemented in routine practice, but that “early detection will allow earlier initiation of supportive care strategies such as physical therapy and exercise, as well as dose modifications, which may be helpful for preventing permanent damage and improving quality of life.”
The investigators and Dr. Lustberg report no relevant financial relationships.
A version of this article appeared on Medscape.com.
Investigators found Nfl levels increased in cancer patients following a first infusion of the medication paclitaxel and corresponded to neuropathy severity 6-12 months post-treatment, suggesting the blood protein may provide an early CIPN biomarker.
“Nfl after a single cycle could detect axonal degeneration,” said lead investigator Masarra Joda, a researcher and PhD candidate at the University of Sydney in Australia. She added that “quantification of Nfl may provide a clinically useful marker of emerging neurotoxicity in patients vulnerable to CIPN.”
The findings were presented at the Peripheral Nerve Society (PNS) 2024 annual meeting.
Common, Burdensome Side Effect
A common side effect of chemotherapy, CIPN manifests as sensory neuropathy and causes degeneration of the peripheral axons. A protein biomarker of axonal degeneration, Nfl has previously been investigated as a way of identifying patients at risk of CIPN.
The goal of the current study was to identify the potential link between Nfl with neurophysiological markers of axon degeneration in patients receiving the neurotoxin chemotherapy paclitaxel.
The study included 93 cancer patients. All were assessed at the beginning, middle, and end of treatment. CIPN was assessed using blood samples of Nfl and the Total Neuropathy Score (TNS), the Common Terminology Criteria for Adverse Events (CTCAE) neuropathy scale, and patient-reported measures using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire–Chemotherapy-Induced Peripheral Neuropathy Module (EORTC-CIPN20).
Axonal degeneration was measured with neurophysiological tests including sural nerve compound sensory action potential (CSAP) for the lower limbs, and sensory median nerve CSAP, as well as stimulus threshold testing, for the upper limbs.
Almost all of study participants (97%) were female. The majority (66%) had breast cancer and 30% had gynecological cancer. Most (73%) were receiving a weekly regimen of paclitaxel, and the remainder were treated with taxanes plus platinum once every 3 weeks. By the end of treatment, 82% of the patients had developed CIPN, which was mild in 44% and moderate/severe in 38%.
Nfl levels increased significantly from baseline to after the first dose of chemotherapy (P < .001), “highlighting that nerve damage occurs from the very beginning of treatment,” senior investigator Susanna Park, PhD, told this news organization.
In addition, “patients with higher Nfl levels after a single paclitaxel treatment had greater neuropathy at the end of treatment (higher EORTC scores [P ≤ .026], and higher TNS scores [P ≤ .00]),” added Dr. Park, who is associate professor at the University of Sydney.
“Importantly, we also looked at long-term outcomes beyond the end of chemotherapy, because chronic neuropathy produces a significant burden in cancer survivors,” said Dr. Park.
“Among a total of 44 patients who completed the 6- to 12-month post-treatment follow-up, NfL levels after a single treatment were linked to severity of nerve damage quantified with neurophysiological tests, and greater Nfl levels at mid-treatment were correlated with worse patient and neurologically graded neuropathy at 6-12 months.”
Dr. Park said the results suggest that NfL may provide a biomarker of long-term axon damage and that Nfl assays “may enable clinicians to evaluate the risk of long-term toxicity early during paclitaxel treatment to hopefully provide clinically significant information to guide better treatment titration.”
Currently, she said, CIPN is a prominent cause of dose reduction and early chemotherapy cessation.
“For example, in early breast cancer around 25% of patients experience a dose reduction due to the severity of neuropathy symptoms.” But, she said, “there is no standardized way of identifying which patients are at risk of long-term neuropathy and therefore, may benefit more from dose reduction. In this setting, a biomarker such as Nfl could provide oncologists with more information about the risk of long-term toxicity and take that into account in dose decision-making.”
For some cancers, she added, there are multiple potential therapy options.
“A biomarker such as NfL could assist in determining risk-benefit profile in terms of switching to alternate therapies. However, further studies will be needed to fully define the utility of NfL as a biomarker of paclitaxel neuropathy.”
Promising Research
Commenting on the research for this news organization, Maryam Lustberg, MD, associate professor, director of the Center for Breast Cancer at Smilow Cancer Hospital and Yale Cancer Center, and chief of Breast Medical Oncology at Yale Cancer Center, in New Haven, Connecticut, said the study “builds on a body of work previously reported by others showing that neurofilament light chains as detected in the blood can be associated with early signs of neurotoxic injury.”
She added that the research “is promising, since existing clinical and patient-reported measures tend to under-detect chemotherapy-induced neuropathy until more permanent injury might have occurred.”
Dr. Lustberg, who is immediate past president of the Multinational Association of Supportive Care in Cancer, said future studies are needed before Nfl testing can be implemented in routine practice, but that “early detection will allow earlier initiation of supportive care strategies such as physical therapy and exercise, as well as dose modifications, which may be helpful for preventing permanent damage and improving quality of life.”
The investigators and Dr. Lustberg report no relevant financial relationships.
A version of this article appeared on Medscape.com.
Investigators found Nfl levels increased in cancer patients following a first infusion of the medication paclitaxel and corresponded to neuropathy severity 6-12 months post-treatment, suggesting the blood protein may provide an early CIPN biomarker.
“Nfl after a single cycle could detect axonal degeneration,” said lead investigator Masarra Joda, a researcher and PhD candidate at the University of Sydney in Australia. She added that “quantification of Nfl may provide a clinically useful marker of emerging neurotoxicity in patients vulnerable to CIPN.”
The findings were presented at the Peripheral Nerve Society (PNS) 2024 annual meeting.
Common, Burdensome Side Effect
A common side effect of chemotherapy, CIPN manifests as sensory neuropathy and causes degeneration of the peripheral axons. A protein biomarker of axonal degeneration, Nfl has previously been investigated as a way of identifying patients at risk of CIPN.
The goal of the current study was to identify the potential link between Nfl with neurophysiological markers of axon degeneration in patients receiving the neurotoxin chemotherapy paclitaxel.
The study included 93 cancer patients. All were assessed at the beginning, middle, and end of treatment. CIPN was assessed using blood samples of Nfl and the Total Neuropathy Score (TNS), the Common Terminology Criteria for Adverse Events (CTCAE) neuropathy scale, and patient-reported measures using the European Organization for Research and Treatment of Cancer Quality of Life Questionnaire–Chemotherapy-Induced Peripheral Neuropathy Module (EORTC-CIPN20).
Axonal degeneration was measured with neurophysiological tests including sural nerve compound sensory action potential (CSAP) for the lower limbs, and sensory median nerve CSAP, as well as stimulus threshold testing, for the upper limbs.
Almost all of study participants (97%) were female. The majority (66%) had breast cancer and 30% had gynecological cancer. Most (73%) were receiving a weekly regimen of paclitaxel, and the remainder were treated with taxanes plus platinum once every 3 weeks. By the end of treatment, 82% of the patients had developed CIPN, which was mild in 44% and moderate/severe in 38%.
Nfl levels increased significantly from baseline to after the first dose of chemotherapy (P < .001), “highlighting that nerve damage occurs from the very beginning of treatment,” senior investigator Susanna Park, PhD, told this news organization.
In addition, “patients with higher Nfl levels after a single paclitaxel treatment had greater neuropathy at the end of treatment (higher EORTC scores [P ≤ .026], and higher TNS scores [P ≤ .00]),” added Dr. Park, who is associate professor at the University of Sydney.
“Importantly, we also looked at long-term outcomes beyond the end of chemotherapy, because chronic neuropathy produces a significant burden in cancer survivors,” said Dr. Park.
“Among a total of 44 patients who completed the 6- to 12-month post-treatment follow-up, NfL levels after a single treatment were linked to severity of nerve damage quantified with neurophysiological tests, and greater Nfl levels at mid-treatment were correlated with worse patient and neurologically graded neuropathy at 6-12 months.”
Dr. Park said the results suggest that NfL may provide a biomarker of long-term axon damage and that Nfl assays “may enable clinicians to evaluate the risk of long-term toxicity early during paclitaxel treatment to hopefully provide clinically significant information to guide better treatment titration.”
Currently, she said, CIPN is a prominent cause of dose reduction and early chemotherapy cessation.
“For example, in early breast cancer around 25% of patients experience a dose reduction due to the severity of neuropathy symptoms.” But, she said, “there is no standardized way of identifying which patients are at risk of long-term neuropathy and therefore, may benefit more from dose reduction. In this setting, a biomarker such as Nfl could provide oncologists with more information about the risk of long-term toxicity and take that into account in dose decision-making.”
For some cancers, she added, there are multiple potential therapy options.
“A biomarker such as NfL could assist in determining risk-benefit profile in terms of switching to alternate therapies. However, further studies will be needed to fully define the utility of NfL as a biomarker of paclitaxel neuropathy.”
Promising Research
Commenting on the research for this news organization, Maryam Lustberg, MD, associate professor, director of the Center for Breast Cancer at Smilow Cancer Hospital and Yale Cancer Center, and chief of Breast Medical Oncology at Yale Cancer Center, in New Haven, Connecticut, said the study “builds on a body of work previously reported by others showing that neurofilament light chains as detected in the blood can be associated with early signs of neurotoxic injury.”
She added that the research “is promising, since existing clinical and patient-reported measures tend to under-detect chemotherapy-induced neuropathy until more permanent injury might have occurred.”
Dr. Lustberg, who is immediate past president of the Multinational Association of Supportive Care in Cancer, said future studies are needed before Nfl testing can be implemented in routine practice, but that “early detection will allow earlier initiation of supportive care strategies such as physical therapy and exercise, as well as dose modifications, which may be helpful for preventing permanent damage and improving quality of life.”
The investigators and Dr. Lustberg report no relevant financial relationships.
A version of this article appeared on Medscape.com.
AT PNS 2024
Study Addresses Litigation Related to Cutaneous Energy-based Based Device Treatments
“The utilization of laser and energy-based devices (LEBD) has grown substantially,” corresponding author Scott Stratman, MD, MPH, and coauthors wrote in their study, which was published online in the Journal of the American Academy of Dermatology. “This has led to a rise in practitioners, both physicians and nonphysicians, who may lack the requisite training in LEBD procedures. Subsequently, procedures performed by these untrained practitioners have resulted in more lawsuits related to patient complications. As the demand for LEBD procedures and the number of practitioners performing these procedures increase, it remains paramount to characterize the trends of malpractice cases involving these procedures.”
Dr. Stratman, a dermatology resident at the Icahn School of Medicine at Mount Sinai, New York City, and colleagues queried the LexisNexis database from 1985 to Sept. 30, 2023, for all state, federal, and appellate cases that included the terms “negligence” or “malpractice” and “skin” and “laser.” After they removed duplicate cases and excluded cases that did not report dermatologic complications or cutaneous energy-based procedures, the final analysis included 75 cases.
Most of the appellants/plaintiffs (66; 88%) were women, a greater number of cases were in the Northeast (26; 34.7%) and the South (23; 30.7%), and the fewest cases were in the Midwest (12 [16%]). The most common anatomical sites were the face, head, and/or neck, and 43 of the cases (57.3%) were decided in favor of the appellee/defendant or the party defending against the appeal, while 29 (38.7%) were in favor of the appellant/plaintiff or the party appealing, and three cases (4%) did not report a verdict.
In other findings, plastic surgeons were the most litigated healthcare professionals (18; 24%), while 39 of the overall cases (52%) involved nonphysician operators (NPOs), 32 (42.7%) involved a physician operator, and 4 cases (5.3%) did not name a device operator. The most common procedure performed in the included cases was laser hair removal (33; 44%). Complications from energy-based devices included burns, scarring, and pigmentation changes. Statistically significant associations were neither found between verdict outcome and appellee/defendant type nor found between energy-device operator or anatomical site.
The authors acknowledged certain limitations of the study, including the fact that the LexisNexis database does not contain cases handled in out-of-court settlements and cases that underwent third-party arbitration.
“Physicians must recognize their responsibility when delegating procedures to NPOs and their role in supervision of these procedures,” they concluded. “Comprehensive training for physicians and their agents is necessary to diminish adverse outcomes and legal risks. Moreover, all practitioners should be held to the same standard of care. Familiarity with malpractice trends not only strengthens the patient-provider relationship but also equips providers with effective strategies to minimize the risk of legal repercussions.”
Mathew M. Avram, MD, JD, director of laser, cosmetics, and dermatologic surgery at Massachusetts General Hospital, Boston, who was asked to comment on the study, said that it “reaffirms previous studies which show that laser hair removal continues to be the most litigated procedure in laser surgery, and that nonphysician operators are most commonly litigated against. It further reiterates the importance of close supervision and expert training of procedures delegated by physicians.”
Neither the authors nor Dr. Avram reported having relevant financial disclosures.
A version of this article first appeared on Medscape.com.
“The utilization of laser and energy-based devices (LEBD) has grown substantially,” corresponding author Scott Stratman, MD, MPH, and coauthors wrote in their study, which was published online in the Journal of the American Academy of Dermatology. “This has led to a rise in practitioners, both physicians and nonphysicians, who may lack the requisite training in LEBD procedures. Subsequently, procedures performed by these untrained practitioners have resulted in more lawsuits related to patient complications. As the demand for LEBD procedures and the number of practitioners performing these procedures increase, it remains paramount to characterize the trends of malpractice cases involving these procedures.”
Dr. Stratman, a dermatology resident at the Icahn School of Medicine at Mount Sinai, New York City, and colleagues queried the LexisNexis database from 1985 to Sept. 30, 2023, for all state, federal, and appellate cases that included the terms “negligence” or “malpractice” and “skin” and “laser.” After they removed duplicate cases and excluded cases that did not report dermatologic complications or cutaneous energy-based procedures, the final analysis included 75 cases.
Most of the appellants/plaintiffs (66; 88%) were women, a greater number of cases were in the Northeast (26; 34.7%) and the South (23; 30.7%), and the fewest cases were in the Midwest (12 [16%]). The most common anatomical sites were the face, head, and/or neck, and 43 of the cases (57.3%) were decided in favor of the appellee/defendant or the party defending against the appeal, while 29 (38.7%) were in favor of the appellant/plaintiff or the party appealing, and three cases (4%) did not report a verdict.
In other findings, plastic surgeons were the most litigated healthcare professionals (18; 24%), while 39 of the overall cases (52%) involved nonphysician operators (NPOs), 32 (42.7%) involved a physician operator, and 4 cases (5.3%) did not name a device operator. The most common procedure performed in the included cases was laser hair removal (33; 44%). Complications from energy-based devices included burns, scarring, and pigmentation changes. Statistically significant associations were neither found between verdict outcome and appellee/defendant type nor found between energy-device operator or anatomical site.
The authors acknowledged certain limitations of the study, including the fact that the LexisNexis database does not contain cases handled in out-of-court settlements and cases that underwent third-party arbitration.
“Physicians must recognize their responsibility when delegating procedures to NPOs and their role in supervision of these procedures,” they concluded. “Comprehensive training for physicians and their agents is necessary to diminish adverse outcomes and legal risks. Moreover, all practitioners should be held to the same standard of care. Familiarity with malpractice trends not only strengthens the patient-provider relationship but also equips providers with effective strategies to minimize the risk of legal repercussions.”
Mathew M. Avram, MD, JD, director of laser, cosmetics, and dermatologic surgery at Massachusetts General Hospital, Boston, who was asked to comment on the study, said that it “reaffirms previous studies which show that laser hair removal continues to be the most litigated procedure in laser surgery, and that nonphysician operators are most commonly litigated against. It further reiterates the importance of close supervision and expert training of procedures delegated by physicians.”
Neither the authors nor Dr. Avram reported having relevant financial disclosures.
A version of this article first appeared on Medscape.com.
“The utilization of laser and energy-based devices (LEBD) has grown substantially,” corresponding author Scott Stratman, MD, MPH, and coauthors wrote in their study, which was published online in the Journal of the American Academy of Dermatology. “This has led to a rise in practitioners, both physicians and nonphysicians, who may lack the requisite training in LEBD procedures. Subsequently, procedures performed by these untrained practitioners have resulted in more lawsuits related to patient complications. As the demand for LEBD procedures and the number of practitioners performing these procedures increase, it remains paramount to characterize the trends of malpractice cases involving these procedures.”
Dr. Stratman, a dermatology resident at the Icahn School of Medicine at Mount Sinai, New York City, and colleagues queried the LexisNexis database from 1985 to Sept. 30, 2023, for all state, federal, and appellate cases that included the terms “negligence” or “malpractice” and “skin” and “laser.” After they removed duplicate cases and excluded cases that did not report dermatologic complications or cutaneous energy-based procedures, the final analysis included 75 cases.
Most of the appellants/plaintiffs (66; 88%) were women, a greater number of cases were in the Northeast (26; 34.7%) and the South (23; 30.7%), and the fewest cases were in the Midwest (12 [16%]). The most common anatomical sites were the face, head, and/or neck, and 43 of the cases (57.3%) were decided in favor of the appellee/defendant or the party defending against the appeal, while 29 (38.7%) were in favor of the appellant/plaintiff or the party appealing, and three cases (4%) did not report a verdict.
In other findings, plastic surgeons were the most litigated healthcare professionals (18; 24%), while 39 of the overall cases (52%) involved nonphysician operators (NPOs), 32 (42.7%) involved a physician operator, and 4 cases (5.3%) did not name a device operator. The most common procedure performed in the included cases was laser hair removal (33; 44%). Complications from energy-based devices included burns, scarring, and pigmentation changes. Statistically significant associations were neither found between verdict outcome and appellee/defendant type nor found between energy-device operator or anatomical site.
The authors acknowledged certain limitations of the study, including the fact that the LexisNexis database does not contain cases handled in out-of-court settlements and cases that underwent third-party arbitration.
“Physicians must recognize their responsibility when delegating procedures to NPOs and their role in supervision of these procedures,” they concluded. “Comprehensive training for physicians and their agents is necessary to diminish adverse outcomes and legal risks. Moreover, all practitioners should be held to the same standard of care. Familiarity with malpractice trends not only strengthens the patient-provider relationship but also equips providers with effective strategies to minimize the risk of legal repercussions.”
Mathew M. Avram, MD, JD, director of laser, cosmetics, and dermatologic surgery at Massachusetts General Hospital, Boston, who was asked to comment on the study, said that it “reaffirms previous studies which show that laser hair removal continues to be the most litigated procedure in laser surgery, and that nonphysician operators are most commonly litigated against. It further reiterates the importance of close supervision and expert training of procedures delegated by physicians.”
Neither the authors nor Dr. Avram reported having relevant financial disclosures.
A version of this article first appeared on Medscape.com.
FROM THE JOURNAL OF THE AMERICAN ACADEMY OF DERMATOLOGY
‘Therapeutic Continuums’ Guide Systemic Sclerosis Treatment in Updated EULAR Recommendations
VIENNA – The use of immunosuppressive and antifibrotic drugs to treat skin and lung fibrosis leads updated recommendations from the European Alliance of Associations for Rheumatology (EULAR) for the treatment of systemic sclerosis.
“The most impactful new recommendation relates to the evidence for immunosuppressive agents and antifibrotics for the treatment of skin fibrosis and lung fibrosis,” said Francesco Del Galdo, MD, PhD, professor of experimental medicine, consultant rheumatologist, and scleroderma and connective tissue diseases specialist at Leeds Teaching Hospitals NHS Trust, Leeds, England. Dr. Del Galdo presented the update at the annual European Congress of Rheumatology.
“But there are also new recommendations, including a redefined target population for hematopoietic stem cell transplantation following cyclophosphamide, the upfront combination treatment at the time of diagnosis of pulmonary arterial hypertension [PAH], and a negative recommendation for the use of anticoagulants for pulmonary arterial hypertension,” noted Dr. Del Galdo, highlighting key updates in the 2024 recommendations.
Robert B.M. Landewé, MD, PhD, professor and rheumatologist at Amsterdam University Medical Center, Amsterdam, the Netherlands, and Zuyderland Medical Center, Heerlen, the Netherlands, co-moderated the session on EULAR recommendations. “The management of systemic sclerosis is a field in which a lot is happening,” he said. “The last update goes back to 2017, and in the meantime, many new approaches have seen the light, especially pertaining to skin fibrosis and interstitial lung disease. Six new recommendations have been coined, covering drugs like mycophenolate mofetil, nintedanib, rituximab, and tocilizumab. None of these therapies were present in the 2017 recommendations. It seems the field is now ready to further expand on targeted therapies for the management of musculoskeletal and gastrointestinal manifestations, calcinosis, and the local management of digital ulcers.”
‘Therapeutic Continuums’ Aid Disease Management
Dr. Del Galdo and his colleagues grouped the various interventions across what the recommendations label as evidence-backed “therapeutic continuums.” These span six of the eight different clinical manifestations of systemic sclerosis: Raynaud’s phenomenon, digital ulcers, pulmonary hypertension, musculoskeletal manifestations, skin fibrosis, interstitial lung disease (ILD), and gastrointestinal and renal crisis.
A slide showing the different strengths of evidence for various drugs across the eight manifestations illustrated the principle behind the therapeutic continuums. “These ‘therapeutic continuums’ suggest a common pathogenetic mechanism driving the various manifestations of disease,” said Dr. Del Galdo. For example, he noted, “If rituximab had a positive response in skin and in lung, it suggests that B cells play a role in the clinical manifestations of skin and lung in this disease.”
Dr. Del Galdo highlighted the new immunosuppression continuum and associated treatments for skin and lung fibrosis. “For skin involvement, the task force recommended mycophenolate, methotrexate, and rituximab, with tocilizumab having a lower level of evidence and lower recommendation strength; similarly, in interstitial lung disease, we have rituximab, mycophenolate, cyclophosphamide, and nintedanib, and these all have the highest strength of evidence. Tocilizumab is assigned one strength of evidence below the other drugs.”
He also cited the phosphodiesterase 5 inhibitor (PDE5i) drugs that are used across Raynaud’s phenomenon, digital ulcers, and pulmonary arterial hypertension, which together form a vascular therapeutic continuum.
The complexity of systemic sclerosis and multiple manifestations was a major determinant of the recommendations, Dr. Del Galdo pointed out. “The task force realized that since this is such a complex disease, we cannot recommend one treatment unconditionally. For example, with mycophenolate mofetil, what works for most patients for the skin and lung manifestations might not for someone who experiences severe diarrhea, in which mycophenolate is contraindicated. So, the highest degree of recommendation that the task force felt comfortable with was ‘should be considered.’ ”
Dr. Del Galdo stressed that the complex nature of systemic sclerosis means that “when thinking of treating one manifestation, you also always need to consider all the other clinical manifestations as experienced by the patient, and it is this multifaceted scenario that will ultimately lead to your final choice.”
Turning to new evidence around drug use, Dr. Del Galdo said that rituximab has the highest level of evidence across skin and lung manifestations, nintedanib is new in lung, and tocilizumab is new across both skin and lung.
To treat systemic sclerosis–pulmonary arterial hypertension (SSc-PAH), as long as there are no contraindications, the task force recommends using PDE5i and endothelin receptor antagonists (ERAs) at diagnosis. Data from phase 3 trials show a better outcome when the combination is established early.
The task force suggests avoiding the use of warfarin in PAH. “This is supported by a signal from two trials showing an increase in morbidity and mortality in these patients,” noted Dr. Del Galdo.
He also pointed out that selexipag and riociguat were new and important second-line additions for the treatment of PAH, and — consistent with the ERA approach — the EULAR recommendation supports frequent follow-up to establish a treat-to-target approach to maximizing clinical outcomes in SSc-PAH and SSc-ILD. “Specifically, for the first time, we recommend monitoring the effect of any chosen intervention selected within 3-6 months of starting. The evidence suggests there is a group of patients who respond and some who respond less well and who might benefit from a second-line intervention.”
For example, results of one trial support the approach of adding an antifibrotic agent to reduce progression in people with progressive lung fibrosis. “Similarly, for pulmonary hypertension, we recommend putting patients on dual treatment, and if this fails, place them on selexipag or switch the PDE5i to riociguat,” Dr. Del Galdo said.
Systemic Sclerosis Research Agenda and Recommendations Align
Dr. Del Galdo highlighted the value of therapeutic continuums in advancing disease understanding. “It is starting to teach us what we know and what we don’t and where do we need to build more evidence. Effectively, they determine where the gaps in therapy lie, and this starts to guide the research agenda.
“In fact, what is really interesting about this recommendation update — certainly from the perspective of disease understanding — is that we are starting to have a bird’s-eye view of the clinical manifestations of scleroderma that have so often been dealt with separately. Now we are starting to build a cumulative evidence map of this disease.”
In 2017, the research agenda largely advocated identifying immune-targeting drugs for skin and lung fibrosis, Dr. Del Galdo pointed out. “Now, we’ve done that — we’ve identified appropriate immunosuppressive drugs — and this is testimony to the importance of these recommendations because what prioritized the research agenda 10 years ago ended up informing the clinical trials and made it into the recommendations.”
“We definitely are one step forward compared to this 2017 recommendation and closer to what we would like to do,” he asserted.
Remission Elusive but Getting Closer
In some respects, according to Dr. Del Galdo, research and development is making relatively slow progress, especially compared with other rheumatologic diseases such as rheumatoid arthritis. “We cannot put patients with systemic sclerosis in remission yet. But I think we are one step ahead in that we’ve now established the treat-to-target approach to maximize the efficacy with which we can stall disease progression, but we cannot yet put these patients into remission,” he said. Systemic sclerosis has multiple manifestations, and fibrotic damage cannot be reversed. “Right now, the scar will remain there forever,” he noted.
Until remission is achievable, Dr. Del Galdo advises diagnosing and treating patients earlier to prevent fibrotic manifestations.
Dr. Del Galdo explained the three leading priorities on the systemic sclerosis research agenda. “There are three because it is such a complex disease. The first is considering the patient voice — this is the most important one, and the patients say they want a more holistic approach — so trialing and treating multiple manifestations together.”
Second, Dr. Del Galdo said, he would like to see a patient-reported measure developed that can capture the entire disease.
Third, from a physician’s point of view, Dr. Del Galdo said, “We want to send the patients into remission. We need to continue to further deconvolute the clinical manifestations and find the bottleneck at the beginning of the natural history of disease.
“If we can find a drug that is effective very early on, before the patients start getting the eight different manifestations with different levels of severity, then we will be on the right road, which we hope will end in remission.”
Dr. Del Galdo has served on the speakers bureau for AstraZeneca and Janssen; consulted for AstraZeneca, Boehringer Ingelheim, Capella, Chemomab, Janssen, and Mitsubishi-Tanabe; and received grant or research support from AbbVie, AstraZeneca, Boheringer Ingelheim, Capella, Chemomab, Kymab, Janssen, and Mitsubishi-Tanabe. Dr. Landewé had no relevant disclosures.
A version of this article first appeared on Medscape.com.
VIENNA – The use of immunosuppressive and antifibrotic drugs to treat skin and lung fibrosis leads updated recommendations from the European Alliance of Associations for Rheumatology (EULAR) for the treatment of systemic sclerosis.
“The most impactful new recommendation relates to the evidence for immunosuppressive agents and antifibrotics for the treatment of skin fibrosis and lung fibrosis,” said Francesco Del Galdo, MD, PhD, professor of experimental medicine, consultant rheumatologist, and scleroderma and connective tissue diseases specialist at Leeds Teaching Hospitals NHS Trust, Leeds, England. Dr. Del Galdo presented the update at the annual European Congress of Rheumatology.
“But there are also new recommendations, including a redefined target population for hematopoietic stem cell transplantation following cyclophosphamide, the upfront combination treatment at the time of diagnosis of pulmonary arterial hypertension [PAH], and a negative recommendation for the use of anticoagulants for pulmonary arterial hypertension,” noted Dr. Del Galdo, highlighting key updates in the 2024 recommendations.
Robert B.M. Landewé, MD, PhD, professor and rheumatologist at Amsterdam University Medical Center, Amsterdam, the Netherlands, and Zuyderland Medical Center, Heerlen, the Netherlands, co-moderated the session on EULAR recommendations. “The management of systemic sclerosis is a field in which a lot is happening,” he said. “The last update goes back to 2017, and in the meantime, many new approaches have seen the light, especially pertaining to skin fibrosis and interstitial lung disease. Six new recommendations have been coined, covering drugs like mycophenolate mofetil, nintedanib, rituximab, and tocilizumab. None of these therapies were present in the 2017 recommendations. It seems the field is now ready to further expand on targeted therapies for the management of musculoskeletal and gastrointestinal manifestations, calcinosis, and the local management of digital ulcers.”
‘Therapeutic Continuums’ Aid Disease Management
Dr. Del Galdo and his colleagues grouped the various interventions across what the recommendations label as evidence-backed “therapeutic continuums.” These span six of the eight different clinical manifestations of systemic sclerosis: Raynaud’s phenomenon, digital ulcers, pulmonary hypertension, musculoskeletal manifestations, skin fibrosis, interstitial lung disease (ILD), and gastrointestinal and renal crisis.
A slide showing the different strengths of evidence for various drugs across the eight manifestations illustrated the principle behind the therapeutic continuums. “These ‘therapeutic continuums’ suggest a common pathogenetic mechanism driving the various manifestations of disease,” said Dr. Del Galdo. For example, he noted, “If rituximab had a positive response in skin and in lung, it suggests that B cells play a role in the clinical manifestations of skin and lung in this disease.”
Dr. Del Galdo highlighted the new immunosuppression continuum and associated treatments for skin and lung fibrosis. “For skin involvement, the task force recommended mycophenolate, methotrexate, and rituximab, with tocilizumab having a lower level of evidence and lower recommendation strength; similarly, in interstitial lung disease, we have rituximab, mycophenolate, cyclophosphamide, and nintedanib, and these all have the highest strength of evidence. Tocilizumab is assigned one strength of evidence below the other drugs.”
He also cited the phosphodiesterase 5 inhibitor (PDE5i) drugs that are used across Raynaud’s phenomenon, digital ulcers, and pulmonary arterial hypertension, which together form a vascular therapeutic continuum.
The complexity of systemic sclerosis and multiple manifestations was a major determinant of the recommendations, Dr. Del Galdo pointed out. “The task force realized that since this is such a complex disease, we cannot recommend one treatment unconditionally. For example, with mycophenolate mofetil, what works for most patients for the skin and lung manifestations might not for someone who experiences severe diarrhea, in which mycophenolate is contraindicated. So, the highest degree of recommendation that the task force felt comfortable with was ‘should be considered.’ ”
Dr. Del Galdo stressed that the complex nature of systemic sclerosis means that “when thinking of treating one manifestation, you also always need to consider all the other clinical manifestations as experienced by the patient, and it is this multifaceted scenario that will ultimately lead to your final choice.”
Turning to new evidence around drug use, Dr. Del Galdo said that rituximab has the highest level of evidence across skin and lung manifestations, nintedanib is new in lung, and tocilizumab is new across both skin and lung.
To treat systemic sclerosis–pulmonary arterial hypertension (SSc-PAH), as long as there are no contraindications, the task force recommends using PDE5i and endothelin receptor antagonists (ERAs) at diagnosis. Data from phase 3 trials show a better outcome when the combination is established early.
The task force suggests avoiding the use of warfarin in PAH. “This is supported by a signal from two trials showing an increase in morbidity and mortality in these patients,” noted Dr. Del Galdo.
He also pointed out that selexipag and riociguat were new and important second-line additions for the treatment of PAH, and — consistent with the ERA approach — the EULAR recommendation supports frequent follow-up to establish a treat-to-target approach to maximizing clinical outcomes in SSc-PAH and SSc-ILD. “Specifically, for the first time, we recommend monitoring the effect of any chosen intervention selected within 3-6 months of starting. The evidence suggests there is a group of patients who respond and some who respond less well and who might benefit from a second-line intervention.”
For example, results of one trial support the approach of adding an antifibrotic agent to reduce progression in people with progressive lung fibrosis. “Similarly, for pulmonary hypertension, we recommend putting patients on dual treatment, and if this fails, place them on selexipag or switch the PDE5i to riociguat,” Dr. Del Galdo said.
Systemic Sclerosis Research Agenda and Recommendations Align
Dr. Del Galdo highlighted the value of therapeutic continuums in advancing disease understanding. “It is starting to teach us what we know and what we don’t and where do we need to build more evidence. Effectively, they determine where the gaps in therapy lie, and this starts to guide the research agenda.
“In fact, what is really interesting about this recommendation update — certainly from the perspective of disease understanding — is that we are starting to have a bird’s-eye view of the clinical manifestations of scleroderma that have so often been dealt with separately. Now we are starting to build a cumulative evidence map of this disease.”
In 2017, the research agenda largely advocated identifying immune-targeting drugs for skin and lung fibrosis, Dr. Del Galdo pointed out. “Now, we’ve done that — we’ve identified appropriate immunosuppressive drugs — and this is testimony to the importance of these recommendations because what prioritized the research agenda 10 years ago ended up informing the clinical trials and made it into the recommendations.”
“We definitely are one step forward compared to this 2017 recommendation and closer to what we would like to do,” he asserted.
Remission Elusive but Getting Closer
In some respects, according to Dr. Del Galdo, research and development is making relatively slow progress, especially compared with other rheumatologic diseases such as rheumatoid arthritis. “We cannot put patients with systemic sclerosis in remission yet. But I think we are one step ahead in that we’ve now established the treat-to-target approach to maximize the efficacy with which we can stall disease progression, but we cannot yet put these patients into remission,” he said. Systemic sclerosis has multiple manifestations, and fibrotic damage cannot be reversed. “Right now, the scar will remain there forever,” he noted.
Until remission is achievable, Dr. Del Galdo advises diagnosing and treating patients earlier to prevent fibrotic manifestations.
Dr. Del Galdo explained the three leading priorities on the systemic sclerosis research agenda. “There are three because it is such a complex disease. The first is considering the patient voice — this is the most important one, and the patients say they want a more holistic approach — so trialing and treating multiple manifestations together.”
Second, Dr. Del Galdo said, he would like to see a patient-reported measure developed that can capture the entire disease.
Third, from a physician’s point of view, Dr. Del Galdo said, “We want to send the patients into remission. We need to continue to further deconvolute the clinical manifestations and find the bottleneck at the beginning of the natural history of disease.
“If we can find a drug that is effective very early on, before the patients start getting the eight different manifestations with different levels of severity, then we will be on the right road, which we hope will end in remission.”
Dr. Del Galdo has served on the speakers bureau for AstraZeneca and Janssen; consulted for AstraZeneca, Boehringer Ingelheim, Capella, Chemomab, Janssen, and Mitsubishi-Tanabe; and received grant or research support from AbbVie, AstraZeneca, Boheringer Ingelheim, Capella, Chemomab, Kymab, Janssen, and Mitsubishi-Tanabe. Dr. Landewé had no relevant disclosures.
A version of this article first appeared on Medscape.com.
VIENNA – The use of immunosuppressive and antifibrotic drugs to treat skin and lung fibrosis leads updated recommendations from the European Alliance of Associations for Rheumatology (EULAR) for the treatment of systemic sclerosis.
“The most impactful new recommendation relates to the evidence for immunosuppressive agents and antifibrotics for the treatment of skin fibrosis and lung fibrosis,” said Francesco Del Galdo, MD, PhD, professor of experimental medicine, consultant rheumatologist, and scleroderma and connective tissue diseases specialist at Leeds Teaching Hospitals NHS Trust, Leeds, England. Dr. Del Galdo presented the update at the annual European Congress of Rheumatology.
“But there are also new recommendations, including a redefined target population for hematopoietic stem cell transplantation following cyclophosphamide, the upfront combination treatment at the time of diagnosis of pulmonary arterial hypertension [PAH], and a negative recommendation for the use of anticoagulants for pulmonary arterial hypertension,” noted Dr. Del Galdo, highlighting key updates in the 2024 recommendations.
Robert B.M. Landewé, MD, PhD, professor and rheumatologist at Amsterdam University Medical Center, Amsterdam, the Netherlands, and Zuyderland Medical Center, Heerlen, the Netherlands, co-moderated the session on EULAR recommendations. “The management of systemic sclerosis is a field in which a lot is happening,” he said. “The last update goes back to 2017, and in the meantime, many new approaches have seen the light, especially pertaining to skin fibrosis and interstitial lung disease. Six new recommendations have been coined, covering drugs like mycophenolate mofetil, nintedanib, rituximab, and tocilizumab. None of these therapies were present in the 2017 recommendations. It seems the field is now ready to further expand on targeted therapies for the management of musculoskeletal and gastrointestinal manifestations, calcinosis, and the local management of digital ulcers.”
‘Therapeutic Continuums’ Aid Disease Management
Dr. Del Galdo and his colleagues grouped the various interventions across what the recommendations label as evidence-backed “therapeutic continuums.” These span six of the eight different clinical manifestations of systemic sclerosis: Raynaud’s phenomenon, digital ulcers, pulmonary hypertension, musculoskeletal manifestations, skin fibrosis, interstitial lung disease (ILD), and gastrointestinal and renal crisis.
A slide showing the different strengths of evidence for various drugs across the eight manifestations illustrated the principle behind the therapeutic continuums. “These ‘therapeutic continuums’ suggest a common pathogenetic mechanism driving the various manifestations of disease,” said Dr. Del Galdo. For example, he noted, “If rituximab had a positive response in skin and in lung, it suggests that B cells play a role in the clinical manifestations of skin and lung in this disease.”
Dr. Del Galdo highlighted the new immunosuppression continuum and associated treatments for skin and lung fibrosis. “For skin involvement, the task force recommended mycophenolate, methotrexate, and rituximab, with tocilizumab having a lower level of evidence and lower recommendation strength; similarly, in interstitial lung disease, we have rituximab, mycophenolate, cyclophosphamide, and nintedanib, and these all have the highest strength of evidence. Tocilizumab is assigned one strength of evidence below the other drugs.”
He also cited the phosphodiesterase 5 inhibitor (PDE5i) drugs that are used across Raynaud’s phenomenon, digital ulcers, and pulmonary arterial hypertension, which together form a vascular therapeutic continuum.
The complexity of systemic sclerosis and multiple manifestations was a major determinant of the recommendations, Dr. Del Galdo pointed out. “The task force realized that since this is such a complex disease, we cannot recommend one treatment unconditionally. For example, with mycophenolate mofetil, what works for most patients for the skin and lung manifestations might not for someone who experiences severe diarrhea, in which mycophenolate is contraindicated. So, the highest degree of recommendation that the task force felt comfortable with was ‘should be considered.’ ”
Dr. Del Galdo stressed that the complex nature of systemic sclerosis means that “when thinking of treating one manifestation, you also always need to consider all the other clinical manifestations as experienced by the patient, and it is this multifaceted scenario that will ultimately lead to your final choice.”
Turning to new evidence around drug use, Dr. Del Galdo said that rituximab has the highest level of evidence across skin and lung manifestations, nintedanib is new in lung, and tocilizumab is new across both skin and lung.
To treat systemic sclerosis–pulmonary arterial hypertension (SSc-PAH), as long as there are no contraindications, the task force recommends using PDE5i and endothelin receptor antagonists (ERAs) at diagnosis. Data from phase 3 trials show a better outcome when the combination is established early.
The task force suggests avoiding the use of warfarin in PAH. “This is supported by a signal from two trials showing an increase in morbidity and mortality in these patients,” noted Dr. Del Galdo.
He also pointed out that selexipag and riociguat were new and important second-line additions for the treatment of PAH, and — consistent with the ERA approach — the EULAR recommendation supports frequent follow-up to establish a treat-to-target approach to maximizing clinical outcomes in SSc-PAH and SSc-ILD. “Specifically, for the first time, we recommend monitoring the effect of any chosen intervention selected within 3-6 months of starting. The evidence suggests there is a group of patients who respond and some who respond less well and who might benefit from a second-line intervention.”
For example, results of one trial support the approach of adding an antifibrotic agent to reduce progression in people with progressive lung fibrosis. “Similarly, for pulmonary hypertension, we recommend putting patients on dual treatment, and if this fails, place them on selexipag or switch the PDE5i to riociguat,” Dr. Del Galdo said.
Systemic Sclerosis Research Agenda and Recommendations Align
Dr. Del Galdo highlighted the value of therapeutic continuums in advancing disease understanding. “It is starting to teach us what we know and what we don’t and where do we need to build more evidence. Effectively, they determine where the gaps in therapy lie, and this starts to guide the research agenda.
“In fact, what is really interesting about this recommendation update — certainly from the perspective of disease understanding — is that we are starting to have a bird’s-eye view of the clinical manifestations of scleroderma that have so often been dealt with separately. Now we are starting to build a cumulative evidence map of this disease.”
In 2017, the research agenda largely advocated identifying immune-targeting drugs for skin and lung fibrosis, Dr. Del Galdo pointed out. “Now, we’ve done that — we’ve identified appropriate immunosuppressive drugs — and this is testimony to the importance of these recommendations because what prioritized the research agenda 10 years ago ended up informing the clinical trials and made it into the recommendations.”
“We definitely are one step forward compared to this 2017 recommendation and closer to what we would like to do,” he asserted.
Remission Elusive but Getting Closer
In some respects, according to Dr. Del Galdo, research and development is making relatively slow progress, especially compared with other rheumatologic diseases such as rheumatoid arthritis. “We cannot put patients with systemic sclerosis in remission yet. But I think we are one step ahead in that we’ve now established the treat-to-target approach to maximize the efficacy with which we can stall disease progression, but we cannot yet put these patients into remission,” he said. Systemic sclerosis has multiple manifestations, and fibrotic damage cannot be reversed. “Right now, the scar will remain there forever,” he noted.
Until remission is achievable, Dr. Del Galdo advises diagnosing and treating patients earlier to prevent fibrotic manifestations.
Dr. Del Galdo explained the three leading priorities on the systemic sclerosis research agenda. “There are three because it is such a complex disease. The first is considering the patient voice — this is the most important one, and the patients say they want a more holistic approach — so trialing and treating multiple manifestations together.”
Second, Dr. Del Galdo said, he would like to see a patient-reported measure developed that can capture the entire disease.
Third, from a physician’s point of view, Dr. Del Galdo said, “We want to send the patients into remission. We need to continue to further deconvolute the clinical manifestations and find the bottleneck at the beginning of the natural history of disease.
“If we can find a drug that is effective very early on, before the patients start getting the eight different manifestations with different levels of severity, then we will be on the right road, which we hope will end in remission.”
Dr. Del Galdo has served on the speakers bureau for AstraZeneca and Janssen; consulted for AstraZeneca, Boehringer Ingelheim, Capella, Chemomab, Janssen, and Mitsubishi-Tanabe; and received grant or research support from AbbVie, AstraZeneca, Boheringer Ingelheim, Capella, Chemomab, Kymab, Janssen, and Mitsubishi-Tanabe. Dr. Landewé had no relevant disclosures.
A version of this article first appeared on Medscape.com.
FROM EULAR 2024
Extensive Multidrug-Resistant Dermatophytosis From Trichophyton indotineae
To the Editor:
Historically, commonly available antifungal medications have been effective for treating dermatophytosis (tinea). However, recent tinea outbreaks caused by Trichophyton indotineae—a dermatophyte often resistant to terbinafine and sometimes to other antifungals—have been reported in South Asia, Europe, the Middle East, Southeast Asia, and Australia.1-5
Three confirmed cases of T indotineae dermatophytosis in the United States were reported in 2023 in New York3,6; a fourth confirmed case was reported in 2024 in Pennsylvania.7 Post hoc laboratory testing of fungal isolates in New York in 2022 and 2023 identified an additional 11 cases.8 We present a case of extensive multidrug-resistant tinea caused by T indotineae in a man in California.
An otherwise healthy 65-year-old man who had traveled to Europe in the past 3 months presented to his primary care physician with a widespread pruritic rash (Figure 1). He was treated with 2 weeks of oral terbinafine 250 mg/d and topical medicines, including clotrimazole cream 1%, fluocinonide ointment 0.05%, and clobetasol ointment 0.05% without improvement. Subsequently, 2 weeks of oral griseofulvin microsize 500 mg/d also proved ineffective. An antibody test was negative for HIV. His hemoglobin A1c was 6.2% (reference range, ≤5.6%). The patient was referred to dermatology.
Erythematous plaques—many scaly throughout and some annular with central clearing—were present on the arms, legs, and torso as well as in the groin. Honey crust was present on some plaques on the leg. A potassium hydroxide preparation showed abundant fungal hyphae. Material for fungal and bacterial cultures was collected. The patient was treated again with oral terbinafine 250 mg/d, an oral prednisone taper starting at 60 mg/d for a presumed id reaction, and various oral antihistamines for pruritus; all were ineffective. A bacterial culture showed only mixed skin flora. Oral fluconazole 200 mg/d was prescribed. A skin biopsy specimen showed compact orthokeratosis and parakeratosis of the stratum corneum with few neutrophils and focal pustule formation (Figure 2). Superficial perivascular inflammation, including lymphocytes, histiocytes, and few neutrophils, was present. A periodic acid–Schiff stain showed fungal hyphae in the stratum corneum and a hair follicle (Figure 3). After approximately 2 weeks, mold was identified in the fungal culture. Approximately 2 weeks thereafter, the organism was reported as Trichophyton species.

The rash did not improve; resistance to terbinafine, griseofulvin, and fluconazole was suspected clinically. The fungal isolate was sent to a reference laboratory (University of Texas Health Science Center, San Antonio). Meanwhile, oral itraconazole 200 mg twice daily and ketoconazole cream 2% were prescribed; the rash began to improve. A serum itraconazole trough level obtained 4 days after treatment initiation was 0.5 μg/mL (reference range, ≥0.6 μg/mL). The evening itraconazole dose was increased to 300 mg; a subsequent trough level was 0.8 μg/mL.


Approximately 1 month after the fungal isolate was sent to the reference laboratory, T indotineae was confirmed based on polymerase chain reaction (PCR) testing of internal transcribed spacer region sequences. Minimum inhibitory concentrations (MICs) obtained through antifungal susceptibility testing (AFST) were reported for fluconazole (8 μg/mL), griseofulvin (2 μg/mL), itraconazole (≤0.03 μg/mL), posaconazole (≤0.03 μg/mL), terbinafine (≥2 μg/mL), and voriconazole (0.125 μg/mL).
Approximately 7 weeks after itraconazole and ketoconazole were started, the rash had completely resolved. Nearly 8 months later (at the time this article was written), the rash had not recurred.
We report a unique case of T indotineae in a patient residing in California. Post hoc laboratory testing of dermatophyte isolates sent to the University of Texas reference laboratory identified terbinafine-resistant T indotineae specimens from the United States and Canada dating to 2017; clinical characteristics of patients from whom those isolates were obtained were unavailable.9
Trichophyton indotineae dermatophytosis typically is more extensive, inflamed, and pruritic, as well as likely more contagious, than tinea caused by other dermatophytes.5 Previously called Trichophyton mentagrophytes genotype VIII when first isolated in 2017, the pathogen was renamed T indotineae in 2020 after important genetic differences were discovered between it and other T mentagrophytes species.5 The emergence of T indotineae has been attributed to concomitant use of topical steroids and antifungals,5,10 inappropriate prescribing of antifungals,5 and nonadherence to antifungal treatment.5
Likely risk factors for T indotineae infection include suboptimal hygiene, overcrowded conditions, hot and humid environments, and tight-fitting synthetic clothing.4 Transmission from family members appears common,5 especially when fomites are shared.4 A case reported in Pennsylvania likely was acquired through sexual contact.7 Travel to South Asia has been associated with acquisition of T indotineae infection,3,5-7 though our patient and some others had not traveled there.3,8 It is not clear whether immunosuppression and diabetes mellitus are associated with T indotineae infection.4,5,8Trichophyton indotineae also can affect animals,11 though zoonotic transmission has not been reported.4
Not all T indotineae isolates are resistant to one or more antifungals; furthermore, antifungal resistance in other dermatophyte species has been reported.5 Terbinafine resistance in T indotineae is conferred by mutations in the gene encoding squalene epoxidase, which helps synthesize ergosterol—a component of the cell membrane in fungi.2,4,5,12 Although clinical cut-points for MIC obtained by AFST are not well established, T indotineae MICs for terbinafine of 0.5 μg/mL or more correlate with resistance.9 Resistance to azoles has been linked to overexpression of transporter genes, which increase azole efflux from cells, as well as to mutations in the gene encoding lanosterol 14α demethylase.4,12,13
Potassium hydroxide preparations and fungal cultures cannot differentiate T indotineae from other dermatophytes that typically cause tinea.5,14 Histopathologic findings in our case were no different than those of non–T indotineae dermatophytes. Only molecular testing using PCR assays to sequence internal transcribed spacer genes can confirm T indotineae infection. However, PCR assays and AFST are not available in many US laboratories.5 Matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry has shown promise in distinguishing T indotineae from other dermatophytes, though its clinical use is limited and it cannot assess terbinafine sensitivity.15,16 Clinicians in the United States who want to test specimens from cases suspicious for T indotineae infection should contact their local or state health department or the Centers for Disease Control and Prevention for assistance.3,5
Systemic treatment typically is necessary for T indotineae infection.5 Combinations of oral and topical azoles have been used, as well as topical ciclopirox, amorolfine (not available in the United States), and luliconazole.1,5,17-21
Itraconazole has emerged as the treatment of choice for T indotineae tinea, typically at 200 mg/d and often for courses of more than 3 months.5 Testing for serum itraconazole trough levels, as done for our patient, typically is not recommended. Clinicians should counsel patients to take itraconazole with high-fat foods and an acidic beverage to increase bioavailability.5 Potential adverse effects of itraconazole include heart failure and numerous drug-drug interactions.5,22 Patients with T indotineae dermatophytosis should avoid sharing personal belongings and having skin-to-skin contact of affected areas with others.4
Dermatologists who suspect T indotineae infection should work with public health agencies that can assist with testing and undertake infection surveillance, prevention, and control.5,23 Challenges to diagnosing and managing T indotineae infection include lack of awareness among dermatology providers, the need for specialized laboratory testing to confirm infection, lack of established clinical cut-points for MICs from AFST, the need for longer duration of treatment vs what is needed for typical tinea, and potential challenges with insurance coverage for testing and treatment. Empiric treatment with itraconazole should be considered when terbinafine-resistant dermatophytosis is suspected or when terbinafine-resistant T indotineae infection is confirmed.
Acknowledgments—Jeremy Gold, MD; Dallas J. Smith, PharmD; and Shawn Lockhart, PhD, all of the Centers for Disease Control and Prevention, Mycotic Diseases Branch (Atlanta, Georgia), provided helpful comments to the authors in preparing the manuscript of this article.
- Uhrlaß S, Verma SB, Gräser Y, al. Trichophyton indotineae—an emerging pathogen causing recalcitrant dermatophytoses in India and worldwide—a multidimensional perspective. J Fungi (Basel). 2022;8:757. doi:10.3390/jof8070757
- Jabet A, Brun S, Normand A-C, et al. Extensive dermatophytosis caused by terbinafine-resistant Trichophyton indotineae, France. Emerg Infect Dis. 2022;28:229-233. doi:10.3201/eid2801.210883
- Caplan AS, Chaturvedi S, Zhu Y, et al. Notes from the field. First reported U.S. cases of tinea caused by Trichophyton indotineae—New York City, December 2021-March 2023. MMWR Morb Mortal Wkly Rep. 2023;72:536-537. doi:10.15585/mmwr.mm7219a4
- Jabet A, Normand A-C, Brun S, et al. Trichophyton indotineae, from epidemiology to therapeutic. J Mycol Med. 2023;33:101383. doi:10.1016/j.mycmed.2023.101383
- Hill RC, Caplan AS, Elewski B, et al. Expert panel review of skin and hair dermatophytoses in an era of antifungal resistance. Am J Clin Dermatol. 2024;25:359-389. doi:10.1007/s40257-024-00848-1
- Caplan AS, Zakhem GA, Pomeranz MK. Trichophyton mentagrophytes internal transcribed spacer genotype VIII. JAMA Dermatol. 2023;159:1130. doi:10.1001/jamadermatol.2023.2645
- Spivack S, Gold JAW, Lockhart SR, et al. Potential sexual transmission of antifungal-resistant Trichophyton indotineae. Emerg Infect Dis. 2024;30:807-809. doi:10.3201/eid3004.240115
- Caplan AS, Todd GC, Zhu Y, et al. Clinical course, antifungal susceptibility, and genomic sequencing of Trichophyton indotineae. JAMA Dermatol. Published online May 15, 2024. doi:10.1001/jamadermatol.2024.1126
- Cañete-Gibas CF, Mele J, Patterson HP, et al. Terbinafine-resistant dermatophytes and the presence of Trichophyton indotineae in North America. J Clin Microbiol. 2023;61:e0056223. doi:10.1128/jcm.00562-23
- Gupta AK, Venkataraman M, Hall DC, et al. The emergence of Trichophyton indotineae: implications for clinical practice. Int J Dermatol. 2023;62:857-861.
- Oladzad V, Nasrollahi Omran A, Haghani I, et al. Multi-drug resistance Trichophyton indotineae in a stray dog. Res Vet Sci. 2024;166:105105. doi:10.1016/j.rvsc.2023.105105
- Martinez-Rossi NM, Bitencourt TA, Peres NTA, et al. Dermatophyte resistance to antifungal drugs: mechanisms and prospectus. Front Microbiol. 2018;9:1108. doi:10.3389/fmicb.2018.01108
- Sacheli R, Hayette MP. Antifungal resistance in dermatophytes: genetic considerations, clinical presentations and alternative therapies. J Fungi (Basel). 2021;711:983. doi:10.3390/jof7110983
- Gupta AK, Cooper EA. Dermatophytosis (tinea) and other superficial fungal infections. In: Hospenthal DR, Rinaldi MG, eds. Diagnosis and Treatment of Human Mycoses. Humana Press; 2008:355-381.
- Normand A-C, Moreno-Sabater A, Jabet A, et al. MALDI-TOF mass spectrometry online identification of Trichophyton indotineae using the MSI-2 application. J Fungi (Basel). 2022;8:1103. doi:10.3390/jof8101103
- De Paepe R, Normand A-C, Uhrlaß S, et al. Resistance profile, terbinafine resistance screening and MALDI-TOF MS identification of the emerging pathogen Trichophyton indotineae. Mycopathologia. 2024;189:29. doi:10.1007/s11046-024-00835-4
- Rajagopalan M, Inamadar A, Mittal A, et al. Expert consensus on the management of dermatophytosis in India (ECTODERM India). BMC Dermatol. 2018;18:6. doi:10.1186/s12895-018-0073-1
- Verma SB, Panda S, Nenoff P, et al. The unprecedented epidemic-like scenario of dermatophytosis in India: III. Antifungal resistance and treatment options. Indian J Dermatol Venereol Leprol. 2021;87:468-482. doi:10.25259/IJDVL_303_20
- Shaw D, Singh S, Dogra S, et al. MIC and upper limit of wild-type distribution for 13 antifungal agents against a Trichophyton mentagrophytes–Trichophyton interdigitale complex of Indian origin. Antimicrob Agents Chemother. 2020;64:E01964-19. doi:10.1128/AAC.01964-19
- Burmester A, Hipler U-C, Uhrlaß S, et al. Indian Trichophyton mentagrophytes squalene epoxidase erg1 double mutants show high proportion of combined fluconazole and terbinafine resistance. Mycoses. 2020;63:1175-1180. doi:10.1111/myc.13150
- Khurana A, Agarwal A, Agrawal D, et al. Effect of different itraconazole dosing regimens on cure rates, treatment duration, safety, and relapse rates in adult patients with tinea corporis/cruris: a randomized clinical trial. JAMA Dermatol. 2022;158:1269-1278. doi:10.1001/jamadermatol.2022.3745
- Itraconazole capsule. DailyMed [Internet]. Updated June 3, 2024. Accessed June 19, 2024. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=2ab38a8a-3708-4b97-9f7f-8e554a15348d
- Bui TS, Katz KA. Resistant Trichophyton indotineae dermatophytosis—an emerging pandemic, now in the US. JAMA Dermatol. Published online May 15, 2024. doi:10.1001/jamadermatol.2024.1125
To the Editor:
Historically, commonly available antifungal medications have been effective for treating dermatophytosis (tinea). However, recent tinea outbreaks caused by Trichophyton indotineae—a dermatophyte often resistant to terbinafine and sometimes to other antifungals—have been reported in South Asia, Europe, the Middle East, Southeast Asia, and Australia.1-5
Three confirmed cases of T indotineae dermatophytosis in the United States were reported in 2023 in New York3,6; a fourth confirmed case was reported in 2024 in Pennsylvania.7 Post hoc laboratory testing of fungal isolates in New York in 2022 and 2023 identified an additional 11 cases.8 We present a case of extensive multidrug-resistant tinea caused by T indotineae in a man in California.
An otherwise healthy 65-year-old man who had traveled to Europe in the past 3 months presented to his primary care physician with a widespread pruritic rash (Figure 1). He was treated with 2 weeks of oral terbinafine 250 mg/d and topical medicines, including clotrimazole cream 1%, fluocinonide ointment 0.05%, and clobetasol ointment 0.05% without improvement. Subsequently, 2 weeks of oral griseofulvin microsize 500 mg/d also proved ineffective. An antibody test was negative for HIV. His hemoglobin A1c was 6.2% (reference range, ≤5.6%). The patient was referred to dermatology.
Erythematous plaques—many scaly throughout and some annular with central clearing—were present on the arms, legs, and torso as well as in the groin. Honey crust was present on some plaques on the leg. A potassium hydroxide preparation showed abundant fungal hyphae. Material for fungal and bacterial cultures was collected. The patient was treated again with oral terbinafine 250 mg/d, an oral prednisone taper starting at 60 mg/d for a presumed id reaction, and various oral antihistamines for pruritus; all were ineffective. A bacterial culture showed only mixed skin flora. Oral fluconazole 200 mg/d was prescribed. A skin biopsy specimen showed compact orthokeratosis and parakeratosis of the stratum corneum with few neutrophils and focal pustule formation (Figure 2). Superficial perivascular inflammation, including lymphocytes, histiocytes, and few neutrophils, was present. A periodic acid–Schiff stain showed fungal hyphae in the stratum corneum and a hair follicle (Figure 3). After approximately 2 weeks, mold was identified in the fungal culture. Approximately 2 weeks thereafter, the organism was reported as Trichophyton species.

The rash did not improve; resistance to terbinafine, griseofulvin, and fluconazole was suspected clinically. The fungal isolate was sent to a reference laboratory (University of Texas Health Science Center, San Antonio). Meanwhile, oral itraconazole 200 mg twice daily and ketoconazole cream 2% were prescribed; the rash began to improve. A serum itraconazole trough level obtained 4 days after treatment initiation was 0.5 μg/mL (reference range, ≥0.6 μg/mL). The evening itraconazole dose was increased to 300 mg; a subsequent trough level was 0.8 μg/mL.


Approximately 1 month after the fungal isolate was sent to the reference laboratory, T indotineae was confirmed based on polymerase chain reaction (PCR) testing of internal transcribed spacer region sequences. Minimum inhibitory concentrations (MICs) obtained through antifungal susceptibility testing (AFST) were reported for fluconazole (8 μg/mL), griseofulvin (2 μg/mL), itraconazole (≤0.03 μg/mL), posaconazole (≤0.03 μg/mL), terbinafine (≥2 μg/mL), and voriconazole (0.125 μg/mL).
Approximately 7 weeks after itraconazole and ketoconazole were started, the rash had completely resolved. Nearly 8 months later (at the time this article was written), the rash had not recurred.
We report a unique case of T indotineae in a patient residing in California. Post hoc laboratory testing of dermatophyte isolates sent to the University of Texas reference laboratory identified terbinafine-resistant T indotineae specimens from the United States and Canada dating to 2017; clinical characteristics of patients from whom those isolates were obtained were unavailable.9
Trichophyton indotineae dermatophytosis typically is more extensive, inflamed, and pruritic, as well as likely more contagious, than tinea caused by other dermatophytes.5 Previously called Trichophyton mentagrophytes genotype VIII when first isolated in 2017, the pathogen was renamed T indotineae in 2020 after important genetic differences were discovered between it and other T mentagrophytes species.5 The emergence of T indotineae has been attributed to concomitant use of topical steroids and antifungals,5,10 inappropriate prescribing of antifungals,5 and nonadherence to antifungal treatment.5
Likely risk factors for T indotineae infection include suboptimal hygiene, overcrowded conditions, hot and humid environments, and tight-fitting synthetic clothing.4 Transmission from family members appears common,5 especially when fomites are shared.4 A case reported in Pennsylvania likely was acquired through sexual contact.7 Travel to South Asia has been associated with acquisition of T indotineae infection,3,5-7 though our patient and some others had not traveled there.3,8 It is not clear whether immunosuppression and diabetes mellitus are associated with T indotineae infection.4,5,8Trichophyton indotineae also can affect animals,11 though zoonotic transmission has not been reported.4
Not all T indotineae isolates are resistant to one or more antifungals; furthermore, antifungal resistance in other dermatophyte species has been reported.5 Terbinafine resistance in T indotineae is conferred by mutations in the gene encoding squalene epoxidase, which helps synthesize ergosterol—a component of the cell membrane in fungi.2,4,5,12 Although clinical cut-points for MIC obtained by AFST are not well established, T indotineae MICs for terbinafine of 0.5 μg/mL or more correlate with resistance.9 Resistance to azoles has been linked to overexpression of transporter genes, which increase azole efflux from cells, as well as to mutations in the gene encoding lanosterol 14α demethylase.4,12,13
Potassium hydroxide preparations and fungal cultures cannot differentiate T indotineae from other dermatophytes that typically cause tinea.5,14 Histopathologic findings in our case were no different than those of non–T indotineae dermatophytes. Only molecular testing using PCR assays to sequence internal transcribed spacer genes can confirm T indotineae infection. However, PCR assays and AFST are not available in many US laboratories.5 Matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry has shown promise in distinguishing T indotineae from other dermatophytes, though its clinical use is limited and it cannot assess terbinafine sensitivity.15,16 Clinicians in the United States who want to test specimens from cases suspicious for T indotineae infection should contact their local or state health department or the Centers for Disease Control and Prevention for assistance.3,5
Systemic treatment typically is necessary for T indotineae infection.5 Combinations of oral and topical azoles have been used, as well as topical ciclopirox, amorolfine (not available in the United States), and luliconazole.1,5,17-21
Itraconazole has emerged as the treatment of choice for T indotineae tinea, typically at 200 mg/d and often for courses of more than 3 months.5 Testing for serum itraconazole trough levels, as done for our patient, typically is not recommended. Clinicians should counsel patients to take itraconazole with high-fat foods and an acidic beverage to increase bioavailability.5 Potential adverse effects of itraconazole include heart failure and numerous drug-drug interactions.5,22 Patients with T indotineae dermatophytosis should avoid sharing personal belongings and having skin-to-skin contact of affected areas with others.4
Dermatologists who suspect T indotineae infection should work with public health agencies that can assist with testing and undertake infection surveillance, prevention, and control.5,23 Challenges to diagnosing and managing T indotineae infection include lack of awareness among dermatology providers, the need for specialized laboratory testing to confirm infection, lack of established clinical cut-points for MICs from AFST, the need for longer duration of treatment vs what is needed for typical tinea, and potential challenges with insurance coverage for testing and treatment. Empiric treatment with itraconazole should be considered when terbinafine-resistant dermatophytosis is suspected or when terbinafine-resistant T indotineae infection is confirmed.
Acknowledgments—Jeremy Gold, MD; Dallas J. Smith, PharmD; and Shawn Lockhart, PhD, all of the Centers for Disease Control and Prevention, Mycotic Diseases Branch (Atlanta, Georgia), provided helpful comments to the authors in preparing the manuscript of this article.
To the Editor:
Historically, commonly available antifungal medications have been effective for treating dermatophytosis (tinea). However, recent tinea outbreaks caused by Trichophyton indotineae—a dermatophyte often resistant to terbinafine and sometimes to other antifungals—have been reported in South Asia, Europe, the Middle East, Southeast Asia, and Australia.1-5
Three confirmed cases of T indotineae dermatophytosis in the United States were reported in 2023 in New York3,6; a fourth confirmed case was reported in 2024 in Pennsylvania.7 Post hoc laboratory testing of fungal isolates in New York in 2022 and 2023 identified an additional 11 cases.8 We present a case of extensive multidrug-resistant tinea caused by T indotineae in a man in California.
An otherwise healthy 65-year-old man who had traveled to Europe in the past 3 months presented to his primary care physician with a widespread pruritic rash (Figure 1). He was treated with 2 weeks of oral terbinafine 250 mg/d and topical medicines, including clotrimazole cream 1%, fluocinonide ointment 0.05%, and clobetasol ointment 0.05% without improvement. Subsequently, 2 weeks of oral griseofulvin microsize 500 mg/d also proved ineffective. An antibody test was negative for HIV. His hemoglobin A1c was 6.2% (reference range, ≤5.6%). The patient was referred to dermatology.
Erythematous plaques—many scaly throughout and some annular with central clearing—were present on the arms, legs, and torso as well as in the groin. Honey crust was present on some plaques on the leg. A potassium hydroxide preparation showed abundant fungal hyphae. Material for fungal and bacterial cultures was collected. The patient was treated again with oral terbinafine 250 mg/d, an oral prednisone taper starting at 60 mg/d for a presumed id reaction, and various oral antihistamines for pruritus; all were ineffective. A bacterial culture showed only mixed skin flora. Oral fluconazole 200 mg/d was prescribed. A skin biopsy specimen showed compact orthokeratosis and parakeratosis of the stratum corneum with few neutrophils and focal pustule formation (Figure 2). Superficial perivascular inflammation, including lymphocytes, histiocytes, and few neutrophils, was present. A periodic acid–Schiff stain showed fungal hyphae in the stratum corneum and a hair follicle (Figure 3). After approximately 2 weeks, mold was identified in the fungal culture. Approximately 2 weeks thereafter, the organism was reported as Trichophyton species.

The rash did not improve; resistance to terbinafine, griseofulvin, and fluconazole was suspected clinically. The fungal isolate was sent to a reference laboratory (University of Texas Health Science Center, San Antonio). Meanwhile, oral itraconazole 200 mg twice daily and ketoconazole cream 2% were prescribed; the rash began to improve. A serum itraconazole trough level obtained 4 days after treatment initiation was 0.5 μg/mL (reference range, ≥0.6 μg/mL). The evening itraconazole dose was increased to 300 mg; a subsequent trough level was 0.8 μg/mL.


Approximately 1 month after the fungal isolate was sent to the reference laboratory, T indotineae was confirmed based on polymerase chain reaction (PCR) testing of internal transcribed spacer region sequences. Minimum inhibitory concentrations (MICs) obtained through antifungal susceptibility testing (AFST) were reported for fluconazole (8 μg/mL), griseofulvin (2 μg/mL), itraconazole (≤0.03 μg/mL), posaconazole (≤0.03 μg/mL), terbinafine (≥2 μg/mL), and voriconazole (0.125 μg/mL).
Approximately 7 weeks after itraconazole and ketoconazole were started, the rash had completely resolved. Nearly 8 months later (at the time this article was written), the rash had not recurred.
We report a unique case of T indotineae in a patient residing in California. Post hoc laboratory testing of dermatophyte isolates sent to the University of Texas reference laboratory identified terbinafine-resistant T indotineae specimens from the United States and Canada dating to 2017; clinical characteristics of patients from whom those isolates were obtained were unavailable.9
Trichophyton indotineae dermatophytosis typically is more extensive, inflamed, and pruritic, as well as likely more contagious, than tinea caused by other dermatophytes.5 Previously called Trichophyton mentagrophytes genotype VIII when first isolated in 2017, the pathogen was renamed T indotineae in 2020 after important genetic differences were discovered between it and other T mentagrophytes species.5 The emergence of T indotineae has been attributed to concomitant use of topical steroids and antifungals,5,10 inappropriate prescribing of antifungals,5 and nonadherence to antifungal treatment.5
Likely risk factors for T indotineae infection include suboptimal hygiene, overcrowded conditions, hot and humid environments, and tight-fitting synthetic clothing.4 Transmission from family members appears common,5 especially when fomites are shared.4 A case reported in Pennsylvania likely was acquired through sexual contact.7 Travel to South Asia has been associated with acquisition of T indotineae infection,3,5-7 though our patient and some others had not traveled there.3,8 It is not clear whether immunosuppression and diabetes mellitus are associated with T indotineae infection.4,5,8Trichophyton indotineae also can affect animals,11 though zoonotic transmission has not been reported.4
Not all T indotineae isolates are resistant to one or more antifungals; furthermore, antifungal resistance in other dermatophyte species has been reported.5 Terbinafine resistance in T indotineae is conferred by mutations in the gene encoding squalene epoxidase, which helps synthesize ergosterol—a component of the cell membrane in fungi.2,4,5,12 Although clinical cut-points for MIC obtained by AFST are not well established, T indotineae MICs for terbinafine of 0.5 μg/mL or more correlate with resistance.9 Resistance to azoles has been linked to overexpression of transporter genes, which increase azole efflux from cells, as well as to mutations in the gene encoding lanosterol 14α demethylase.4,12,13
Potassium hydroxide preparations and fungal cultures cannot differentiate T indotineae from other dermatophytes that typically cause tinea.5,14 Histopathologic findings in our case were no different than those of non–T indotineae dermatophytes. Only molecular testing using PCR assays to sequence internal transcribed spacer genes can confirm T indotineae infection. However, PCR assays and AFST are not available in many US laboratories.5 Matrix-assisted laser desorption ionization-time of flight (MALDI-TOF) mass spectrometry has shown promise in distinguishing T indotineae from other dermatophytes, though its clinical use is limited and it cannot assess terbinafine sensitivity.15,16 Clinicians in the United States who want to test specimens from cases suspicious for T indotineae infection should contact their local or state health department or the Centers for Disease Control and Prevention for assistance.3,5
Systemic treatment typically is necessary for T indotineae infection.5 Combinations of oral and topical azoles have been used, as well as topical ciclopirox, amorolfine (not available in the United States), and luliconazole.1,5,17-21
Itraconazole has emerged as the treatment of choice for T indotineae tinea, typically at 200 mg/d and often for courses of more than 3 months.5 Testing for serum itraconazole trough levels, as done for our patient, typically is not recommended. Clinicians should counsel patients to take itraconazole with high-fat foods and an acidic beverage to increase bioavailability.5 Potential adverse effects of itraconazole include heart failure and numerous drug-drug interactions.5,22 Patients with T indotineae dermatophytosis should avoid sharing personal belongings and having skin-to-skin contact of affected areas with others.4
Dermatologists who suspect T indotineae infection should work with public health agencies that can assist with testing and undertake infection surveillance, prevention, and control.5,23 Challenges to diagnosing and managing T indotineae infection include lack of awareness among dermatology providers, the need for specialized laboratory testing to confirm infection, lack of established clinical cut-points for MICs from AFST, the need for longer duration of treatment vs what is needed for typical tinea, and potential challenges with insurance coverage for testing and treatment. Empiric treatment with itraconazole should be considered when terbinafine-resistant dermatophytosis is suspected or when terbinafine-resistant T indotineae infection is confirmed.
Acknowledgments—Jeremy Gold, MD; Dallas J. Smith, PharmD; and Shawn Lockhart, PhD, all of the Centers for Disease Control and Prevention, Mycotic Diseases Branch (Atlanta, Georgia), provided helpful comments to the authors in preparing the manuscript of this article.
- Uhrlaß S, Verma SB, Gräser Y, al. Trichophyton indotineae—an emerging pathogen causing recalcitrant dermatophytoses in India and worldwide—a multidimensional perspective. J Fungi (Basel). 2022;8:757. doi:10.3390/jof8070757
- Jabet A, Brun S, Normand A-C, et al. Extensive dermatophytosis caused by terbinafine-resistant Trichophyton indotineae, France. Emerg Infect Dis. 2022;28:229-233. doi:10.3201/eid2801.210883
- Caplan AS, Chaturvedi S, Zhu Y, et al. Notes from the field. First reported U.S. cases of tinea caused by Trichophyton indotineae—New York City, December 2021-March 2023. MMWR Morb Mortal Wkly Rep. 2023;72:536-537. doi:10.15585/mmwr.mm7219a4
- Jabet A, Normand A-C, Brun S, et al. Trichophyton indotineae, from epidemiology to therapeutic. J Mycol Med. 2023;33:101383. doi:10.1016/j.mycmed.2023.101383
- Hill RC, Caplan AS, Elewski B, et al. Expert panel review of skin and hair dermatophytoses in an era of antifungal resistance. Am J Clin Dermatol. 2024;25:359-389. doi:10.1007/s40257-024-00848-1
- Caplan AS, Zakhem GA, Pomeranz MK. Trichophyton mentagrophytes internal transcribed spacer genotype VIII. JAMA Dermatol. 2023;159:1130. doi:10.1001/jamadermatol.2023.2645
- Spivack S, Gold JAW, Lockhart SR, et al. Potential sexual transmission of antifungal-resistant Trichophyton indotineae. Emerg Infect Dis. 2024;30:807-809. doi:10.3201/eid3004.240115
- Caplan AS, Todd GC, Zhu Y, et al. Clinical course, antifungal susceptibility, and genomic sequencing of Trichophyton indotineae. JAMA Dermatol. Published online May 15, 2024. doi:10.1001/jamadermatol.2024.1126
- Cañete-Gibas CF, Mele J, Patterson HP, et al. Terbinafine-resistant dermatophytes and the presence of Trichophyton indotineae in North America. J Clin Microbiol. 2023;61:e0056223. doi:10.1128/jcm.00562-23
- Gupta AK, Venkataraman M, Hall DC, et al. The emergence of Trichophyton indotineae: implications for clinical practice. Int J Dermatol. 2023;62:857-861.
- Oladzad V, Nasrollahi Omran A, Haghani I, et al. Multi-drug resistance Trichophyton indotineae in a stray dog. Res Vet Sci. 2024;166:105105. doi:10.1016/j.rvsc.2023.105105
- Martinez-Rossi NM, Bitencourt TA, Peres NTA, et al. Dermatophyte resistance to antifungal drugs: mechanisms and prospectus. Front Microbiol. 2018;9:1108. doi:10.3389/fmicb.2018.01108
- Sacheli R, Hayette MP. Antifungal resistance in dermatophytes: genetic considerations, clinical presentations and alternative therapies. J Fungi (Basel). 2021;711:983. doi:10.3390/jof7110983
- Gupta AK, Cooper EA. Dermatophytosis (tinea) and other superficial fungal infections. In: Hospenthal DR, Rinaldi MG, eds. Diagnosis and Treatment of Human Mycoses. Humana Press; 2008:355-381.
- Normand A-C, Moreno-Sabater A, Jabet A, et al. MALDI-TOF mass spectrometry online identification of Trichophyton indotineae using the MSI-2 application. J Fungi (Basel). 2022;8:1103. doi:10.3390/jof8101103
- De Paepe R, Normand A-C, Uhrlaß S, et al. Resistance profile, terbinafine resistance screening and MALDI-TOF MS identification of the emerging pathogen Trichophyton indotineae. Mycopathologia. 2024;189:29. doi:10.1007/s11046-024-00835-4
- Rajagopalan M, Inamadar A, Mittal A, et al. Expert consensus on the management of dermatophytosis in India (ECTODERM India). BMC Dermatol. 2018;18:6. doi:10.1186/s12895-018-0073-1
- Verma SB, Panda S, Nenoff P, et al. The unprecedented epidemic-like scenario of dermatophytosis in India: III. Antifungal resistance and treatment options. Indian J Dermatol Venereol Leprol. 2021;87:468-482. doi:10.25259/IJDVL_303_20
- Shaw D, Singh S, Dogra S, et al. MIC and upper limit of wild-type distribution for 13 antifungal agents against a Trichophyton mentagrophytes–Trichophyton interdigitale complex of Indian origin. Antimicrob Agents Chemother. 2020;64:E01964-19. doi:10.1128/AAC.01964-19
- Burmester A, Hipler U-C, Uhrlaß S, et al. Indian Trichophyton mentagrophytes squalene epoxidase erg1 double mutants show high proportion of combined fluconazole and terbinafine resistance. Mycoses. 2020;63:1175-1180. doi:10.1111/myc.13150
- Khurana A, Agarwal A, Agrawal D, et al. Effect of different itraconazole dosing regimens on cure rates, treatment duration, safety, and relapse rates in adult patients with tinea corporis/cruris: a randomized clinical trial. JAMA Dermatol. 2022;158:1269-1278. doi:10.1001/jamadermatol.2022.3745
- Itraconazole capsule. DailyMed [Internet]. Updated June 3, 2024. Accessed June 19, 2024. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=2ab38a8a-3708-4b97-9f7f-8e554a15348d
- Bui TS, Katz KA. Resistant Trichophyton indotineae dermatophytosis—an emerging pandemic, now in the US. JAMA Dermatol. Published online May 15, 2024. doi:10.1001/jamadermatol.2024.1125
- Uhrlaß S, Verma SB, Gräser Y, al. Trichophyton indotineae—an emerging pathogen causing recalcitrant dermatophytoses in India and worldwide—a multidimensional perspective. J Fungi (Basel). 2022;8:757. doi:10.3390/jof8070757
- Jabet A, Brun S, Normand A-C, et al. Extensive dermatophytosis caused by terbinafine-resistant Trichophyton indotineae, France. Emerg Infect Dis. 2022;28:229-233. doi:10.3201/eid2801.210883
- Caplan AS, Chaturvedi S, Zhu Y, et al. Notes from the field. First reported U.S. cases of tinea caused by Trichophyton indotineae—New York City, December 2021-March 2023. MMWR Morb Mortal Wkly Rep. 2023;72:536-537. doi:10.15585/mmwr.mm7219a4
- Jabet A, Normand A-C, Brun S, et al. Trichophyton indotineae, from epidemiology to therapeutic. J Mycol Med. 2023;33:101383. doi:10.1016/j.mycmed.2023.101383
- Hill RC, Caplan AS, Elewski B, et al. Expert panel review of skin and hair dermatophytoses in an era of antifungal resistance. Am J Clin Dermatol. 2024;25:359-389. doi:10.1007/s40257-024-00848-1
- Caplan AS, Zakhem GA, Pomeranz MK. Trichophyton mentagrophytes internal transcribed spacer genotype VIII. JAMA Dermatol. 2023;159:1130. doi:10.1001/jamadermatol.2023.2645
- Spivack S, Gold JAW, Lockhart SR, et al. Potential sexual transmission of antifungal-resistant Trichophyton indotineae. Emerg Infect Dis. 2024;30:807-809. doi:10.3201/eid3004.240115
- Caplan AS, Todd GC, Zhu Y, et al. Clinical course, antifungal susceptibility, and genomic sequencing of Trichophyton indotineae. JAMA Dermatol. Published online May 15, 2024. doi:10.1001/jamadermatol.2024.1126
- Cañete-Gibas CF, Mele J, Patterson HP, et al. Terbinafine-resistant dermatophytes and the presence of Trichophyton indotineae in North America. J Clin Microbiol. 2023;61:e0056223. doi:10.1128/jcm.00562-23
- Gupta AK, Venkataraman M, Hall DC, et al. The emergence of Trichophyton indotineae: implications for clinical practice. Int J Dermatol. 2023;62:857-861.
- Oladzad V, Nasrollahi Omran A, Haghani I, et al. Multi-drug resistance Trichophyton indotineae in a stray dog. Res Vet Sci. 2024;166:105105. doi:10.1016/j.rvsc.2023.105105
- Martinez-Rossi NM, Bitencourt TA, Peres NTA, et al. Dermatophyte resistance to antifungal drugs: mechanisms and prospectus. Front Microbiol. 2018;9:1108. doi:10.3389/fmicb.2018.01108
- Sacheli R, Hayette MP. Antifungal resistance in dermatophytes: genetic considerations, clinical presentations and alternative therapies. J Fungi (Basel). 2021;711:983. doi:10.3390/jof7110983
- Gupta AK, Cooper EA. Dermatophytosis (tinea) and other superficial fungal infections. In: Hospenthal DR, Rinaldi MG, eds. Diagnosis and Treatment of Human Mycoses. Humana Press; 2008:355-381.
- Normand A-C, Moreno-Sabater A, Jabet A, et al. MALDI-TOF mass spectrometry online identification of Trichophyton indotineae using the MSI-2 application. J Fungi (Basel). 2022;8:1103. doi:10.3390/jof8101103
- De Paepe R, Normand A-C, Uhrlaß S, et al. Resistance profile, terbinafine resistance screening and MALDI-TOF MS identification of the emerging pathogen Trichophyton indotineae. Mycopathologia. 2024;189:29. doi:10.1007/s11046-024-00835-4
- Rajagopalan M, Inamadar A, Mittal A, et al. Expert consensus on the management of dermatophytosis in India (ECTODERM India). BMC Dermatol. 2018;18:6. doi:10.1186/s12895-018-0073-1
- Verma SB, Panda S, Nenoff P, et al. The unprecedented epidemic-like scenario of dermatophytosis in India: III. Antifungal resistance and treatment options. Indian J Dermatol Venereol Leprol. 2021;87:468-482. doi:10.25259/IJDVL_303_20
- Shaw D, Singh S, Dogra S, et al. MIC and upper limit of wild-type distribution for 13 antifungal agents against a Trichophyton mentagrophytes–Trichophyton interdigitale complex of Indian origin. Antimicrob Agents Chemother. 2020;64:E01964-19. doi:10.1128/AAC.01964-19
- Burmester A, Hipler U-C, Uhrlaß S, et al. Indian Trichophyton mentagrophytes squalene epoxidase erg1 double mutants show high proportion of combined fluconazole and terbinafine resistance. Mycoses. 2020;63:1175-1180. doi:10.1111/myc.13150
- Khurana A, Agarwal A, Agrawal D, et al. Effect of different itraconazole dosing regimens on cure rates, treatment duration, safety, and relapse rates in adult patients with tinea corporis/cruris: a randomized clinical trial. JAMA Dermatol. 2022;158:1269-1278. doi:10.1001/jamadermatol.2022.3745
- Itraconazole capsule. DailyMed [Internet]. Updated June 3, 2024. Accessed June 19, 2024. https://dailymed.nlm.nih.gov/dailymed/lookup.cfm?setid=2ab38a8a-3708-4b97-9f7f-8e554a15348d
- Bui TS, Katz KA. Resistant Trichophyton indotineae dermatophytosis—an emerging pandemic, now in the US. JAMA Dermatol. Published online May 15, 2024. doi:10.1001/jamadermatol.2024.1125
Practice Points
- Trichophyton indotineae can cause extensive dermatophytosis that often is resistant to terbinafine and in some cases to other antifungals.
- Only molecular testing, which is not widely available, can distinguish T indotineae from other dermatophytes.
- Suspected or confirmed cases of T indotineae dermatophytosis should be reported to public health agencies to provide assistance with testing, as well as surveillance, prevention, and control of infection.
CMS Announces End to Cyberattack Relief Program
The Centers for Medicare & Medicaid Services (CMS) has announced the conclusion of a program that provided billions in early Medicare payments to those affected by the Change Healthcare/UnitedHealth Group cyberattack last winter.
CMS reported that the program advanced more than $2.55 billion in Medicare payments to > 4200 Part A providers, including hospitals, and more than $717.18 million in payments to Part B suppliers such as physicians, nonphysician practitioners, and durable medical equipment suppliers.
According to CMS, the Medicare billing system is now functioning properly, and 96% of the early payments have been recovered. The advances were to represent ≤ 30 days of typical claims payments in a 3-month period of 2023, with full repayment expected within 90 days through “automatic recoupment from Medicare claims” — no extensions allowed.
The agency took a victory lap regarding its response. “In the face of one of the most widespread cyberattacks on the US health care industry, CMS promptly took action to get providers and suppliers access to the funds they needed to continue providing patients with vital care,” CMS Administrator Chiquita Brooks-LaSure said in a statement. “Our efforts helped minimize the disruptive fallout from this incident, and we will remain vigilant to be ready to address future events.”
Ongoing Concerns from Health Care Organizations
Ben Teicher, an American Hospital Association spokesman, said that the organization hopes that CMS will be responsive if there’s more need for action after the advance payment program expires. The organization represents about 5000 hospitals, health care systems, and other providers.
“Our members report that the aftereffects of this event will likely be felt throughout the remainder of the year,” he said. According to Teicher, hospitals remain concerned about their ability to process claims and appeal denials, the safety of reconnecting to cyber services, and access to information needed to bill patients and reconcile payments.
In addition, hospitals are concerned about “financial support to mitigate the considerable costs incurred as a result of the cyberattack,” he said.
Charlene MacDonald, executive vice-president of public affairs at the Federation of American Hospitals, which represents more than 1000 for-profit hospitals, sent a statement to this news organization that said some providers “are still feeling the effects of care denials and delays caused by insurer inaction.
“We appreciate that the Administration acted within its authority to support providers during this unprecedented crisis and blunt these devastating impacts, especially because a vast majority of managed care companies failed to step up to the plate,” she said. “It is now time to shift our focus to holding plans accountable for using tactics to delay and deny needed patient care.”
Cyberattack Impact and Response
The ransom-based cyberattack against Change Healthcare/UnitedHealth Group targeted an electronic data interchange clearing house processing payer reimbursement systems, disrupting cash flows at hospitals and medical practices, and affecting patient access to prescriptions and life-saving therapy.
Change Healthcare — part of the UnitedHealth Group subsidiary Optum — processes half of all medical claims, according to a Department of Justice lawsuit. The American Hospital Association described the cyberattack as “the most significant and consequential incident of its kind” in US history.
By late March, UnitedHealth Group said nearly all medical and pharmacy claims were processing properly, while a deputy secretary of the US Department of Health & Human Services told clinicians that officials were focusing on the last group of clinicians who were facing cash-flow problems.
Still, a senior advisor with CMS told providers at that time that “we have heard from so many providers over the last several weeks who are really struggling to make ends meet right now or who are worried that they will not be able to make payroll in the weeks to come.”
Randy Dotinga is a freelance health/medical reporter and board member of the Association of Health Care Journalists.
A version of this article appeared on Medscape.com.
The Centers for Medicare & Medicaid Services (CMS) has announced the conclusion of a program that provided billions in early Medicare payments to those affected by the Change Healthcare/UnitedHealth Group cyberattack last winter.
CMS reported that the program advanced more than $2.55 billion in Medicare payments to > 4200 Part A providers, including hospitals, and more than $717.18 million in payments to Part B suppliers such as physicians, nonphysician practitioners, and durable medical equipment suppliers.
According to CMS, the Medicare billing system is now functioning properly, and 96% of the early payments have been recovered. The advances were to represent ≤ 30 days of typical claims payments in a 3-month period of 2023, with full repayment expected within 90 days through “automatic recoupment from Medicare claims” — no extensions allowed.
The agency took a victory lap regarding its response. “In the face of one of the most widespread cyberattacks on the US health care industry, CMS promptly took action to get providers and suppliers access to the funds they needed to continue providing patients with vital care,” CMS Administrator Chiquita Brooks-LaSure said in a statement. “Our efforts helped minimize the disruptive fallout from this incident, and we will remain vigilant to be ready to address future events.”
Ongoing Concerns from Health Care Organizations
Ben Teicher, an American Hospital Association spokesman, said that the organization hopes that CMS will be responsive if there’s more need for action after the advance payment program expires. The organization represents about 5000 hospitals, health care systems, and other providers.
“Our members report that the aftereffects of this event will likely be felt throughout the remainder of the year,” he said. According to Teicher, hospitals remain concerned about their ability to process claims and appeal denials, the safety of reconnecting to cyber services, and access to information needed to bill patients and reconcile payments.
In addition, hospitals are concerned about “financial support to mitigate the considerable costs incurred as a result of the cyberattack,” he said.
Charlene MacDonald, executive vice-president of public affairs at the Federation of American Hospitals, which represents more than 1000 for-profit hospitals, sent a statement to this news organization that said some providers “are still feeling the effects of care denials and delays caused by insurer inaction.
“We appreciate that the Administration acted within its authority to support providers during this unprecedented crisis and blunt these devastating impacts, especially because a vast majority of managed care companies failed to step up to the plate,” she said. “It is now time to shift our focus to holding plans accountable for using tactics to delay and deny needed patient care.”
Cyberattack Impact and Response
The ransom-based cyberattack against Change Healthcare/UnitedHealth Group targeted an electronic data interchange clearing house processing payer reimbursement systems, disrupting cash flows at hospitals and medical practices, and affecting patient access to prescriptions and life-saving therapy.
Change Healthcare — part of the UnitedHealth Group subsidiary Optum — processes half of all medical claims, according to a Department of Justice lawsuit. The American Hospital Association described the cyberattack as “the most significant and consequential incident of its kind” in US history.
By late March, UnitedHealth Group said nearly all medical and pharmacy claims were processing properly, while a deputy secretary of the US Department of Health & Human Services told clinicians that officials were focusing on the last group of clinicians who were facing cash-flow problems.
Still, a senior advisor with CMS told providers at that time that “we have heard from so many providers over the last several weeks who are really struggling to make ends meet right now or who are worried that they will not be able to make payroll in the weeks to come.”
Randy Dotinga is a freelance health/medical reporter and board member of the Association of Health Care Journalists.
A version of this article appeared on Medscape.com.
The Centers for Medicare & Medicaid Services (CMS) has announced the conclusion of a program that provided billions in early Medicare payments to those affected by the Change Healthcare/UnitedHealth Group cyberattack last winter.
CMS reported that the program advanced more than $2.55 billion in Medicare payments to > 4200 Part A providers, including hospitals, and more than $717.18 million in payments to Part B suppliers such as physicians, nonphysician practitioners, and durable medical equipment suppliers.
According to CMS, the Medicare billing system is now functioning properly, and 96% of the early payments have been recovered. The advances were to represent ≤ 30 days of typical claims payments in a 3-month period of 2023, with full repayment expected within 90 days through “automatic recoupment from Medicare claims” — no extensions allowed.
The agency took a victory lap regarding its response. “In the face of one of the most widespread cyberattacks on the US health care industry, CMS promptly took action to get providers and suppliers access to the funds they needed to continue providing patients with vital care,” CMS Administrator Chiquita Brooks-LaSure said in a statement. “Our efforts helped minimize the disruptive fallout from this incident, and we will remain vigilant to be ready to address future events.”
Ongoing Concerns from Health Care Organizations
Ben Teicher, an American Hospital Association spokesman, said that the organization hopes that CMS will be responsive if there’s more need for action after the advance payment program expires. The organization represents about 5000 hospitals, health care systems, and other providers.
“Our members report that the aftereffects of this event will likely be felt throughout the remainder of the year,” he said. According to Teicher, hospitals remain concerned about their ability to process claims and appeal denials, the safety of reconnecting to cyber services, and access to information needed to bill patients and reconcile payments.
In addition, hospitals are concerned about “financial support to mitigate the considerable costs incurred as a result of the cyberattack,” he said.
Charlene MacDonald, executive vice-president of public affairs at the Federation of American Hospitals, which represents more than 1000 for-profit hospitals, sent a statement to this news organization that said some providers “are still feeling the effects of care denials and delays caused by insurer inaction.
“We appreciate that the Administration acted within its authority to support providers during this unprecedented crisis and blunt these devastating impacts, especially because a vast majority of managed care companies failed to step up to the plate,” she said. “It is now time to shift our focus to holding plans accountable for using tactics to delay and deny needed patient care.”
Cyberattack Impact and Response
The ransom-based cyberattack against Change Healthcare/UnitedHealth Group targeted an electronic data interchange clearing house processing payer reimbursement systems, disrupting cash flows at hospitals and medical practices, and affecting patient access to prescriptions and life-saving therapy.
Change Healthcare — part of the UnitedHealth Group subsidiary Optum — processes half of all medical claims, according to a Department of Justice lawsuit. The American Hospital Association described the cyberattack as “the most significant and consequential incident of its kind” in US history.
By late March, UnitedHealth Group said nearly all medical and pharmacy claims were processing properly, while a deputy secretary of the US Department of Health & Human Services told clinicians that officials were focusing on the last group of clinicians who were facing cash-flow problems.
Still, a senior advisor with CMS told providers at that time that “we have heard from so many providers over the last several weeks who are really struggling to make ends meet right now or who are worried that they will not be able to make payroll in the weeks to come.”
Randy Dotinga is a freelance health/medical reporter and board member of the Association of Health Care Journalists.
A version of this article appeared on Medscape.com.
Is This Journal Legit? Predatory Publishers
This transcript has been edited for clarity.
Andrew N. Wilner, MD: My guest today is Dr. Jose Merino, editor in chief of the Neurology family of journals and professor of neurology and co-vice chair of education at Georgetown University in Washington, DC.
Our program today is a follow-up of Dr. Merino’s presentation at the recent American Academy of Neurology meeting in Denver, Colorado. Along with two other panelists, Dr. Merino discussed the role of open-access publication and the dangers of predatory journals.
Jose G. Merino, MD, MPhil: Thank you for having me here. It’s a pleasure.
Open Access Defined
Dr. Wilner: I remember when publication in neurology was pretty straightforward. It was either the green journal or the blue journal, but things have certainly changed. I think one topic that is not clear to everyone is this concept of open access. Could you define that for us?
Dr. Merino: Sure. Open access is a mode of publication that fosters more open or accessible science. The idea of open access is that it combines two main elements. One is that the papers that are published become immediately available to anybody with an internet connection anywhere in the world without any restrictions.
The second important element from open access, which makes it different from other models we can talk about, is the fact that the authors retain the copyright of their work, but they give the journal and readers a license to use, reproduce, and modify the content.
This is different, for example, from instances where we have funder mandates. For example, NIH papers have to become available 6 months after publication, so they’re available to everybody but not immediately.
Dr. Wilner: I remember that when a journal article was published, say, in Neurology, if you didn’t have a subscription to Neurology, you went to the library that hopefully had a subscription.
If they didn’t have it, you would write to the author and say, “Hey, I heard you have this great paper because the abstract was out there. Could you send me a reprint?” Has that whole universe evaporated?
Dr. Merino: It depends on how the paper is published. For example, in Neurology, some of the research we publish is open access. Basically, if you have an internet connection, you can access the paper.
That’s the case for papers published in our wholly open-access journals in the Neurology family like Neurology Neuroimmunology & Neuroinflammation, Neurology Genetics, or Neurology Education.
For other papers that are published in Neurology, not under open access, there is a paywall. For some of them, the paywall comes down after a few months based on funder mandates and so on. As I was mentioning, the NIH-funded papers are available 6 months later.
In the first 6 months, you may have to go to your library, and if your library has a subscription, you can download it directly. [This is also true for] those that always stay behind the paywall, where you have to have a subscription or your library has to have a subscription.
Is Pay to Publish a Red Flag?
Dr. Wilner: I’m a professional writer. With any luck, when I write something, I get paid to write it. There’s been a long tradition in academic medicine that when you submit an article to, say, Neurology, you don’t get paid as an author for the publication. Your reward is the honor of it being published.
Neurology supports itself in various ways, including advertising and so on. That’s been the contract: free publication for work that merits it, and the journal survives on its own.
With open access, one of the things that’s happened is that — and I’ve published open access myself — is that I get a notification that I need to pay to have my article that I’ve slaved over published. Explain that, please.
Dr. Merino: This is the issue with open access. As I mentioned, the paper gets published. You’re giving the journal a license to publish it. You’re retaining the copyright of your work. That means that the journal cannot make money or support itself by just publishing open access because they belong to you.
Typically, open-access journals are not in print and don’t have much in terms of advertising. The contract is you’re giving me a license to publish it, but it’s your journal, so you’re paying a fee for the journal expenses to basically produce your paper. That’s what’s happening with open access.
That’s been recognized with many funders, for example, with NIH funding or many of the European funders, they’re including open-access fees as part of their funding for research. Now, of course, this doesn’t help if you’re not a funded researcher or if you’re a fellow who’s doing work and so on.
Typically, most journals will have waived fees or lower fees for these situations. The reason for the open-access fee is the fact that you’re retaining the copyright. You’re not giving it to the journal who can then use it to generate its revenue for supporting itself, the editorial staff, and so on.
Dr. Wilner: This idea of charging for publication has created a satellite business of what are called predatory journals. How does one know if the open-access journal that I’m submitting to is really just in the business of wanting my $300 or my $900 to get published? How do I know if that’s a reasonable place to publish?
Predatory Journals
Dr. Merino: That’s a big challenge that has come with this whole idea of open access and the fact that now, many journals are online only, so you’re no longer seeing a physical copy. That has given rise to the predatory journals.
The predatory journal, by definition, is a journal that claims to be open access. They’ll take your paper and publish it, but they don’t provide all the other services that you would typically expect from the fact that you’re paying an open-access fee. This includes getting appropriate peer review, production of the manuscript, and long-term curation and storage of the manuscript.
Many predatory journals will take your open-access fee, accept any paper that you submit, regardless of the quality, because they’re charging the fees for that. They don’t send it to real peer review, and then in a few months, the journal disappears so there’s no way for anybody to actually find your paper anymore.
There are certain checklists. Dr. David Moher at the University of Toronto has produced some work trying to help us identify predatory journals.
One thing I typically suggest to people who ask me this question is: Have you ever heard of this journal before? Does the journal have a track record? How far back does the story of the journal go? Is it supported by a publisher that you know? Do you know anybody who has published there? Is it something you can easily access?
If in doubt, always ask your friendly medical librarian. There used to be lists that were kept in terms of predatory journals that were being constantly updated, but those had to be shut down. As far as I understand, there were legal issues in terms of how things got on that list.
I think that overall, if you’ve heard of it, if it’s relevant, if it’s known in your field, and if your librarian knows it, it’s probably a good legitimate open-access journal. There are many very good legitimate open-access journals.
I mentioned the two that we have in our family, but all the other major journals have their own open-access journal within their family. There are some, like BMC or PLOS, that are completely open-access and legitimate journals.
Impact Factor
Dr. Wilner: What about impact factor? Many journals boast about their impact factor. I’m not sure how to interpret that number.
Dr. Merino: Impact factor is very interesting. The impact factor was developed by medical librarians to try to identify the journals they should be subscribing to. It’s a measure of the average citations to an average paper in the journal.
It doesn’t tell you about specific papers. It tells you, on average, how many of the papers in this journal get cited so many times. It’s calculated by the number of articles that were cited divided by the number of articles that were published. Journals that publish many papers, like Neurology, have a hard time bringing up their impact factor beyond a certain level.
Similarly, very small journals with one or two very highly cited papers have a very high impact factor. It’s being used as a measure, perhaps inappropriately, of how good or how reputable a journal is. We all say we don’t care about journal impact factors, but we all know our journal impact factor and we used to know it to three decimals. Now, they changed the system, and there’s only one decimal point, which makes more sense.
This is more important, for example, for authors when deciding where to submit papers. I know that in some countries, particularly in Europe, the impact factor of the journal where you publish has an impact on your promotion decisions.
I would say what’s even more important than the impact factor, is to say, “Well, is this the journal that fits the scope of my paper? Is this the journal that reaches the audience that I want to reach when I write my paper?”
There are some papers, for example, that are very influential. The impact factor just captures citations. There are some papers that are very influential that may not get cited very often. There may be papers that change clinical practice.
If you read a paper that tells you that you should be changing how you treat your patients with myasthenia based on this paper, that may not get cited. It’s a very clinically focused paper, but it’s probably more impactful than one that gets cited very much in some respect, or they make it to public policy decisions, and so on.
I think it’s important to look more at the audience and the journal scope when you submit your papers.
Dr. Wilner: One other technical question. The journals also say they’re indexed in PubMed or Google Scholar. If I want to publish my paper and I want it indexed where the right people are going to find it, where does it need to be indexed?
Dr. Merino: I grew up using Index Medicus, MedlinePlus, and the Library of Science. I still do. If I need to find something, I go to PubMed. Ideally, papers are listed in MedlinePlus or can be found in PubMed. They’re not the same thing, but you can find them through them.
That would be an important thing. Nowadays, a lot more people are using Google Scholar or Google just to identify papers. It may be a little bit less relevant, but it’s still a measure of the quality of the journal before they get indexed in some of these. For example, if you get listed in MedlinePlus, it has gone through certain quality checks by the index itself to see whether they would accept the journal or not. That’s something you want to check.
Typically, most of the large journals or the journals you and I know about are listed in more than one place, right? They’re listed in Scopus and Web of Science. They’re listed in MedlinePlus and so on. Again, if you’re submitting your paper, go somewhere where you know the journal and you’ve heard about it.
Dr. Wilner: I’m not going to ask you about artificial intelligence. We can do that another time. I want to ask something closer to me, which is this question of publish or perish.
There seems to be, in academics, more emphasis on the number of papers that one has published rather than their quality. How does a younger academician or one who really needs to publish cope with that?
Dr. Merino: Many people are writing up research that may not be relevant or that may not be high quality just because you need to have a long list of papers to get promoted, for example, if you’re an academician.
Doug Altman, who was a very influential person in the field quality of not only medical statistics but also medical publishing, had the idea that we need less research, but we need better research.
We often receive papers where you say, well, what’s the rationale behind the question in this paper? It’s like they had a large amount of data and were trying to squeeze as much as they could out of that. I think, as a young academician, the important thing to think about is whether it is an important question that matters to you and to the field, from whatever perspective, whether it’s going to advance research, advance clinical care, or have public policy implications.
Is this one where the answer will be important no matter what the answer is? If you’re thinking of that, your work will be well recognized, people will know you, and you’ll get invited to collaborate. I think that’s the most important thing rather than just churning out a large number of papers.
The productivity will come from the fact that you start by saying, let me ask something that’s really meaningful to me and to the field, with a good question and using strong research methodology.
Dr. Wilner: Thanks for that, Dr. Merino. I think that’s very valuable for all of us. This has been a great discussion. Do you have any final comments before we wrap up?
Dr. Merino: I want to encourage people to continue reading medical journals all the time and submitting to us, again, good research and important questions with robust methodology. That’s what we’re looking for in Neurology and most serious medical journals.
Dr. Wilner is an associate professor of neurology at the University of Tennessee Health Science Center, Memphis. Dr. Merino is a professor in the department of neurology at Georgetown University Medical Center, Washington, DC. Dr. Wilner reported conflicts of interest with Accordant Health Services and Lulu Publishing. Dr. Merino reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Andrew N. Wilner, MD: My guest today is Dr. Jose Merino, editor in chief of the Neurology family of journals and professor of neurology and co-vice chair of education at Georgetown University in Washington, DC.
Our program today is a follow-up of Dr. Merino’s presentation at the recent American Academy of Neurology meeting in Denver, Colorado. Along with two other panelists, Dr. Merino discussed the role of open-access publication and the dangers of predatory journals.
Jose G. Merino, MD, MPhil: Thank you for having me here. It’s a pleasure.
Open Access Defined
Dr. Wilner: I remember when publication in neurology was pretty straightforward. It was either the green journal or the blue journal, but things have certainly changed. I think one topic that is not clear to everyone is this concept of open access. Could you define that for us?
Dr. Merino: Sure. Open access is a mode of publication that fosters more open or accessible science. The idea of open access is that it combines two main elements. One is that the papers that are published become immediately available to anybody with an internet connection anywhere in the world without any restrictions.
The second important element from open access, which makes it different from other models we can talk about, is the fact that the authors retain the copyright of their work, but they give the journal and readers a license to use, reproduce, and modify the content.
This is different, for example, from instances where we have funder mandates. For example, NIH papers have to become available 6 months after publication, so they’re available to everybody but not immediately.
Dr. Wilner: I remember that when a journal article was published, say, in Neurology, if you didn’t have a subscription to Neurology, you went to the library that hopefully had a subscription.
If they didn’t have it, you would write to the author and say, “Hey, I heard you have this great paper because the abstract was out there. Could you send me a reprint?” Has that whole universe evaporated?
Dr. Merino: It depends on how the paper is published. For example, in Neurology, some of the research we publish is open access. Basically, if you have an internet connection, you can access the paper.
That’s the case for papers published in our wholly open-access journals in the Neurology family like Neurology Neuroimmunology & Neuroinflammation, Neurology Genetics, or Neurology Education.
For other papers that are published in Neurology, not under open access, there is a paywall. For some of them, the paywall comes down after a few months based on funder mandates and so on. As I was mentioning, the NIH-funded papers are available 6 months later.
In the first 6 months, you may have to go to your library, and if your library has a subscription, you can download it directly. [This is also true for] those that always stay behind the paywall, where you have to have a subscription or your library has to have a subscription.
Is Pay to Publish a Red Flag?
Dr. Wilner: I’m a professional writer. With any luck, when I write something, I get paid to write it. There’s been a long tradition in academic medicine that when you submit an article to, say, Neurology, you don’t get paid as an author for the publication. Your reward is the honor of it being published.
Neurology supports itself in various ways, including advertising and so on. That’s been the contract: free publication for work that merits it, and the journal survives on its own.
With open access, one of the things that’s happened is that — and I’ve published open access myself — is that I get a notification that I need to pay to have my article that I’ve slaved over published. Explain that, please.
Dr. Merino: This is the issue with open access. As I mentioned, the paper gets published. You’re giving the journal a license to publish it. You’re retaining the copyright of your work. That means that the journal cannot make money or support itself by just publishing open access because they belong to you.
Typically, open-access journals are not in print and don’t have much in terms of advertising. The contract is you’re giving me a license to publish it, but it’s your journal, so you’re paying a fee for the journal expenses to basically produce your paper. That’s what’s happening with open access.
That’s been recognized with many funders, for example, with NIH funding or many of the European funders, they’re including open-access fees as part of their funding for research. Now, of course, this doesn’t help if you’re not a funded researcher or if you’re a fellow who’s doing work and so on.
Typically, most journals will have waived fees or lower fees for these situations. The reason for the open-access fee is the fact that you’re retaining the copyright. You’re not giving it to the journal who can then use it to generate its revenue for supporting itself, the editorial staff, and so on.
Dr. Wilner: This idea of charging for publication has created a satellite business of what are called predatory journals. How does one know if the open-access journal that I’m submitting to is really just in the business of wanting my $300 or my $900 to get published? How do I know if that’s a reasonable place to publish?
Predatory Journals
Dr. Merino: That’s a big challenge that has come with this whole idea of open access and the fact that now, many journals are online only, so you’re no longer seeing a physical copy. That has given rise to the predatory journals.
The predatory journal, by definition, is a journal that claims to be open access. They’ll take your paper and publish it, but they don’t provide all the other services that you would typically expect from the fact that you’re paying an open-access fee. This includes getting appropriate peer review, production of the manuscript, and long-term curation and storage of the manuscript.
Many predatory journals will take your open-access fee, accept any paper that you submit, regardless of the quality, because they’re charging the fees for that. They don’t send it to real peer review, and then in a few months, the journal disappears so there’s no way for anybody to actually find your paper anymore.
There are certain checklists. Dr. David Moher at the University of Toronto has produced some work trying to help us identify predatory journals.
One thing I typically suggest to people who ask me this question is: Have you ever heard of this journal before? Does the journal have a track record? How far back does the story of the journal go? Is it supported by a publisher that you know? Do you know anybody who has published there? Is it something you can easily access?
If in doubt, always ask your friendly medical librarian. There used to be lists that were kept in terms of predatory journals that were being constantly updated, but those had to be shut down. As far as I understand, there were legal issues in terms of how things got on that list.
I think that overall, if you’ve heard of it, if it’s relevant, if it’s known in your field, and if your librarian knows it, it’s probably a good legitimate open-access journal. There are many very good legitimate open-access journals.
I mentioned the two that we have in our family, but all the other major journals have their own open-access journal within their family. There are some, like BMC or PLOS, that are completely open-access and legitimate journals.
Impact Factor
Dr. Wilner: What about impact factor? Many journals boast about their impact factor. I’m not sure how to interpret that number.
Dr. Merino: Impact factor is very interesting. The impact factor was developed by medical librarians to try to identify the journals they should be subscribing to. It’s a measure of the average citations to an average paper in the journal.
It doesn’t tell you about specific papers. It tells you, on average, how many of the papers in this journal get cited so many times. It’s calculated by the number of articles that were cited divided by the number of articles that were published. Journals that publish many papers, like Neurology, have a hard time bringing up their impact factor beyond a certain level.
Similarly, very small journals with one or two very highly cited papers have a very high impact factor. It’s being used as a measure, perhaps inappropriately, of how good or how reputable a journal is. We all say we don’t care about journal impact factors, but we all know our journal impact factor and we used to know it to three decimals. Now, they changed the system, and there’s only one decimal point, which makes more sense.
This is more important, for example, for authors when deciding where to submit papers. I know that in some countries, particularly in Europe, the impact factor of the journal where you publish has an impact on your promotion decisions.
I would say what’s even more important than the impact factor, is to say, “Well, is this the journal that fits the scope of my paper? Is this the journal that reaches the audience that I want to reach when I write my paper?”
There are some papers, for example, that are very influential. The impact factor just captures citations. There are some papers that are very influential that may not get cited very often. There may be papers that change clinical practice.
If you read a paper that tells you that you should be changing how you treat your patients with myasthenia based on this paper, that may not get cited. It’s a very clinically focused paper, but it’s probably more impactful than one that gets cited very much in some respect, or they make it to public policy decisions, and so on.
I think it’s important to look more at the audience and the journal scope when you submit your papers.
Dr. Wilner: One other technical question. The journals also say they’re indexed in PubMed or Google Scholar. If I want to publish my paper and I want it indexed where the right people are going to find it, where does it need to be indexed?
Dr. Merino: I grew up using Index Medicus, MedlinePlus, and the Library of Science. I still do. If I need to find something, I go to PubMed. Ideally, papers are listed in MedlinePlus or can be found in PubMed. They’re not the same thing, but you can find them through them.
That would be an important thing. Nowadays, a lot more people are using Google Scholar or Google just to identify papers. It may be a little bit less relevant, but it’s still a measure of the quality of the journal before they get indexed in some of these. For example, if you get listed in MedlinePlus, it has gone through certain quality checks by the index itself to see whether they would accept the journal or not. That’s something you want to check.
Typically, most of the large journals or the journals you and I know about are listed in more than one place, right? They’re listed in Scopus and Web of Science. They’re listed in MedlinePlus and so on. Again, if you’re submitting your paper, go somewhere where you know the journal and you’ve heard about it.
Dr. Wilner: I’m not going to ask you about artificial intelligence. We can do that another time. I want to ask something closer to me, which is this question of publish or perish.
There seems to be, in academics, more emphasis on the number of papers that one has published rather than their quality. How does a younger academician or one who really needs to publish cope with that?
Dr. Merino: Many people are writing up research that may not be relevant or that may not be high quality just because you need to have a long list of papers to get promoted, for example, if you’re an academician.
Doug Altman, who was a very influential person in the field quality of not only medical statistics but also medical publishing, had the idea that we need less research, but we need better research.
We often receive papers where you say, well, what’s the rationale behind the question in this paper? It’s like they had a large amount of data and were trying to squeeze as much as they could out of that. I think, as a young academician, the important thing to think about is whether it is an important question that matters to you and to the field, from whatever perspective, whether it’s going to advance research, advance clinical care, or have public policy implications.
Is this one where the answer will be important no matter what the answer is? If you’re thinking of that, your work will be well recognized, people will know you, and you’ll get invited to collaborate. I think that’s the most important thing rather than just churning out a large number of papers.
The productivity will come from the fact that you start by saying, let me ask something that’s really meaningful to me and to the field, with a good question and using strong research methodology.
Dr. Wilner: Thanks for that, Dr. Merino. I think that’s very valuable for all of us. This has been a great discussion. Do you have any final comments before we wrap up?
Dr. Merino: I want to encourage people to continue reading medical journals all the time and submitting to us, again, good research and important questions with robust methodology. That’s what we’re looking for in Neurology and most serious medical journals.
Dr. Wilner is an associate professor of neurology at the University of Tennessee Health Science Center, Memphis. Dr. Merino is a professor in the department of neurology at Georgetown University Medical Center, Washington, DC. Dr. Wilner reported conflicts of interest with Accordant Health Services and Lulu Publishing. Dr. Merino reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
This transcript has been edited for clarity.
Andrew N. Wilner, MD: My guest today is Dr. Jose Merino, editor in chief of the Neurology family of journals and professor of neurology and co-vice chair of education at Georgetown University in Washington, DC.
Our program today is a follow-up of Dr. Merino’s presentation at the recent American Academy of Neurology meeting in Denver, Colorado. Along with two other panelists, Dr. Merino discussed the role of open-access publication and the dangers of predatory journals.
Jose G. Merino, MD, MPhil: Thank you for having me here. It’s a pleasure.
Open Access Defined
Dr. Wilner: I remember when publication in neurology was pretty straightforward. It was either the green journal or the blue journal, but things have certainly changed. I think one topic that is not clear to everyone is this concept of open access. Could you define that for us?
Dr. Merino: Sure. Open access is a mode of publication that fosters more open or accessible science. The idea of open access is that it combines two main elements. One is that the papers that are published become immediately available to anybody with an internet connection anywhere in the world without any restrictions.
The second important element from open access, which makes it different from other models we can talk about, is the fact that the authors retain the copyright of their work, but they give the journal and readers a license to use, reproduce, and modify the content.
This is different, for example, from instances where we have funder mandates. For example, NIH papers have to become available 6 months after publication, so they’re available to everybody but not immediately.
Dr. Wilner: I remember that when a journal article was published, say, in Neurology, if you didn’t have a subscription to Neurology, you went to the library that hopefully had a subscription.
If they didn’t have it, you would write to the author and say, “Hey, I heard you have this great paper because the abstract was out there. Could you send me a reprint?” Has that whole universe evaporated?
Dr. Merino: It depends on how the paper is published. For example, in Neurology, some of the research we publish is open access. Basically, if you have an internet connection, you can access the paper.
That’s the case for papers published in our wholly open-access journals in the Neurology family like Neurology Neuroimmunology & Neuroinflammation, Neurology Genetics, or Neurology Education.
For other papers that are published in Neurology, not under open access, there is a paywall. For some of them, the paywall comes down after a few months based on funder mandates and so on. As I was mentioning, the NIH-funded papers are available 6 months later.
In the first 6 months, you may have to go to your library, and if your library has a subscription, you can download it directly. [This is also true for] those that always stay behind the paywall, where you have to have a subscription or your library has to have a subscription.
Is Pay to Publish a Red Flag?
Dr. Wilner: I’m a professional writer. With any luck, when I write something, I get paid to write it. There’s been a long tradition in academic medicine that when you submit an article to, say, Neurology, you don’t get paid as an author for the publication. Your reward is the honor of it being published.
Neurology supports itself in various ways, including advertising and so on. That’s been the contract: free publication for work that merits it, and the journal survives on its own.
With open access, one of the things that’s happened is that — and I’ve published open access myself — is that I get a notification that I need to pay to have my article that I’ve slaved over published. Explain that, please.
Dr. Merino: This is the issue with open access. As I mentioned, the paper gets published. You’re giving the journal a license to publish it. You’re retaining the copyright of your work. That means that the journal cannot make money or support itself by just publishing open access because they belong to you.
Typically, open-access journals are not in print and don’t have much in terms of advertising. The contract is you’re giving me a license to publish it, but it’s your journal, so you’re paying a fee for the journal expenses to basically produce your paper. That’s what’s happening with open access.
That’s been recognized with many funders, for example, with NIH funding or many of the European funders, they’re including open-access fees as part of their funding for research. Now, of course, this doesn’t help if you’re not a funded researcher or if you’re a fellow who’s doing work and so on.
Typically, most journals will have waived fees or lower fees for these situations. The reason for the open-access fee is the fact that you’re retaining the copyright. You’re not giving it to the journal who can then use it to generate its revenue for supporting itself, the editorial staff, and so on.
Dr. Wilner: This idea of charging for publication has created a satellite business of what are called predatory journals. How does one know if the open-access journal that I’m submitting to is really just in the business of wanting my $300 or my $900 to get published? How do I know if that’s a reasonable place to publish?
Predatory Journals
Dr. Merino: That’s a big challenge that has come with this whole idea of open access and the fact that now, many journals are online only, so you’re no longer seeing a physical copy. That has given rise to the predatory journals.
The predatory journal, by definition, is a journal that claims to be open access. They’ll take your paper and publish it, but they don’t provide all the other services that you would typically expect from the fact that you’re paying an open-access fee. This includes getting appropriate peer review, production of the manuscript, and long-term curation and storage of the manuscript.
Many predatory journals will take your open-access fee, accept any paper that you submit, regardless of the quality, because they’re charging the fees for that. They don’t send it to real peer review, and then in a few months, the journal disappears so there’s no way for anybody to actually find your paper anymore.
There are certain checklists. Dr. David Moher at the University of Toronto has produced some work trying to help us identify predatory journals.
One thing I typically suggest to people who ask me this question is: Have you ever heard of this journal before? Does the journal have a track record? How far back does the story of the journal go? Is it supported by a publisher that you know? Do you know anybody who has published there? Is it something you can easily access?
If in doubt, always ask your friendly medical librarian. There used to be lists that were kept in terms of predatory journals that were being constantly updated, but those had to be shut down. As far as I understand, there were legal issues in terms of how things got on that list.
I think that overall, if you’ve heard of it, if it’s relevant, if it’s known in your field, and if your librarian knows it, it’s probably a good legitimate open-access journal. There are many very good legitimate open-access journals.
I mentioned the two that we have in our family, but all the other major journals have their own open-access journal within their family. There are some, like BMC or PLOS, that are completely open-access and legitimate journals.
Impact Factor
Dr. Wilner: What about impact factor? Many journals boast about their impact factor. I’m not sure how to interpret that number.
Dr. Merino: Impact factor is very interesting. The impact factor was developed by medical librarians to try to identify the journals they should be subscribing to. It’s a measure of the average citations to an average paper in the journal.
It doesn’t tell you about specific papers. It tells you, on average, how many of the papers in this journal get cited so many times. It’s calculated by the number of articles that were cited divided by the number of articles that were published. Journals that publish many papers, like Neurology, have a hard time bringing up their impact factor beyond a certain level.
Similarly, very small journals with one or two very highly cited papers have a very high impact factor. It’s being used as a measure, perhaps inappropriately, of how good or how reputable a journal is. We all say we don’t care about journal impact factors, but we all know our journal impact factor and we used to know it to three decimals. Now, they changed the system, and there’s only one decimal point, which makes more sense.
This is more important, for example, for authors when deciding where to submit papers. I know that in some countries, particularly in Europe, the impact factor of the journal where you publish has an impact on your promotion decisions.
I would say what’s even more important than the impact factor, is to say, “Well, is this the journal that fits the scope of my paper? Is this the journal that reaches the audience that I want to reach when I write my paper?”
There are some papers, for example, that are very influential. The impact factor just captures citations. There are some papers that are very influential that may not get cited very often. There may be papers that change clinical practice.
If you read a paper that tells you that you should be changing how you treat your patients with myasthenia based on this paper, that may not get cited. It’s a very clinically focused paper, but it’s probably more impactful than one that gets cited very much in some respect, or they make it to public policy decisions, and so on.
I think it’s important to look more at the audience and the journal scope when you submit your papers.
Dr. Wilner: One other technical question. The journals also say they’re indexed in PubMed or Google Scholar. If I want to publish my paper and I want it indexed where the right people are going to find it, where does it need to be indexed?
Dr. Merino: I grew up using Index Medicus, MedlinePlus, and the Library of Science. I still do. If I need to find something, I go to PubMed. Ideally, papers are listed in MedlinePlus or can be found in PubMed. They’re not the same thing, but you can find them through them.
That would be an important thing. Nowadays, a lot more people are using Google Scholar or Google just to identify papers. It may be a little bit less relevant, but it’s still a measure of the quality of the journal before they get indexed in some of these. For example, if you get listed in MedlinePlus, it has gone through certain quality checks by the index itself to see whether they would accept the journal or not. That’s something you want to check.
Typically, most of the large journals or the journals you and I know about are listed in more than one place, right? They’re listed in Scopus and Web of Science. They’re listed in MedlinePlus and so on. Again, if you’re submitting your paper, go somewhere where you know the journal and you’ve heard about it.
Dr. Wilner: I’m not going to ask you about artificial intelligence. We can do that another time. I want to ask something closer to me, which is this question of publish or perish.
There seems to be, in academics, more emphasis on the number of papers that one has published rather than their quality. How does a younger academician or one who really needs to publish cope with that?
Dr. Merino: Many people are writing up research that may not be relevant or that may not be high quality just because you need to have a long list of papers to get promoted, for example, if you’re an academician.
Doug Altman, who was a very influential person in the field quality of not only medical statistics but also medical publishing, had the idea that we need less research, but we need better research.
We often receive papers where you say, well, what’s the rationale behind the question in this paper? It’s like they had a large amount of data and were trying to squeeze as much as they could out of that. I think, as a young academician, the important thing to think about is whether it is an important question that matters to you and to the field, from whatever perspective, whether it’s going to advance research, advance clinical care, or have public policy implications.
Is this one where the answer will be important no matter what the answer is? If you’re thinking of that, your work will be well recognized, people will know you, and you’ll get invited to collaborate. I think that’s the most important thing rather than just churning out a large number of papers.
The productivity will come from the fact that you start by saying, let me ask something that’s really meaningful to me and to the field, with a good question and using strong research methodology.
Dr. Wilner: Thanks for that, Dr. Merino. I think that’s very valuable for all of us. This has been a great discussion. Do you have any final comments before we wrap up?
Dr. Merino: I want to encourage people to continue reading medical journals all the time and submitting to us, again, good research and important questions with robust methodology. That’s what we’re looking for in Neurology and most serious medical journals.
Dr. Wilner is an associate professor of neurology at the University of Tennessee Health Science Center, Memphis. Dr. Merino is a professor in the department of neurology at Georgetown University Medical Center, Washington, DC. Dr. Wilner reported conflicts of interest with Accordant Health Services and Lulu Publishing. Dr. Merino reported no relevant conflicts of interest.
A version of this article first appeared on Medscape.com.
Teaching Tips for Dermatology Residents
Dermatology residents interact with trainees of various levels throughout the workday—from undergraduate or even high school students to postgraduate fellows. Depending on the institution’s training program, residents may have responsibilities to teach through lecture series such as Grand Rounds and didactics. Therefore, it is an integral part of resident training to become educators in addition to being learners; however, formal pedagogy education is rare in dermatology programs. 1,2 Herein, I discuss several techniques that residents can apply to their practice to cultivate ideal learning environments and outcomes for trainees.
Creating Effective Teaching and Learning Experiences
Planning to teach can be as important as teaching itself. Developing learning objectives can help to create effective teaching and learning experiences. Learning objectives should be specific, time bound, attainable, and learner centered (Table 1). It is recommended that residents aim for no more than 4 objectives per hour of learning.3 By creating clear learning objectives, residents can make connections between the content and any assessments. Bloom’s taxonomy of cognitive learning objectives gives guidance on action verbs to use in writing learning objectives depending on the cognitive process being tested (Table 2).4
Creating a Safe Educational Environment
Psychological safety is the belief that a learning environment is a safe place in which to take risks.5 A clinical learning environment that is psychologically safe can support trainee well-being and learning. Cultivating a safe educational environment may include addressing microaggressions and bias in the clinical workplace. Table 3 provides examples of statements using the 6 Ds, which can be used to mitigate these issues.6 The first 4—direct, distract, delegate, and defer—represent ways to respond to racism, microaggressions, and bias, and the last 2—display discomfort and debrief—are responses that may be utilized in any problematic incident. Residents can play an important supportive role in scenarios where learners are faced with an incident that may not be regarded as psychologically safe. This is especially true if the learner is at a lower training level than the dermatology resident. We all play a role in creating a safe workplace for our teams.



Teaching in the Clinic and Hospital
There are multiple challenges to teaching in both inpatient and outpatient environments, including limited space and time; thus, more informal teaching methods are common. For example, in an outpatient dermatology clinic, the patient schedule can become a “table of contents” of potential teaching and learning opportunities. This technique is called the focused half day.3,7 By reviewing the clinic schedule, students can focus on a specific area of interest or theme throughout the course of the day.3
Priming and framing are other focused techniques that work well in both outpatient and inpatient settings.3,8,9 Priming means alerting the trainee to upcoming learning objective(s) and focusing their attention on what to observe or do during a shared visit with a patient. Framing—instructing learners to collect information that is relevant to the diagnosis and treatment—allows trainees to help move patient care forward while the resident attends to other patients.3
Modeling involves describing a thought process out loud for a learner3,10; for example, prior to starting a patient encounter, a dermatology resident may clearly state the goal of a patient conversation to the learner, describe their thought process about the topic, summarize the important points, and ask the learner if they have any questions about what was just said. Using this technique, learners may have a better understanding of why and how to go about conducting a patient encounter after the resident models one for them.
Effectively Integrating Visual Media and Presentations
Research supported by the cognitive load theory and cognitive theory of multimedia learning has led to the assertion-evidence approach for creating presentation slides that are built around messages, not topics, and messages are supported with visuals, not bullets.3,11,12 For example, slides should be constructed with 1- to 2-line assertion statements as titles and relevant illustrations or figures as supporting evidence to enhance visual memory.3
Written text on presentation slides often is redundant with spoken narration and also decreases learning because of cognitive load. Busy background colors and/or designs consume working memory and also can be detrimental to learning. Limiting these common distractors in a presentation makes for more effective delivery and retention of knowledge.3
Final Thoughts
There are multiple avenues for teaching as a resident and not all techniques may be applicable depending on the clinical or academic scenario. This column provides a starting point for residents to augment their pedagogical skills, particularly because formal teaching on pedagogy is lacking in medical education.
- Burgin S, Zhong CS, Rana J. A resident-as-teacher program increases dermatology residents’ knowledge and confidence in teaching techniques: a pilot study. J Am Acad Dermatol. 2020;83:651-653. doi:10.1016/j.jaad.2019.12.008
- Burgin S, Homayounfar G, Newman LR, et al. Instruction in teaching and teaching opportunities for residents in US dermatology programs: results of a national survey. J Am Acad Dermatol. 2017;76:703-706. doi:10.1016/j.jaad.2016.08.043
- UNM School of Medicine Continuous Professional Learning. Residents as Educators. UNM School of Medicine; 2023.
- Bloom BS. Taxonomy of Educational Objectives. Book 1, Cognitive Domain. Longman; 1979.
- McClintock AH, Fainstad T, Blau K, et al. Psychological safety in medical education: a scoping review and synthesis of the literature. Med Teach. 2023;45:1290-1299. doi:10.1080/0142159X.2023.2216863
- Ackerman-Barger K, Jacobs NN, Orozco R, et al. Addressing microaggressions in academic health: a workshop for inclusiveexcellence. MedEdPORTAL. 2021;17:11103. doi:10.15766/mep_2374-8265.11103
- Taylor C, Lipsky MS, Bauer L. Focused teaching: facilitating early clinical experience in an office setting. Fam Med. 1998;30:547-548.
- Pan Z, Kosicki G. Framing analysis: an approach to news discourse. Polit Commun. 1993;10:55-75. doi:10.1080/10584609.1993.9962963
- Price V, Tewksbury D, Powers E. Switching trains of thought: the impact of news frames on readers’ cognitive responses. Commun Res. 1997;24:481-506. doi:10.1177/009365097024005002
- Haston W. Teacher modeling as an effective teaching strategy. Music Educators J. 2007;93:26. doi:10.2307/4127130
- Alley M. Build your scientific talk on messages, not topics. Vimeo website. January 18, 2020. Accessed June 14, 2024. https://vimeo.com/385725653
- Alley M. Support your presentation messages with visual evidence, not bullet lists. Vimeo website. January 18, 2020. Accessed June 14, 2024. https://vimeo.com/385729603
Dermatology residents interact with trainees of various levels throughout the workday—from undergraduate or even high school students to postgraduate fellows. Depending on the institution’s training program, residents may have responsibilities to teach through lecture series such as Grand Rounds and didactics. Therefore, it is an integral part of resident training to become educators in addition to being learners; however, formal pedagogy education is rare in dermatology programs. 1,2 Herein, I discuss several techniques that residents can apply to their practice to cultivate ideal learning environments and outcomes for trainees.
Creating Effective Teaching and Learning Experiences
Planning to teach can be as important as teaching itself. Developing learning objectives can help to create effective teaching and learning experiences. Learning objectives should be specific, time bound, attainable, and learner centered (Table 1). It is recommended that residents aim for no more than 4 objectives per hour of learning.3 By creating clear learning objectives, residents can make connections between the content and any assessments. Bloom’s taxonomy of cognitive learning objectives gives guidance on action verbs to use in writing learning objectives depending on the cognitive process being tested (Table 2).4
Creating a Safe Educational Environment
Psychological safety is the belief that a learning environment is a safe place in which to take risks.5 A clinical learning environment that is psychologically safe can support trainee well-being and learning. Cultivating a safe educational environment may include addressing microaggressions and bias in the clinical workplace. Table 3 provides examples of statements using the 6 Ds, which can be used to mitigate these issues.6 The first 4—direct, distract, delegate, and defer—represent ways to respond to racism, microaggressions, and bias, and the last 2—display discomfort and debrief—are responses that may be utilized in any problematic incident. Residents can play an important supportive role in scenarios where learners are faced with an incident that may not be regarded as psychologically safe. This is especially true if the learner is at a lower training level than the dermatology resident. We all play a role in creating a safe workplace for our teams.



Teaching in the Clinic and Hospital
There are multiple challenges to teaching in both inpatient and outpatient environments, including limited space and time; thus, more informal teaching methods are common. For example, in an outpatient dermatology clinic, the patient schedule can become a “table of contents” of potential teaching and learning opportunities. This technique is called the focused half day.3,7 By reviewing the clinic schedule, students can focus on a specific area of interest or theme throughout the course of the day.3
Priming and framing are other focused techniques that work well in both outpatient and inpatient settings.3,8,9 Priming means alerting the trainee to upcoming learning objective(s) and focusing their attention on what to observe or do during a shared visit with a patient. Framing—instructing learners to collect information that is relevant to the diagnosis and treatment—allows trainees to help move patient care forward while the resident attends to other patients.3
Modeling involves describing a thought process out loud for a learner3,10; for example, prior to starting a patient encounter, a dermatology resident may clearly state the goal of a patient conversation to the learner, describe their thought process about the topic, summarize the important points, and ask the learner if they have any questions about what was just said. Using this technique, learners may have a better understanding of why and how to go about conducting a patient encounter after the resident models one for them.
Effectively Integrating Visual Media and Presentations
Research supported by the cognitive load theory and cognitive theory of multimedia learning has led to the assertion-evidence approach for creating presentation slides that are built around messages, not topics, and messages are supported with visuals, not bullets.3,11,12 For example, slides should be constructed with 1- to 2-line assertion statements as titles and relevant illustrations or figures as supporting evidence to enhance visual memory.3
Written text on presentation slides often is redundant with spoken narration and also decreases learning because of cognitive load. Busy background colors and/or designs consume working memory and also can be detrimental to learning. Limiting these common distractors in a presentation makes for more effective delivery and retention of knowledge.3
Final Thoughts
There are multiple avenues for teaching as a resident and not all techniques may be applicable depending on the clinical or academic scenario. This column provides a starting point for residents to augment their pedagogical skills, particularly because formal teaching on pedagogy is lacking in medical education.
Dermatology residents interact with trainees of various levels throughout the workday—from undergraduate or even high school students to postgraduate fellows. Depending on the institution’s training program, residents may have responsibilities to teach through lecture series such as Grand Rounds and didactics. Therefore, it is an integral part of resident training to become educators in addition to being learners; however, formal pedagogy education is rare in dermatology programs. 1,2 Herein, I discuss several techniques that residents can apply to their practice to cultivate ideal learning environments and outcomes for trainees.
Creating Effective Teaching and Learning Experiences
Planning to teach can be as important as teaching itself. Developing learning objectives can help to create effective teaching and learning experiences. Learning objectives should be specific, time bound, attainable, and learner centered (Table 1). It is recommended that residents aim for no more than 4 objectives per hour of learning.3 By creating clear learning objectives, residents can make connections between the content and any assessments. Bloom’s taxonomy of cognitive learning objectives gives guidance on action verbs to use in writing learning objectives depending on the cognitive process being tested (Table 2).4
Creating a Safe Educational Environment
Psychological safety is the belief that a learning environment is a safe place in which to take risks.5 A clinical learning environment that is psychologically safe can support trainee well-being and learning. Cultivating a safe educational environment may include addressing microaggressions and bias in the clinical workplace. Table 3 provides examples of statements using the 6 Ds, which can be used to mitigate these issues.6 The first 4—direct, distract, delegate, and defer—represent ways to respond to racism, microaggressions, and bias, and the last 2—display discomfort and debrief—are responses that may be utilized in any problematic incident. Residents can play an important supportive role in scenarios where learners are faced with an incident that may not be regarded as psychologically safe. This is especially true if the learner is at a lower training level than the dermatology resident. We all play a role in creating a safe workplace for our teams.



Teaching in the Clinic and Hospital
There are multiple challenges to teaching in both inpatient and outpatient environments, including limited space and time; thus, more informal teaching methods are common. For example, in an outpatient dermatology clinic, the patient schedule can become a “table of contents” of potential teaching and learning opportunities. This technique is called the focused half day.3,7 By reviewing the clinic schedule, students can focus on a specific area of interest or theme throughout the course of the day.3
Priming and framing are other focused techniques that work well in both outpatient and inpatient settings.3,8,9 Priming means alerting the trainee to upcoming learning objective(s) and focusing their attention on what to observe or do during a shared visit with a patient. Framing—instructing learners to collect information that is relevant to the diagnosis and treatment—allows trainees to help move patient care forward while the resident attends to other patients.3
Modeling involves describing a thought process out loud for a learner3,10; for example, prior to starting a patient encounter, a dermatology resident may clearly state the goal of a patient conversation to the learner, describe their thought process about the topic, summarize the important points, and ask the learner if they have any questions about what was just said. Using this technique, learners may have a better understanding of why and how to go about conducting a patient encounter after the resident models one for them.
Effectively Integrating Visual Media and Presentations
Research supported by the cognitive load theory and cognitive theory of multimedia learning has led to the assertion-evidence approach for creating presentation slides that are built around messages, not topics, and messages are supported with visuals, not bullets.3,11,12 For example, slides should be constructed with 1- to 2-line assertion statements as titles and relevant illustrations or figures as supporting evidence to enhance visual memory.3
Written text on presentation slides often is redundant with spoken narration and also decreases learning because of cognitive load. Busy background colors and/or designs consume working memory and also can be detrimental to learning. Limiting these common distractors in a presentation makes for more effective delivery and retention of knowledge.3
Final Thoughts
There are multiple avenues for teaching as a resident and not all techniques may be applicable depending on the clinical or academic scenario. This column provides a starting point for residents to augment their pedagogical skills, particularly because formal teaching on pedagogy is lacking in medical education.
- Burgin S, Zhong CS, Rana J. A resident-as-teacher program increases dermatology residents’ knowledge and confidence in teaching techniques: a pilot study. J Am Acad Dermatol. 2020;83:651-653. doi:10.1016/j.jaad.2019.12.008
- Burgin S, Homayounfar G, Newman LR, et al. Instruction in teaching and teaching opportunities for residents in US dermatology programs: results of a national survey. J Am Acad Dermatol. 2017;76:703-706. doi:10.1016/j.jaad.2016.08.043
- UNM School of Medicine Continuous Professional Learning. Residents as Educators. UNM School of Medicine; 2023.
- Bloom BS. Taxonomy of Educational Objectives. Book 1, Cognitive Domain. Longman; 1979.
- McClintock AH, Fainstad T, Blau K, et al. Psychological safety in medical education: a scoping review and synthesis of the literature. Med Teach. 2023;45:1290-1299. doi:10.1080/0142159X.2023.2216863
- Ackerman-Barger K, Jacobs NN, Orozco R, et al. Addressing microaggressions in academic health: a workshop for inclusiveexcellence. MedEdPORTAL. 2021;17:11103. doi:10.15766/mep_2374-8265.11103
- Taylor C, Lipsky MS, Bauer L. Focused teaching: facilitating early clinical experience in an office setting. Fam Med. 1998;30:547-548.
- Pan Z, Kosicki G. Framing analysis: an approach to news discourse. Polit Commun. 1993;10:55-75. doi:10.1080/10584609.1993.9962963
- Price V, Tewksbury D, Powers E. Switching trains of thought: the impact of news frames on readers’ cognitive responses. Commun Res. 1997;24:481-506. doi:10.1177/009365097024005002
- Haston W. Teacher modeling as an effective teaching strategy. Music Educators J. 2007;93:26. doi:10.2307/4127130
- Alley M. Build your scientific talk on messages, not topics. Vimeo website. January 18, 2020. Accessed June 14, 2024. https://vimeo.com/385725653
- Alley M. Support your presentation messages with visual evidence, not bullet lists. Vimeo website. January 18, 2020. Accessed June 14, 2024. https://vimeo.com/385729603
- Burgin S, Zhong CS, Rana J. A resident-as-teacher program increases dermatology residents’ knowledge and confidence in teaching techniques: a pilot study. J Am Acad Dermatol. 2020;83:651-653. doi:10.1016/j.jaad.2019.12.008
- Burgin S, Homayounfar G, Newman LR, et al. Instruction in teaching and teaching opportunities for residents in US dermatology programs: results of a national survey. J Am Acad Dermatol. 2017;76:703-706. doi:10.1016/j.jaad.2016.08.043
- UNM School of Medicine Continuous Professional Learning. Residents as Educators. UNM School of Medicine; 2023.
- Bloom BS. Taxonomy of Educational Objectives. Book 1, Cognitive Domain. Longman; 1979.
- McClintock AH, Fainstad T, Blau K, et al. Psychological safety in medical education: a scoping review and synthesis of the literature. Med Teach. 2023;45:1290-1299. doi:10.1080/0142159X.2023.2216863
- Ackerman-Barger K, Jacobs NN, Orozco R, et al. Addressing microaggressions in academic health: a workshop for inclusiveexcellence. MedEdPORTAL. 2021;17:11103. doi:10.15766/mep_2374-8265.11103
- Taylor C, Lipsky MS, Bauer L. Focused teaching: facilitating early clinical experience in an office setting. Fam Med. 1998;30:547-548.
- Pan Z, Kosicki G. Framing analysis: an approach to news discourse. Polit Commun. 1993;10:55-75. doi:10.1080/10584609.1993.9962963
- Price V, Tewksbury D, Powers E. Switching trains of thought: the impact of news frames on readers’ cognitive responses. Commun Res. 1997;24:481-506. doi:10.1177/009365097024005002
- Haston W. Teacher modeling as an effective teaching strategy. Music Educators J. 2007;93:26. doi:10.2307/4127130
- Alley M. Build your scientific talk on messages, not topics. Vimeo website. January 18, 2020. Accessed June 14, 2024. https://vimeo.com/385725653
- Alley M. Support your presentation messages with visual evidence, not bullet lists. Vimeo website. January 18, 2020. Accessed June 14, 2024. https://vimeo.com/385729603
Resident Pearls
- Emphasizing specific learning objectives, prioritizing safety in the learning environment, utilizing clinical teaching techniques, and using multimedia to present messages all contribute to effective dermatology teaching by residents.