Mixed Topics

How might AI enhance the detection of key histologic features in drug eruptions compared to traditional microscopy?

DR. BRIDGES: AI offers the potential to enhance detection of histologic features in drug eruptions by systematically analyzing entire whole-slide images. Convolutional neural networks and attention-based models can identify subtle or focal findings such as scattered dyskeratotic keratinocytes, focal spongiosis, early interface change, rare eosinophils, or microvascular injury, which may be overlooked during routine microscopy due to sampling limitations. This capability is particularly relevant in drug eruptions, where histologic changes often are heterogeneous and patchy.

AI-generated attention heatmaps can highlight diagnostically relevant regions across the slide, improving consistency and completeness of slide reviews. While AI has demonstrated high sensitivity and specificity in broader dermatopathology tasks, particularly neoplastic conditions, drug eruption–specific validation data are currently lacking. As such, the most realistic application at present is AI functioning as a sensitivity-enhancing adjunct or “second reader,” improving consistency and completeness of slide review while preserving expert human interpretation.

Which histologic patterns in drug eruptions are hardest to quantify, and how could AI help standardize their assessment?

DR. BRIDGES: AI-based image analysis can standardize the assessment of histologic patterns through objective reproducible quantification. Deep learning algorithms can segment epidermal and dermal compartments, identify inflammatory cell types, and calculate metrics such as eosinophil density per unit area, percentage of epidermis with vacuolar alteration, or number of affected vessels. Studies in quantitative immunohistochemistry demonstrate high accuracy for tissue segmentation and cell counting, suggesting feasibility for similar applications in inflammatory dermatopathology. While these tools would not replace diagnostic interpretation, they could provide standardized measurements that enhance reproducibility and improve clinicopathologic correlation.

What training challenges must be addressed in AI and drug eruption histology?

DR. BRIDGES: Training AI models for drug eruption histopathology faces several challenges, including the limited availability of high-quality, well-annotated datasets, as most existing AI dermatopathology research focuses on neoplastic conditions. Drug eruptions also exhibit marked histologic heterogeneity, ranging from spongiotic and lichenoid to vasculitic and cytotoxic patterns, often with significant overlap. Accurate labeling, therefore, requires robust clinicopathologic correlation, including medication history, timing, laboratory data, and clinical outcomes—information that is often incomplete or retrospective.

Inaccurate or inconsistent annotations can significantly degrade model performance, and expert disagreement in borderline cases further complicates the creation of reliable ground truth. Additionally, training data may reflect institutional or demographic biases, risking unequal performance across patient populations. Addressing these challenges will require multicenter collaboration, standardized annotation protocols, inclusion of diverse patient cohorts, and careful attention to bias mitigation. At present, these barriers place drug eruption AI firmly in the investigational rather than clinical domain.

How important is AI explainability in the interpretation of diagnostic suggestions?

DR. BRIDGES: Explainability is essential for trust, particularly in the evaluation of drug eruptions, where diagnostic decisions can have serious clinical consequences. Dermatopathologists must understand which histologic features are driving an AI model’s assessment to ensure that conclusions align with morphologic reality and clinicopathologic reasoning. Explainable AI tools (such as attention heatmaps, feature importance rankings, and methods like Shapley Additive Explanations or Local Interpretable Model-Agnostic Explanations) can help clarify which histologic features are driving the AI model’s assessment.

Without transparency, AI systems function as “black boxes,” limiting their utility in high-stakes settings where diagnostic accountability and clinical communication are paramount. Explainability also supports appropriate skepticism, allowing pathologists to recognize when model outputs may be unreliable due to artifacts, atypical patterns, or out-of-distribution cases. In cases of drug eruptions—where diagnosis relies on combining histology, clinical timing, and medication history—explainability is essential for proper use.

How could AI pattern recognition be integrated into your workflow to enhance diagnostic efficiency and accuracy? What safeguards would be required?

DR. BRIDGES: In the near term, AI pattern recognition can be useful as an assistive tool rather than a diagnostic authority. One potential application is pre-screening whole-slide images to flag cases with features such as prominent interface change, increased keratinocyte necrosis, eosinophil-rich infiltrates, or vascular injury, prompting expedited review in clinically concerning scenarios. During sign-out, AI overlays could aid efficiency by highlighting rare but relevant features and providing quantitative summaries that support standardized reporting.

Safeguards are essential. AI systems must be validated across diverse practice settings, staining protocols, and scanning platforms. Human oversight is mandatory, with the dermatopathologist retaining full diagnostic responsibility. AI involvement should be clearly documented for medicolegal transparency, and performance should be continuously monitored to detect algorithmic drift as new drug eruption patterns emerge. Given current limitations, AI is best viewed as a tool to refine and support expert judgment, not replace it.

What data-sharing or privacy challenges must be addressed to develop robust AI models for diverse drug-eruption histopathology?

DR. BRIDGES: Developing robust AI models for drug eruptions requires large diverse datasets, raising significant privacy and governance challenges. Rigorous de-identification protocols, clear informed consent frameworks, and strong institutional oversight are therefore essential. Multicenter collaborations must employ secure data-use agreements and governance structures that clearly define access, ownership, and downstream use of data.

Ensuring equitable representation is equally critical, as underrepresentation of certain populations may lead to biased performance and disparities in care. Standardized data formats and interoperable systems are needed to facilitate collaboration while preserving security. Transparent governance structures, clear rules regarding data use, and trust-building with patients and institutions will ultimately determine willingness to participate. Addressing these challenges is foundational to advancing AI research in drug eruptions responsibly and ethically.

How might AI enhance the detection of key histologic features in drug eruptions compared to traditional microscopy?

DR. BRIDGES: AI offers the potential to enhance detection of histologic features in drug eruptions by systematically analyzing entire whole-slide images. Convolutional neural networks and attention-based models can identify subtle or focal findings such as scattered dyskeratotic keratinocytes, focal spongiosis, early interface change, rare eosinophils, or microvascular injury, which may be overlooked during routine microscopy due to sampling limitations. This capability is particularly relevant in drug eruptions, where histologic changes often are heterogeneous and patchy.

AI-generated attention heatmaps can highlight diagnostically relevant regions across the slide, improving consistency and completeness of slide reviews. While AI has demonstrated high sensitivity and specificity in broader dermatopathology tasks, particularly neoplastic conditions, drug eruption–specific validation data are currently lacking. As such, the most realistic application at present is AI functioning as a sensitivity-enhancing adjunct or “second reader,” improving consistency and completeness of slide review while preserving expert human interpretation.

Which histologic patterns in drug eruptions are hardest to quantify, and how could AI help standardize their assessment?

DR. BRIDGES: AI-based image analysis can standardize the assessment of histologic patterns through objective reproducible quantification. Deep learning algorithms can segment epidermal and dermal compartments, identify inflammatory cell types, and calculate metrics such as eosinophil density per unit area, percentage of epidermis with vacuolar alteration, or number of affected vessels. Studies in quantitative immunohistochemistry demonstrate high accuracy for tissue segmentation and cell counting, suggesting feasibility for similar applications in inflammatory dermatopathology. While these tools would not replace diagnostic interpretation, they could provide standardized measurements that enhance reproducibility and improve clinicopathologic correlation.

What training challenges must be addressed in AI and drug eruption histology?

DR. BRIDGES: Training AI models for drug eruption histopathology faces several challenges, including the limited availability of high-quality, well-annotated datasets, as most existing AI dermatopathology research focuses on neoplastic conditions. Drug eruptions also exhibit marked histologic heterogeneity, ranging from spongiotic and lichenoid to vasculitic and cytotoxic patterns, often with significant overlap. Accurate labeling, therefore, requires robust clinicopathologic correlation, including medication history, timing, laboratory data, and clinical outcomes—information that is often incomplete or retrospective.

Inaccurate or inconsistent annotations can significantly degrade model performance, and expert disagreement in borderline cases further complicates the creation of reliable ground truth. Additionally, training data may reflect institutional or demographic biases, risking unequal performance across patient populations. Addressing these challenges will require multicenter collaboration, standardized annotation protocols, inclusion of diverse patient cohorts, and careful attention to bias mitigation. At present, these barriers place drug eruption AI firmly in the investigational rather than clinical domain.

How important is AI explainability in the interpretation of diagnostic suggestions?

DR. BRIDGES: Explainability is essential for trust, particularly in the evaluation of drug eruptions, where diagnostic decisions can have serious clinical consequences. Dermatopathologists must understand which histologic features are driving an AI model’s assessment to ensure that conclusions align with morphologic reality and clinicopathologic reasoning. Explainable AI tools (such as attention heatmaps, feature importance rankings, and methods like Shapley Additive Explanations or Local Interpretable Model-Agnostic Explanations) can help clarify which histologic features are driving the AI model’s assessment.

Without transparency, AI systems function as “black boxes,” limiting their utility in high-stakes settings where diagnostic accountability and clinical communication are paramount. Explainability also supports appropriate skepticism, allowing pathologists to recognize when model outputs may be unreliable due to artifacts, atypical patterns, or out-of-distribution cases. In cases of drug eruptions—where diagnosis relies on combining histology, clinical timing, and medication history—explainability is essential for proper use.

How could AI pattern recognition be integrated into your workflow to enhance diagnostic efficiency and accuracy? What safeguards would be required?

DR. BRIDGES: In the near term, AI pattern recognition can be useful as an assistive tool rather than a diagnostic authority. One potential application is pre-screening whole-slide images to flag cases with features such as prominent interface change, increased keratinocyte necrosis, eosinophil-rich infiltrates, or vascular injury, prompting expedited review in clinically concerning scenarios. During sign-out, AI overlays could aid efficiency by highlighting rare but relevant features and providing quantitative summaries that support standardized reporting.

Safeguards are essential. AI systems must be validated across diverse practice settings, staining protocols, and scanning platforms. Human oversight is mandatory, with the dermatopathologist retaining full diagnostic responsibility. AI involvement should be clearly documented for medicolegal transparency, and performance should be continuously monitored to detect algorithmic drift as new drug eruption patterns emerge. Given current limitations, AI is best viewed as a tool to refine and support expert judgment, not replace it.

What data-sharing or privacy challenges must be addressed to develop robust AI models for diverse drug-eruption histopathology?

DR. BRIDGES: Developing robust AI models for drug eruptions requires large diverse datasets, raising significant privacy and governance challenges. Rigorous de-identification protocols, clear informed consent frameworks, and strong institutional oversight are therefore essential. Multicenter collaborations must employ secure data-use agreements and governance structures that clearly define access, ownership, and downstream use of data.

Ensuring equitable representation is equally critical, as underrepresentation of certain populations may lead to biased performance and disparities in care. Standardized data formats and interoperable systems are needed to facilitate collaboration while preserving security. Transparent governance structures, clear rules regarding data use, and trust-building with patients and institutions will ultimately determine willingness to participate. Addressing these challenges is foundational to advancing AI research in drug eruptions responsibly and ethically.

How might AI enhance the detection of key histologic features in drug eruptions compared to traditional microscopy?

DR. BRIDGES: AI offers the potential to enhance detection of histologic features in drug eruptions by systematically analyzing entire whole-slide images. Convolutional neural networks and attention-based models can identify subtle or focal findings such as scattered dyskeratotic keratinocytes, focal spongiosis, early interface change, rare eosinophils, or microvascular injury, which may be overlooked during routine microscopy due to sampling limitations. This capability is particularly relevant in drug eruptions, where histologic changes often are heterogeneous and patchy.

AI-generated attention heatmaps can highlight diagnostically relevant regions across the slide, improving consistency and completeness of slide reviews. While AI has demonstrated high sensitivity and specificity in broader dermatopathology tasks, particularly neoplastic conditions, drug eruption–specific validation data are currently lacking. As such, the most realistic application at present is AI functioning as a sensitivity-enhancing adjunct or “second reader,” improving consistency and completeness of slide review while preserving expert human interpretation.

Which histologic patterns in drug eruptions are hardest to quantify, and how could AI help standardize their assessment?

DR. BRIDGES: AI-based image analysis can standardize the assessment of histologic patterns through objective reproducible quantification. Deep learning algorithms can segment epidermal and dermal compartments, identify inflammatory cell types, and calculate metrics such as eosinophil density per unit area, percentage of epidermis with vacuolar alteration, or number of affected vessels. Studies in quantitative immunohistochemistry demonstrate high accuracy for tissue segmentation and cell counting, suggesting feasibility for similar applications in inflammatory dermatopathology. While these tools would not replace diagnostic interpretation, they could provide standardized measurements that enhance reproducibility and improve clinicopathologic correlation.

What training challenges must be addressed in AI and drug eruption histology?

DR. BRIDGES: Training AI models for drug eruption histopathology faces several challenges, including the limited availability of high-quality, well-annotated datasets, as most existing AI dermatopathology research focuses on neoplastic conditions. Drug eruptions also exhibit marked histologic heterogeneity, ranging from spongiotic and lichenoid to vasculitic and cytotoxic patterns, often with significant overlap. Accurate labeling, therefore, requires robust clinicopathologic correlation, including medication history, timing, laboratory data, and clinical outcomes—information that is often incomplete or retrospective.

Inaccurate or inconsistent annotations can significantly degrade model performance, and expert disagreement in borderline cases further complicates the creation of reliable ground truth. Additionally, training data may reflect institutional or demographic biases, risking unequal performance across patient populations. Addressing these challenges will require multicenter collaboration, standardized annotation protocols, inclusion of diverse patient cohorts, and careful attention to bias mitigation. At present, these barriers place drug eruption AI firmly in the investigational rather than clinical domain.

How important is AI explainability in the interpretation of diagnostic suggestions?

DR. BRIDGES: Explainability is essential for trust, particularly in the evaluation of drug eruptions, where diagnostic decisions can have serious clinical consequences. Dermatopathologists must understand which histologic features are driving an AI model’s assessment to ensure that conclusions align with morphologic reality and clinicopathologic reasoning. Explainable AI tools (such as attention heatmaps, feature importance rankings, and methods like Shapley Additive Explanations or Local Interpretable Model-Agnostic Explanations) can help clarify which histologic features are driving the AI model’s assessment.

Without transparency, AI systems function as “black boxes,” limiting their utility in high-stakes settings where diagnostic accountability and clinical communication are paramount. Explainability also supports appropriate skepticism, allowing pathologists to recognize when model outputs may be unreliable due to artifacts, atypical patterns, or out-of-distribution cases. In cases of drug eruptions—where diagnosis relies on combining histology, clinical timing, and medication history—explainability is essential for proper use.

How could AI pattern recognition be integrated into your workflow to enhance diagnostic efficiency and accuracy? What safeguards would be required?

DR. BRIDGES: In the near term, AI pattern recognition can be useful as an assistive tool rather than a diagnostic authority. One potential application is pre-screening whole-slide images to flag cases with features such as prominent interface change, increased keratinocyte necrosis, eosinophil-rich infiltrates, or vascular injury, prompting expedited review in clinically concerning scenarios. During sign-out, AI overlays could aid efficiency by highlighting rare but relevant features and providing quantitative summaries that support standardized reporting.

Safeguards are essential. AI systems must be validated across diverse practice settings, staining protocols, and scanning platforms. Human oversight is mandatory, with the dermatopathologist retaining full diagnostic responsibility. AI involvement should be clearly documented for medicolegal transparency, and performance should be continuously monitored to detect algorithmic drift as new drug eruption patterns emerge. Given current limitations, AI is best viewed as a tool to refine and support expert judgment, not replace it.

What data-sharing or privacy challenges must be addressed to develop robust AI models for diverse drug-eruption histopathology?

DR. BRIDGES: Developing robust AI models for drug eruptions requires large diverse datasets, raising significant privacy and governance challenges. Rigorous de-identification protocols, clear informed consent frameworks, and strong institutional oversight are therefore essential. Multicenter collaborations must employ secure data-use agreements and governance structures that clearly define access, ownership, and downstream use of data.

Ensuring equitable representation is equally critical, as underrepresentation of certain populations may lead to biased performance and disparities in care. Standardized data formats and interoperable systems are needed to facilitate collaboration while preserving security. Transparent governance structures, clear rules regarding data use, and trust-building with patients and institutions will ultimately determine willingness to participate. Addressing these challenges is foundational to advancing AI research in drug eruptions responsibly and ethically.

To the Editor:

Mohs micrographic surgery (MMS) is performed in stages and often requires repeated administration of a local anesthetic, most commonly lidocaine. While generally safe, lidocaine administration carries the potential for cumulative toxicity, particularly in patients who have large or multiple lesions or medical comorbidities or who require extensive repair. Current safety guidelines suggest upper limits of 7 mg/kg (or 500 mg) of lidocaine with epinephrine and 4.5 mg/kg (or 300 mg) without epinephrine for adults.¹ However, concerns have been raised about the relevance of these thresholds to MMS, in which anesthetic administration may be prolonged, cumulative, and influenced by surgical complexity.^2-5 While clinical experience often guides anesthetic planning, limited data exist identifying predictors of lidocaine use during MMS.

We performed an institutional review board–approved retrospective chart review of 149 patients who underwent 170 MMS procedures at a single academic dermatologic surgery center between July 2022 and June 2023. The aim of our study was to identify clinical and surgical predictors of lidocaine volume used during MMS. All procedures were performed by board-certified dermatologic surgeons (including A.J.). All patients received 1% lidocaine with epinephrine as the primary anesthetic agent. We collected patient demographic variables (age, sex, race, weight), procedural characteristics (anatomic site, number of Mohs stages, skin cancer type, number of surgical sites treated in one day, preoperative and postoperative lesion size, surgeon, repair type), comorbid conditions (hypertension, diabetes), and time from diagnosis to surgery. Data were extracted from the institutional REDCap system. We used t tests and analysis of variance for categorical variables and linear regression for continuous predictors, with statistical significance set at P<.05.

Baseline characteristics of the study patients are outlined in Table 1. The mean (SD) age was 74.2 (9.4) years, and most patients (98.7% [147/149]) were White. The mean (SD) weight was 83.1 (19.1) kg. Most lesions were either basal cell carcinoma (BCC)(50.6%) or squamous cell carcinoma (SCC)(44.1%), with 5.3% of lesions representing melanoma. The mean (SD) total lidocaine volume administered was 11.8 (8.3) mL. The majority (123/149 [72.4%]) of cases required one Mohs stage, but a subset required multiple stages, with a maximum of 5.

Several procedural and patient factors were significantly associated with the volume of lidocaine used. As expected, lesion size strongly influenced lidocaine volume. Both preoperative and postoperative lesion sizes were highly significant linear predictors (R²=0.28 and 0.41, respectively; P<.001), and postoperative lesion size demonstrated the strongest correlation of all tested variables. Patient weight was also significantly associated with lidocaine use (R²=.03, P=.0202), though the proportion of explained variance was modest. The operating surgeon also was significantly associated with lidocaine use (P=.006), suggesting potential variation in anesthetic technique or threshold for reinfiltration. The number of surgical sites treated in a single session also was significantly associated with greater lidocaine volume (P<.001).

Skin cancer type was a notable categorical predictor. Melanomas required substantially more lidocaine than BCCs or SCCs, with a mean (SD) volume of 25.6 (12.1) mL compared with 10.8 (6.0) mL for BCC and 11.4 (8.8) mL for SCC (P<.001). This difference may reflect disparities in surgical margin requirements, tumor depth, or intraoperative technique. While lesion location and number of stages were not statistically significant overall, mean lidocaine volumes trended higher in lesions on the trunk (18.2 mL) and in procedures requiring 3 or more stages (up to 22.0 mL for a single 4-stage case), though small sample sizes limited the ability to detect statistically significant differences in these subgroups. Detailed comparisons are presented in Table 2.

Wound repair type also was significantly associated with lidocaine volume requirements. Primary closures required a mean (SD) volume of 12.3 (5.0) mL, whereas flap repairs required 19.3 (10.0) mL and graft repairs required 17.5 (8.2) mL. Secondary-intention healing used the lowest lidocaine volumes (mean [SD], 4.9 [2.0] mL). Differences across repair types were statistically significant (analysis of variance, P<.001). These findings indicate that more complex reconstructions, such as flaps and grafts, are associated with higher anesthetic needs when compared with primary closures or secondary-intention healing.

Several other predictors, including age, time from diagnosis to surgery, and comorbid conditions such as hypertension or diabetes, were not significantly associated with anesthetic volume in our cohort. Time from diagnosis to surgery ranged widely but did not correlate with lesion size or lidocaine use, possibly due to scheduling variability or biopsy technique.

These findings offer practical implications for clinical planning. While most MMS cases fall well within safe limits for lidocaine administration, some patients—­particularly those with melanoma, large lesions, or multiple surgical sites—may approach thresholds at which further monitoring or dose tracking becomes relevant. Anticipating higher anesthetic requirements may help surgical teams plan procedure length, anesthesia restocking, or sequencing of multisite cases. Our analysis also showed that the type of wound repair meaningfully influences anesthetic use, with flap and graft repairs requiring substantially higher lidocaine volumes than primary closures and secondary-intention healing. Considering both tumor characteristics and the planned reconstruction may therefore improve the accuracy of anesthetic forecasting during preoperative planning.

We also observed surgeon-level variation in lidocaine volume despite standardized tumor types and case complexity. This suggests a role for individual technique (eg, depth of field block, number of reinfiltrations) and highlights the need for ongoing education around anesthetic optimization.

Our study was limited by its retrospective design, single-institution setting, and demographically homogeneous population. With 98.8% of patients identifying as White, generalizability to skin of color populations may be limited. In addition, lidocaine metabolism may vary across patient factors not captured here (eg, hepatic or renal function). Finally, although lidocaine volume was the outcome of interest, we did not measure patient-reported pain control, which may further clarify anesthetic adequacy. Nonetheless, our analysis demonstrated that routinely available clinical and procedural data can predict lidocaine volume requirements with reasonable reliability. Although no patient in our cohort approached the maximum recommended lidocaine dose, understanding these predictors may help anticipate scenarios nearing maximum dosing thresholds. In future studies, integrating weight-based thresholds (eg, mL/kg received) or serum lidocaine levels may improve safety monitoring and validate toxicity thresholds in complex cases.

In conclusion, we identified several key factors that predict lidocaine volume during MMS, including lesion size, melanoma diagnosis, number of surgical sites, patient weight, planned reconstruction type, and the operating surgeon. Among these factors, melanoma cases required more than twice the volume of lidocaine compared to BCC and SCC cases, and flap and graft repairs demonstrated the highest anesthetic requirements among closure types. Taken together, these findings reinforce the need for advanced anesthetic planning in aggressive, anatomically complex, or reconstruction-intensive cases and may support more informed intraoperative decision-making.

To the Editor:

Mohs micrographic surgery (MMS) is performed in stages and often requires repeated administration of a local anesthetic, most commonly lidocaine. While generally safe, lidocaine administration carries the potential for cumulative toxicity, particularly in patients who have large or multiple lesions or medical comorbidities or who require extensive repair. Current safety guidelines suggest upper limits of 7 mg/kg (or 500 mg) of lidocaine with epinephrine and 4.5 mg/kg (or 300 mg) without epinephrine for adults.¹ However, concerns have been raised about the relevance of these thresholds to MMS, in which anesthetic administration may be prolonged, cumulative, and influenced by surgical complexity.^2-5 While clinical experience often guides anesthetic planning, limited data exist identifying predictors of lidocaine use during MMS.

We performed an institutional review board–approved retrospective chart review of 149 patients who underwent 170 MMS procedures at a single academic dermatologic surgery center between July 2022 and June 2023. The aim of our study was to identify clinical and surgical predictors of lidocaine volume used during MMS. All procedures were performed by board-certified dermatologic surgeons (including A.J.). All patients received 1% lidocaine with epinephrine as the primary anesthetic agent. We collected patient demographic variables (age, sex, race, weight), procedural characteristics (anatomic site, number of Mohs stages, skin cancer type, number of surgical sites treated in one day, preoperative and postoperative lesion size, surgeon, repair type), comorbid conditions (hypertension, diabetes), and time from diagnosis to surgery. Data were extracted from the institutional REDCap system. We used t tests and analysis of variance for categorical variables and linear regression for continuous predictors, with statistical significance set at P<.05.

Baseline characteristics of the study patients are outlined in Table 1. The mean (SD) age was 74.2 (9.4) years, and most patients (98.7% [147/149]) were White. The mean (SD) weight was 83.1 (19.1) kg. Most lesions were either basal cell carcinoma (BCC)(50.6%) or squamous cell carcinoma (SCC)(44.1%), with 5.3% of lesions representing melanoma. The mean (SD) total lidocaine volume administered was 11.8 (8.3) mL. The majority (123/149 [72.4%]) of cases required one Mohs stage, but a subset required multiple stages, with a maximum of 5.

Several procedural and patient factors were significantly associated with the volume of lidocaine used. As expected, lesion size strongly influenced lidocaine volume. Both preoperative and postoperative lesion sizes were highly significant linear predictors (R²=0.28 and 0.41, respectively; P<.001), and postoperative lesion size demonstrated the strongest correlation of all tested variables. Patient weight was also significantly associated with lidocaine use (R²=.03, P=.0202), though the proportion of explained variance was modest. The operating surgeon also was significantly associated with lidocaine use (P=.006), suggesting potential variation in anesthetic technique or threshold for reinfiltration. The number of surgical sites treated in a single session also was significantly associated with greater lidocaine volume (P<.001).

Skin cancer type was a notable categorical predictor. Melanomas required substantially more lidocaine than BCCs or SCCs, with a mean (SD) volume of 25.6 (12.1) mL compared with 10.8 (6.0) mL for BCC and 11.4 (8.8) mL for SCC (P<.001). This difference may reflect disparities in surgical margin requirements, tumor depth, or intraoperative technique. While lesion location and number of stages were not statistically significant overall, mean lidocaine volumes trended higher in lesions on the trunk (18.2 mL) and in procedures requiring 3 or more stages (up to 22.0 mL for a single 4-stage case), though small sample sizes limited the ability to detect statistically significant differences in these subgroups. Detailed comparisons are presented in Table 2.

Wound repair type also was significantly associated with lidocaine volume requirements. Primary closures required a mean (SD) volume of 12.3 (5.0) mL, whereas flap repairs required 19.3 (10.0) mL and graft repairs required 17.5 (8.2) mL. Secondary-intention healing used the lowest lidocaine volumes (mean [SD], 4.9 [2.0] mL). Differences across repair types were statistically significant (analysis of variance, P<.001). These findings indicate that more complex reconstructions, such as flaps and grafts, are associated with higher anesthetic needs when compared with primary closures or secondary-intention healing.

Several other predictors, including age, time from diagnosis to surgery, and comorbid conditions such as hypertension or diabetes, were not significantly associated with anesthetic volume in our cohort. Time from diagnosis to surgery ranged widely but did not correlate with lesion size or lidocaine use, possibly due to scheduling variability or biopsy technique.

These findings offer practical implications for clinical planning. While most MMS cases fall well within safe limits for lidocaine administration, some patients—­particularly those with melanoma, large lesions, or multiple surgical sites—may approach thresholds at which further monitoring or dose tracking becomes relevant. Anticipating higher anesthetic requirements may help surgical teams plan procedure length, anesthesia restocking, or sequencing of multisite cases. Our analysis also showed that the type of wound repair meaningfully influences anesthetic use, with flap and graft repairs requiring substantially higher lidocaine volumes than primary closures and secondary-intention healing. Considering both tumor characteristics and the planned reconstruction may therefore improve the accuracy of anesthetic forecasting during preoperative planning.

We also observed surgeon-level variation in lidocaine volume despite standardized tumor types and case complexity. This suggests a role for individual technique (eg, depth of field block, number of reinfiltrations) and highlights the need for ongoing education around anesthetic optimization.

Our study was limited by its retrospective design, single-institution setting, and demographically homogeneous population. With 98.8% of patients identifying as White, generalizability to skin of color populations may be limited. In addition, lidocaine metabolism may vary across patient factors not captured here (eg, hepatic or renal function). Finally, although lidocaine volume was the outcome of interest, we did not measure patient-reported pain control, which may further clarify anesthetic adequacy. Nonetheless, our analysis demonstrated that routinely available clinical and procedural data can predict lidocaine volume requirements with reasonable reliability. Although no patient in our cohort approached the maximum recommended lidocaine dose, understanding these predictors may help anticipate scenarios nearing maximum dosing thresholds. In future studies, integrating weight-based thresholds (eg, mL/kg received) or serum lidocaine levels may improve safety monitoring and validate toxicity thresholds in complex cases.

In conclusion, we identified several key factors that predict lidocaine volume during MMS, including lesion size, melanoma diagnosis, number of surgical sites, patient weight, planned reconstruction type, and the operating surgeon. Among these factors, melanoma cases required more than twice the volume of lidocaine compared to BCC and SCC cases, and flap and graft repairs demonstrated the highest anesthetic requirements among closure types. Taken together, these findings reinforce the need for advanced anesthetic planning in aggressive, anatomically complex, or reconstruction-intensive cases and may support more informed intraoperative decision-making.

To the Editor:

Mohs micrographic surgery (MMS) is performed in stages and often requires repeated administration of a local anesthetic, most commonly lidocaine. While generally safe, lidocaine administration carries the potential for cumulative toxicity, particularly in patients who have large or multiple lesions or medical comorbidities or who require extensive repair. Current safety guidelines suggest upper limits of 7 mg/kg (or 500 mg) of lidocaine with epinephrine and 4.5 mg/kg (or 300 mg) without epinephrine for adults.¹ However, concerns have been raised about the relevance of these thresholds to MMS, in which anesthetic administration may be prolonged, cumulative, and influenced by surgical complexity.^2-5 While clinical experience often guides anesthetic planning, limited data exist identifying predictors of lidocaine use during MMS.

We performed an institutional review board–approved retrospective chart review of 149 patients who underwent 170 MMS procedures at a single academic dermatologic surgery center between July 2022 and June 2023. The aim of our study was to identify clinical and surgical predictors of lidocaine volume used during MMS. All procedures were performed by board-certified dermatologic surgeons (including A.J.). All patients received 1% lidocaine with epinephrine as the primary anesthetic agent. We collected patient demographic variables (age, sex, race, weight), procedural characteristics (anatomic site, number of Mohs stages, skin cancer type, number of surgical sites treated in one day, preoperative and postoperative lesion size, surgeon, repair type), comorbid conditions (hypertension, diabetes), and time from diagnosis to surgery. Data were extracted from the institutional REDCap system. We used t tests and analysis of variance for categorical variables and linear regression for continuous predictors, with statistical significance set at P<.05.

Baseline characteristics of the study patients are outlined in Table 1. The mean (SD) age was 74.2 (9.4) years, and most patients (98.7% [147/149]) were White. The mean (SD) weight was 83.1 (19.1) kg. Most lesions were either basal cell carcinoma (BCC)(50.6%) or squamous cell carcinoma (SCC)(44.1%), with 5.3% of lesions representing melanoma. The mean (SD) total lidocaine volume administered was 11.8 (8.3) mL. The majority (123/149 [72.4%]) of cases required one Mohs stage, but a subset required multiple stages, with a maximum of 5.

Several procedural and patient factors were significantly associated with the volume of lidocaine used. As expected, lesion size strongly influenced lidocaine volume. Both preoperative and postoperative lesion sizes were highly significant linear predictors (R²=0.28 and 0.41, respectively; P<.001), and postoperative lesion size demonstrated the strongest correlation of all tested variables. Patient weight was also significantly associated with lidocaine use (R²=.03, P=.0202), though the proportion of explained variance was modest. The operating surgeon also was significantly associated with lidocaine use (P=.006), suggesting potential variation in anesthetic technique or threshold for reinfiltration. The number of surgical sites treated in a single session also was significantly associated with greater lidocaine volume (P<.001).

Skin cancer type was a notable categorical predictor. Melanomas required substantially more lidocaine than BCCs or SCCs, with a mean (SD) volume of 25.6 (12.1) mL compared with 10.8 (6.0) mL for BCC and 11.4 (8.8) mL for SCC (P<.001). This difference may reflect disparities in surgical margin requirements, tumor depth, or intraoperative technique. While lesion location and number of stages were not statistically significant overall, mean lidocaine volumes trended higher in lesions on the trunk (18.2 mL) and in procedures requiring 3 or more stages (up to 22.0 mL for a single 4-stage case), though small sample sizes limited the ability to detect statistically significant differences in these subgroups. Detailed comparisons are presented in Table 2.

Wound repair type also was significantly associated with lidocaine volume requirements. Primary closures required a mean (SD) volume of 12.3 (5.0) mL, whereas flap repairs required 19.3 (10.0) mL and graft repairs required 17.5 (8.2) mL. Secondary-intention healing used the lowest lidocaine volumes (mean [SD], 4.9 [2.0] mL). Differences across repair types were statistically significant (analysis of variance, P<.001). These findings indicate that more complex reconstructions, such as flaps and grafts, are associated with higher anesthetic needs when compared with primary closures or secondary-intention healing.

Several other predictors, including age, time from diagnosis to surgery, and comorbid conditions such as hypertension or diabetes, were not significantly associated with anesthetic volume in our cohort. Time from diagnosis to surgery ranged widely but did not correlate with lesion size or lidocaine use, possibly due to scheduling variability or biopsy technique.

These findings offer practical implications for clinical planning. While most MMS cases fall well within safe limits for lidocaine administration, some patients—­particularly those with melanoma, large lesions, or multiple surgical sites—may approach thresholds at which further monitoring or dose tracking becomes relevant. Anticipating higher anesthetic requirements may help surgical teams plan procedure length, anesthesia restocking, or sequencing of multisite cases. Our analysis also showed that the type of wound repair meaningfully influences anesthetic use, with flap and graft repairs requiring substantially higher lidocaine volumes than primary closures and secondary-intention healing. Considering both tumor characteristics and the planned reconstruction may therefore improve the accuracy of anesthetic forecasting during preoperative planning.

We also observed surgeon-level variation in lidocaine volume despite standardized tumor types and case complexity. This suggests a role for individual technique (eg, depth of field block, number of reinfiltrations) and highlights the need for ongoing education around anesthetic optimization.

Our study was limited by its retrospective design, single-institution setting, and demographically homogeneous population. With 98.8% of patients identifying as White, generalizability to skin of color populations may be limited. In addition, lidocaine metabolism may vary across patient factors not captured here (eg, hepatic or renal function). Finally, although lidocaine volume was the outcome of interest, we did not measure patient-reported pain control, which may further clarify anesthetic adequacy. Nonetheless, our analysis demonstrated that routinely available clinical and procedural data can predict lidocaine volume requirements with reasonable reliability. Although no patient in our cohort approached the maximum recommended lidocaine dose, understanding these predictors may help anticipate scenarios nearing maximum dosing thresholds. In future studies, integrating weight-based thresholds (eg, mL/kg received) or serum lidocaine levels may improve safety monitoring and validate toxicity thresholds in complex cases.

In conclusion, we identified several key factors that predict lidocaine volume during MMS, including lesion size, melanoma diagnosis, number of surgical sites, patient weight, planned reconstruction type, and the operating surgeon. Among these factors, melanoma cases required more than twice the volume of lidocaine compared to BCC and SCC cases, and flap and graft repairs demonstrated the highest anesthetic requirements among closure types. Taken together, these findings reinforce the need for advanced anesthetic planning in aggressive, anatomically complex, or reconstruction-intensive cases and may support more informed intraoperative decision-making.

The US Department of Veterans Affairs (VA) recently announced plans to offer $7 million in new transportation services grants that could benefit 4.7 million veterans who live in rural areas. The grants would expand free transportation to medical appointments, something VA Secretary Doug Collins said is designed to “help break down the geographic barriers to health care some rural veterans face.”

Funding could be distributed later in 2026 to veteran service organizations, state agencies, and groups that transport veterans for health care. Eligible veterans would not need to do anything—the transportation is free for those living in qualifying areas.

Travel time and distance from health care facilities are significant barriers to receiving appropriate and timely care. The 2014 Veterans Access, Choice and Accountability Act (Choice) was intended to improve timely access to outpatient health care for veterans by allowing them to receive care from community facilities paid for by the VA. Under Choice, eligible veterans become eligible to receive community care if they have to drive > 40 miles to the nearest VA facility or wait > 30 days for care. 

Even with this provision, many of the 2.7 million rural veterans enrolled in Veterans Health Administration (VHA) remained far from care. For instance, the VA Office of Rural Health says the closest facility for veterans in Hollis, Alaska, is > 1000 miles away. 

Moreover, 56% of rural veterans enrolled in VHA care are aged > 65 years, and more likely to be diagnosed with diabetes, high blood pressure, and heart conditions than veterans living in more urban areas. Although studies comparing health outcomes between rural and urban veterans are sparse, research has long shown that lacking access to routine health care may worsen long-term outcomes.  

The VA has also announced other initiatives aimed at improving health care for veterans, among them the opening of 34 new facilities. Other projects:

• The Electronic Health Record (EHR) modernization project resumed April 11 with new deployments in Michigan. The VA says the new EHR system will result in more consistent medical records, fewer repeated tests, and better coordination between VA facilities and military health services.

• In March, the VA announced a $112 million grant opportunity to strengthen community‑based suicide prevention programs, focusing on outreach outside traditional VA settings.

• In February, the VA said it raised its spending cap for in‑home and community‑based services for veterans with complex medical needs, adding coverage for veterans with spinal cord injuries, Amyotrophic Lateral Sclerosis, and others.

• In January, the VA announced plans to invest $4.8 billion in fiscal year 2026 to modernize, repair, and improve health care facilities nationwide via infrastructure upgrades, major building repairs, and improvements to EHR systems.

The US Department of Veterans Affairs (VA) recently announced plans to offer $7 million in new transportation services grants that could benefit 4.7 million veterans who live in rural areas. The grants would expand free transportation to medical appointments, something VA Secretary Doug Collins said is designed to “help break down the geographic barriers to health care some rural veterans face.”

Funding could be distributed later in 2026 to veteran service organizations, state agencies, and groups that transport veterans for health care. Eligible veterans would not need to do anything—the transportation is free for those living in qualifying areas.

Travel time and distance from health care facilities are significant barriers to receiving appropriate and timely care. The 2014 Veterans Access, Choice and Accountability Act (Choice) was intended to improve timely access to outpatient health care for veterans by allowing them to receive care from community facilities paid for by the VA. Under Choice, eligible veterans become eligible to receive community care if they have to drive > 40 miles to the nearest VA facility or wait > 30 days for care. 

Even with this provision, many of the 2.7 million rural veterans enrolled in Veterans Health Administration (VHA) remained far from care. For instance, the VA Office of Rural Health says the closest facility for veterans in Hollis, Alaska, is > 1000 miles away. 

Moreover, 56% of rural veterans enrolled in VHA care are aged > 65 years, and more likely to be diagnosed with diabetes, high blood pressure, and heart conditions than veterans living in more urban areas. Although studies comparing health outcomes between rural and urban veterans are sparse, research has long shown that lacking access to routine health care may worsen long-term outcomes.  

The VA has also announced other initiatives aimed at improving health care for veterans, among them the opening of 34 new facilities. Other projects:

• The Electronic Health Record (EHR) modernization project resumed April 11 with new deployments in Michigan. The VA says the new EHR system will result in more consistent medical records, fewer repeated tests, and better coordination between VA facilities and military health services.

• In March, the VA announced a $112 million grant opportunity to strengthen community‑based suicide prevention programs, focusing on outreach outside traditional VA settings.

• In February, the VA said it raised its spending cap for in‑home and community‑based services for veterans with complex medical needs, adding coverage for veterans with spinal cord injuries, Amyotrophic Lateral Sclerosis, and others.

• In January, the VA announced plans to invest $4.8 billion in fiscal year 2026 to modernize, repair, and improve health care facilities nationwide via infrastructure upgrades, major building repairs, and improvements to EHR systems.

The US Department of Veterans Affairs (VA) recently announced plans to offer $7 million in new transportation services grants that could benefit 4.7 million veterans who live in rural areas. The grants would expand free transportation to medical appointments, something VA Secretary Doug Collins said is designed to “help break down the geographic barriers to health care some rural veterans face.”

Funding could be distributed later in 2026 to veteran service organizations, state agencies, and groups that transport veterans for health care. Eligible veterans would not need to do anything—the transportation is free for those living in qualifying areas.

Travel time and distance from health care facilities are significant barriers to receiving appropriate and timely care. The 2014 Veterans Access, Choice and Accountability Act (Choice) was intended to improve timely access to outpatient health care for veterans by allowing them to receive care from community facilities paid for by the VA. Under Choice, eligible veterans become eligible to receive community care if they have to drive > 40 miles to the nearest VA facility or wait > 30 days for care. 

Even with this provision, many of the 2.7 million rural veterans enrolled in Veterans Health Administration (VHA) remained far from care. For instance, the VA Office of Rural Health says the closest facility for veterans in Hollis, Alaska, is > 1000 miles away. 

Moreover, 56% of rural veterans enrolled in VHA care are aged > 65 years, and more likely to be diagnosed with diabetes, high blood pressure, and heart conditions than veterans living in more urban areas. Although studies comparing health outcomes between rural and urban veterans are sparse, research has long shown that lacking access to routine health care may worsen long-term outcomes.  

The VA has also announced other initiatives aimed at improving health care for veterans, among them the opening of 34 new facilities. Other projects:

• The Electronic Health Record (EHR) modernization project resumed April 11 with new deployments in Michigan. The VA says the new EHR system will result in more consistent medical records, fewer repeated tests, and better coordination between VA facilities and military health services.

• In March, the VA announced a $112 million grant opportunity to strengthen community‑based suicide prevention programs, focusing on outreach outside traditional VA settings.

• In February, the VA said it raised its spending cap for in‑home and community‑based services for veterans with complex medical needs, adding coverage for veterans with spinal cord injuries, Amyotrophic Lateral Sclerosis, and others.

• In January, the VA announced plans to invest $4.8 billion in fiscal year 2026 to modernize, repair, and improve health care facilities nationwide via infrastructure upgrades, major building repairs, and improvements to EHR systems.

Male veterans are less likely than their female counterparts to be referred for follow-up questions when initial screening suggests they may be at risk of intimate partner violence (IPV), a recent large cross-sectional study finds. 

Among 67,379 patients from 131 US Department of Veterans Affairs (VA) medical centers who screened positive for risk of IPV from October 2022 through September 2023, 17.7% failed to receive a mandated secondary screen to determine whether they were in danger of lethal violence, reported Galina A. Portnoy, PhD, of VA Connecticut Healthcare System and Yale School of Medicine, et al in JAMA Network Open. The rate was higher for men with initial positive screens than women (19.3% vs 12.1%, respectively, adjusted odds ratio [AOR], 1.42, P < .001).

Overall, women who underwent secondary screening were more likely to be considered in lethal danger from IPV than men (27.9% vs 13.3%, respectively, AOR 2.29, P < .001).

“While women face higher lethality risk, men’s IPV experiences are often overlooked, underscoring the need for consistent and reliable screening practices to identify all high-risk patients and connect them to life-saving services,” Portnoy told Federal Practitioner.

“IPV is one of the strongest predictors of homicide with risk escalating over time and especially high during periods of separation.” 

“IPV among men is often underreported, unrecognized, and inadequately addressed in clinical settings,” Portnoy noted. “Men who experience IPV often face barriers to reporting—stigma, shame, and concerns about not being taken seriously.”

The VA has implemented annual screening of IPV in women of reproductive age using a modified version of the 5-question Hurt, Insult, Threaten, Scream (HITS) tool. HITS asks how often a woman’s partner had screamed, cursed, insulted, or talked down to them; threatened to harm or physically hurt them, or forced or pressured them to “have sexual contact against your will, or when you were unable to say no” in the last year.

If a patient answers yes to any of these questions, clinicians should follow up with a secondary lethality screen with 3 questions:

• Has the IPV behavior increased in frequency/severity in the past 6 months?

• Has your partner ever choked or strangled you? and

• Do you believe your partner may kill you?

The test is considered positive if a patient answers yes to any question. 

The study focused on 67,379 patients out of 1,265,115 at the VA who scored positive on HITS (mean age, 52.3 years; 23% women; 62.9% White; 8.2% Hispanic/Latino). More than two-thirds (69.0%) had a service-connected disability rating > 50%.

Portnoy said there are several possible reasons for the gender disparity in misclassification such as time constraints, discomfort, limited resources, and lack of training. Clinician bias can be a factor, too, “with IPV still widely seen as primarily a women’s issue.”

“We don’t know whether IPV screening tools work the same for men as they do for women,” Portnoy added. “The HITS tool was developed and validated using samples of women who experienced IPV, and research is needed to test whether it performs as effectively in men.”

Bethany L. Backes, PhD, associate professor and lead, Violence Against Women Faculty Cluster, University of Central Florida, Orlando, is familiar with the study findings and said in an interview that discomfort among clinicians is a significant factor in preventing follow-up IPV screening. 

“When you’re asking about this and someone says ‘yes,’ how do you respond? You just go to the next thing, the next question: ‘How many drinks have you had in the last week?’” Backes told Federal Practitioner. “We’ve talked about creating some scripts for our student health clinicians on campus about how to talk to someone when they disclose, how to then engage or provide resources.”

This is especially important because “it’s hard for people to admit that they’re experiencing this, and then when they do and it’s brushed over, they’re less likely to tell someone again,” Backes added.

C. Nadine Wathen, PhD, a professor who studies IPV at Western University in London, is also familiar with the study findings, but critiqued the HITS, calling it a “terrible name.” The tool, she said, asks about very different behaviors–being screamed or cursed, for example, and forced sexual contact,” she explained to Federal Practitioner.

“If you’re a physician and you’re asking a man, ‘Does she scream or curse at you?’ and he says ‘Yeah, she screams all the time,’ a provider might say, ‘I’m not actually thinking that he’s experiencing intimate partner violence,” Wathen said. “He might be experiencing a bad relationship.’”

That could be true, Wathen said. Couples may scream and throw things at each other, and “you probably could benefit with some couples counseling on how to have a better relationship and manage stress and anger in your relationship. But that is different than ‘intimate partner terrorism,’ where there‘s a pattern of control.”

Wathen prefers a screening tool she helped develop called the Composite Abuse Scale, which she considers more sensitive and specific than HITS. It differentiates the types of abuse that people experience, and “it also recognizes that men in relationships with other men can experience those forms of intimate terrorism, and women can also be the perpetrator of those forms.”

Recognizing that VA clinicians may not have a choice of screening tool, Wathen suggested they follow up the question about screaming and cursing question this query: “Does that make you afraid?”

The study was funded by US Department of Veterans Affairs Quality Enhancement Research Initiative and the Veterans Health Administration’s Care Management and Social Work Service via the Intimate Partner Violence Center for Implementation, Research, and Evaluation.

Portnoy has no disclosures. One author discloses relationships with the National Council on Family Relations and Military Family Research Institute. Backes and Wathen have no disclosures.

Male veterans are less likely than their female counterparts to be referred for follow-up questions when initial screening suggests they may be at risk of intimate partner violence (IPV), a recent large cross-sectional study finds. 

Among 67,379 patients from 131 US Department of Veterans Affairs (VA) medical centers who screened positive for risk of IPV from October 2022 through September 2023, 17.7% failed to receive a mandated secondary screen to determine whether they were in danger of lethal violence, reported Galina A. Portnoy, PhD, of VA Connecticut Healthcare System and Yale School of Medicine, et al in JAMA Network Open. The rate was higher for men with initial positive screens than women (19.3% vs 12.1%, respectively, adjusted odds ratio [AOR], 1.42, P < .001).

Overall, women who underwent secondary screening were more likely to be considered in lethal danger from IPV than men (27.9% vs 13.3%, respectively, AOR 2.29, P < .001).

“While women face higher lethality risk, men’s IPV experiences are often overlooked, underscoring the need for consistent and reliable screening practices to identify all high-risk patients and connect them to life-saving services,” Portnoy told Federal Practitioner.

“IPV is one of the strongest predictors of homicide with risk escalating over time and especially high during periods of separation.” 

“IPV among men is often underreported, unrecognized, and inadequately addressed in clinical settings,” Portnoy noted. “Men who experience IPV often face barriers to reporting—stigma, shame, and concerns about not being taken seriously.”

The VA has implemented annual screening of IPV in women of reproductive age using a modified version of the 5-question Hurt, Insult, Threaten, Scream (HITS) tool. HITS asks how often a woman’s partner had screamed, cursed, insulted, or talked down to them; threatened to harm or physically hurt them, or forced or pressured them to “have sexual contact against your will, or when you were unable to say no” in the last year.

If a patient answers yes to any of these questions, clinicians should follow up with a secondary lethality screen with 3 questions:

• Has the IPV behavior increased in frequency/severity in the past 6 months?

• Has your partner ever choked or strangled you? and

• Do you believe your partner may kill you?

The test is considered positive if a patient answers yes to any question. 

The study focused on 67,379 patients out of 1,265,115 at the VA who scored positive on HITS (mean age, 52.3 years; 23% women; 62.9% White; 8.2% Hispanic/Latino). More than two-thirds (69.0%) had a service-connected disability rating > 50%.

Portnoy said there are several possible reasons for the gender disparity in misclassification such as time constraints, discomfort, limited resources, and lack of training. Clinician bias can be a factor, too, “with IPV still widely seen as primarily a women’s issue.”

“We don’t know whether IPV screening tools work the same for men as they do for women,” Portnoy added. “The HITS tool was developed and validated using samples of women who experienced IPV, and research is needed to test whether it performs as effectively in men.”

Bethany L. Backes, PhD, associate professor and lead, Violence Against Women Faculty Cluster, University of Central Florida, Orlando, is familiar with the study findings and said in an interview that discomfort among clinicians is a significant factor in preventing follow-up IPV screening. 

“When you’re asking about this and someone says ‘yes,’ how do you respond? You just go to the next thing, the next question: ‘How many drinks have you had in the last week?’” Backes told Federal Practitioner. “We’ve talked about creating some scripts for our student health clinicians on campus about how to talk to someone when they disclose, how to then engage or provide resources.”

This is especially important because “it’s hard for people to admit that they’re experiencing this, and then when they do and it’s brushed over, they’re less likely to tell someone again,” Backes added.

C. Nadine Wathen, PhD, a professor who studies IPV at Western University in London, is also familiar with the study findings, but critiqued the HITS, calling it a “terrible name.” The tool, she said, asks about very different behaviors–being screamed or cursed, for example, and forced sexual contact,” she explained to Federal Practitioner.

“If you’re a physician and you’re asking a man, ‘Does she scream or curse at you?’ and he says ‘Yeah, she screams all the time,’ a provider might say, ‘I’m not actually thinking that he’s experiencing intimate partner violence,” Wathen said. “He might be experiencing a bad relationship.’”

That could be true, Wathen said. Couples may scream and throw things at each other, and “you probably could benefit with some couples counseling on how to have a better relationship and manage stress and anger in your relationship. But that is different than ‘intimate partner terrorism,’ where there‘s a pattern of control.”

Wathen prefers a screening tool she helped develop called the Composite Abuse Scale, which she considers more sensitive and specific than HITS. It differentiates the types of abuse that people experience, and “it also recognizes that men in relationships with other men can experience those forms of intimate terrorism, and women can also be the perpetrator of those forms.”

Recognizing that VA clinicians may not have a choice of screening tool, Wathen suggested they follow up the question about screaming and cursing question this query: “Does that make you afraid?”

The study was funded by US Department of Veterans Affairs Quality Enhancement Research Initiative and the Veterans Health Administration’s Care Management and Social Work Service via the Intimate Partner Violence Center for Implementation, Research, and Evaluation.

Portnoy has no disclosures. One author discloses relationships with the National Council on Family Relations and Military Family Research Institute. Backes and Wathen have no disclosures.

Male veterans are less likely than their female counterparts to be referred for follow-up questions when initial screening suggests they may be at risk of intimate partner violence (IPV), a recent large cross-sectional study finds. 

Among 67,379 patients from 131 US Department of Veterans Affairs (VA) medical centers who screened positive for risk of IPV from October 2022 through September 2023, 17.7% failed to receive a mandated secondary screen to determine whether they were in danger of lethal violence, reported Galina A. Portnoy, PhD, of VA Connecticut Healthcare System and Yale School of Medicine, et al in JAMA Network Open. The rate was higher for men with initial positive screens than women (19.3% vs 12.1%, respectively, adjusted odds ratio [AOR], 1.42, P < .001).

Overall, women who underwent secondary screening were more likely to be considered in lethal danger from IPV than men (27.9% vs 13.3%, respectively, AOR 2.29, P < .001).

“While women face higher lethality risk, men’s IPV experiences are often overlooked, underscoring the need for consistent and reliable screening practices to identify all high-risk patients and connect them to life-saving services,” Portnoy told Federal Practitioner.

“IPV is one of the strongest predictors of homicide with risk escalating over time and especially high during periods of separation.” 

“IPV among men is often underreported, unrecognized, and inadequately addressed in clinical settings,” Portnoy noted. “Men who experience IPV often face barriers to reporting—stigma, shame, and concerns about not being taken seriously.”

The VA has implemented annual screening of IPV in women of reproductive age using a modified version of the 5-question Hurt, Insult, Threaten, Scream (HITS) tool. HITS asks how often a woman’s partner had screamed, cursed, insulted, or talked down to them; threatened to harm or physically hurt them, or forced or pressured them to “have sexual contact against your will, or when you were unable to say no” in the last year.

If a patient answers yes to any of these questions, clinicians should follow up with a secondary lethality screen with 3 questions:

• Has the IPV behavior increased in frequency/severity in the past 6 months?

• Has your partner ever choked or strangled you? and

• Do you believe your partner may kill you?

The test is considered positive if a patient answers yes to any question. 

The study focused on 67,379 patients out of 1,265,115 at the VA who scored positive on HITS (mean age, 52.3 years; 23% women; 62.9% White; 8.2% Hispanic/Latino). More than two-thirds (69.0%) had a service-connected disability rating > 50%.

Portnoy said there are several possible reasons for the gender disparity in misclassification such as time constraints, discomfort, limited resources, and lack of training. Clinician bias can be a factor, too, “with IPV still widely seen as primarily a women’s issue.”

“We don’t know whether IPV screening tools work the same for men as they do for women,” Portnoy added. “The HITS tool was developed and validated using samples of women who experienced IPV, and research is needed to test whether it performs as effectively in men.”

Bethany L. Backes, PhD, associate professor and lead, Violence Against Women Faculty Cluster, University of Central Florida, Orlando, is familiar with the study findings and said in an interview that discomfort among clinicians is a significant factor in preventing follow-up IPV screening. 

“When you’re asking about this and someone says ‘yes,’ how do you respond? You just go to the next thing, the next question: ‘How many drinks have you had in the last week?’” Backes told Federal Practitioner. “We’ve talked about creating some scripts for our student health clinicians on campus about how to talk to someone when they disclose, how to then engage or provide resources.”

This is especially important because “it’s hard for people to admit that they’re experiencing this, and then when they do and it’s brushed over, they’re less likely to tell someone again,” Backes added.

C. Nadine Wathen, PhD, a professor who studies IPV at Western University in London, is also familiar with the study findings, but critiqued the HITS, calling it a “terrible name.” The tool, she said, asks about very different behaviors–being screamed or cursed, for example, and forced sexual contact,” she explained to Federal Practitioner.

“If you’re a physician and you’re asking a man, ‘Does she scream or curse at you?’ and he says ‘Yeah, she screams all the time,’ a provider might say, ‘I’m not actually thinking that he’s experiencing intimate partner violence,” Wathen said. “He might be experiencing a bad relationship.’”

That could be true, Wathen said. Couples may scream and throw things at each other, and “you probably could benefit with some couples counseling on how to have a better relationship and manage stress and anger in your relationship. But that is different than ‘intimate partner terrorism,’ where there‘s a pattern of control.”

Wathen prefers a screening tool she helped develop called the Composite Abuse Scale, which she considers more sensitive and specific than HITS. It differentiates the types of abuse that people experience, and “it also recognizes that men in relationships with other men can experience those forms of intimate terrorism, and women can also be the perpetrator of those forms.”

Recognizing that VA clinicians may not have a choice of screening tool, Wathen suggested they follow up the question about screaming and cursing question this query: “Does that make you afraid?”

The study was funded by US Department of Veterans Affairs Quality Enhancement Research Initiative and the Veterans Health Administration’s Care Management and Social Work Service via the Intimate Partner Violence Center for Implementation, Research, and Evaluation.

Portnoy has no disclosures. One author discloses relationships with the National Council on Family Relations and Military Family Research Institute. Backes and Wathen have no disclosures.

Lichen planus (LP) is a chronic inflammatory condition affecting the skin (cutaneous LP), mucous membranes (oral, ocular, or vulvar LP), hair (lichen planopilaris [LPP]), and nails that predominantly occurs in middle-aged adults. Although the true etiology remains unknown, the pathogenesis of LP is thought to involve multiple factors. Several human leukocyte antigen (HLA) alleles have been associated with LP and its variants, including HLA-B27, HLA-B51, HLA-DR1 (cutaneous and oral LP), HLA-DRB1*11, and HLA-DQB1*03 (LPP). Additionally, HLA-Bw57 has been reported to be associated with oral LP in a cohort of British patients.¹ In addition to HLA alleles, genetic polymorphisms in cytokines including IL-4, IL-6, IL-18, interferon (IFN) γ, and tumor necrosis factor (TNF) α and its receptor have been found to be associated with LP.² Beyond genetics, chronic viral infection has been implicated in the development of LP. Systemic infection with the hepatitis C virus has been linked to the development of oral LP by promoting the recruitment of hepatitis C virus–specific CD8+ T cells from peripheral blood to the oral lesions, where they exhibit a terminally differentiated effector status.³ Another report found an association between human herpesvirus 7 (HHV-7) and cutaneous LP; in this study, HHV-7 RNA was detected in plasmacytoid dendritic cells but not T cells and diminished after treatment, providing evidence for dendritic cells being involved in the HHV-7–mediated pathogenesis of cutaneous LP.⁴ These findings were further corroborated by another study of oral LP patients that found enhanced infiltration of plasmacytoid and myeloid dendritic cells and upregulation in toll-like receptor and IFN-γ signaling.⁴

In addition to immune cell dysregulation, LP and its variants have been linked to neurogenic inflammation. In oral LP lesions, neurokinin 1 receptor and substance P were highly expressed and demonstrated a positive correlation with the expression of apoptotic marker caspase-3 and proliferation marker Ki-67.⁵ These results suggest that neuropeptides may be involved in cell proliferation and turnover in oral LP. Similarly, in patients with LPP, substance P was more abundant in affected areas, whereas another neuropeptide, calcitonin gene-related peptide, was more highly expressed in unaffected areas,⁶ further supporting the pathogenic role of neurogenic inflammation in LP.

A mucosal variant that often goes undiagnosed is vulvar LP. Although no distinct pathologic mechanism for vulvar LP has been established, prior reports found an association with autoantibodies.^7,8 In patients with erosive vulvar LP, epidermal-binding basement membrane zone antibodies were detected in epidermal skin biopsies and in circulation with reactivity to bullous pemphigoid antigens 180 (9/11 [81.8%] patients) and 230 (2/11 [18.2%] patients).⁷ A similar study in patients with vulvar lichen sclerosus found similar proportions of circulating antibodies reactive to bullous pemphigoid antigens 180 (6/7 [85.7%] patients) and 230 (1/7 [14.3%] patients).⁸ Erosive vulvar LP has been shown to be associated with autoimmune disease (eg, alopecia areata, celiac disease and pernicious anemia),⁹ which suggests that the previously reported autoreactive antibodies^7,8 are secondary to autoimmunity rather than primary drivers of vulvar LP pathogenesis.

Certain medications also have been reported to cause cutaneous lichenoid drug eruptions. Although they can clinically and histologically mimic classic LP, lichenoid drug eruptions are a distinct entity. Common inciting medications include thiazide diuretics, angiotensin-converting enzyme inhibitors, anti-inflammatory drugs, antimalarials, checkpoint inhibitors, antimicrobials, antihypertensives, antidiabetics, and psychiatric drugs. The exact pathologic mechanism of lichenoid drug eruptions currently is unclear but is thought to involve the binding of drug molecules to the cell-surface proteins of the epidermis, creating an antigenic hapten stimulus for CD8+T cells and triggering apoptosis of keratinocytes.¹

The clinical severity of LP can range from mild localized disease to widespread and debilitating involvement. Multiple treatment modalities have been developed for management of LP, including topical and intralesional corticosteroids, phototherapy, Janus kinase inhibitors, phosphodiesterase-4 inhibitors, and anti–TNF-α inhibitors. Herein, we provide a narrative review and summary of the use of the TNF-α inhibitor adalimumab as a potential effective treatment for patients with LP.

Methods

We conducted a PubMed search of articles indexed for MEDLINE from 2005 to 2025 using the terms adalimumab AND lichen planus or adalimumab AND lichen. Articles that reported cases of oral LP, cutaneous LP, LPP, or lichenoid eruptions and adalimumab therapy were included in our review. Articles that used non-adalimumab TNF-α inhibitors were excluded. Using the search terms, 2 independent reviewers (M.G. and N.E.) conducted the literature review then screened the articles based on the inclusion and exclusion criteria. Our literature search yielded 40 articles, of which 20 met the criteria for inclusion in our narrative review.

Results

Our literature search yielded 11 patients with LP who were treated with adalimumab across studies (Table 1).^10-16 Prior LP treatments included topical corticosteroids (11/11 [100%]), disease-modifying antirheumatic drugs (6/11 [54.5%]), retinoids (4/11 [36.4%]), and psoralen plus UVA (1/11 [36.4%]). Adalimumab was administered subcutaneously following 4 treatment regimens: (1) 160 mg in week 1, then 80 mg in week 2, then 40 mg weekly for a median duration of 36 weeks (6/11 [54.5%]); (2) 80 mg in week 1, then 40 mg in week 2, 40 mg every 2 weeks for 20 weeks (1/11 [9.1%]); (3) 80 mg in week 1, then 40 mg every 2 weeks for a median duration of 12 weeks (2/11 [18.2%]); and (4) 40 mg every 2 weeks (2/11 [18.2%]). Adalimumab generally was well tolerated, with only 1 (9.1%) patient experiencing minor stress-related mucocutaneous flares on the tongue and extremities that resolved spontaneously.¹² Remission was achieved in 5 (45.5%) patients, with time to remission ranging from 2 to 4 months after adalimumab therapy, with a median of 2.5 months. In 1 (9.1%) patient with bullous LP, adalimumab therapy led to remission after 10 weeks. In both cases of oral and cutaneous LP (2/11 [18.2%]), remission was achieved after 2 months of treatment. Of the 2 LPP patients reported, 1 had hair regrowth after 9 months, and the other experienced remission after 3 months of adalimumab therapy. In the 1 (9.1%) case of annular LP, adalimumab treatment led to remission after 4 months. Five (45.5%) patients with vulvar LP treated with adalimumab for at least 9 months demonstrated improved Vulvar Quality of Life Index scores without improvement in their mucosal LP lesions. In 4 of the 5 (80.0%) patients who experienced remission after adalimumab treatment, remission lasted at least 6 to 10 months, with a median of 6 months; remission duration was not reported in 1 (20.0%) patient.

Paradoxically, our review of the literature yielded 12 patients in whom adalimumab was associated with lichenoid-type eruptions across 9 studies (Table 2).^17-29 The conditions for which these patients were undergoing treatment with adalimumab included ulcerative colitis,¹⁷ psoriasis,^18,19 Crohn disease,^20,26 rheumatoid arthritis,^21-23,26 oligoarthritis,²⁴ and ankylosing spondylitis.²⁵ Lichenoid drug eruptions occurred on the legs (5/12 [41.7%]), arms (3/12 [25%]), oral mucosa (2/12 [16.7%]), and forehead or scalp (2/12 [16.7%]). Onset of time to these lichenoid eruptions ranged from 2 weeks to 17 months, with a median of 4 months. Adalimumab was discontinued in 9 (75.0%) patients and was continued in 3 (25.0%). One patient who had an onset of their lichenoid eruption after 17 months of treatment with adalimumab continued to receive adalimumab therapy with the addition of topical corticosteroids, which led to resolution of their oral lesions and partial remission of their cutaneous lesions. In 1 (8.3%) patient with localized buccal lichenoid eruptions, discontinuation of adalimumab on its own was sufficient to completely clear the lesions. Seven patients (7/12 [58.3%]) received topical corticosteroids with minimal (2/12 [16.7%]) or moderate (4/12 [33.3%]) improvement, and 1 (8.3%) patient did not have reported outcomes data. Eosinophils were detected within the adalimumab-associated lichenoid eruptions in 3 (25.0%) patients.^17,20,22

In addition to its association with lichenoid drug eruptions, adalimumab also was reported to induce LPP in a patient who was being treated for Behçet disease,²⁹ oral LP in a patient being treated for Crohn disease,²⁷ and cutaneous LP in a patient being treated for Crohn disease (Table 2).²⁸ Time to onset ranged from 4 to 10 months, with a median of 6 months. Adalimumab was discontinued in 2 of 3 (66.7%) patients and was continued in the other patient (33.3%). After cessation of adalimumab therapy, administration of topical steroids led to complete resolution in the case of associated oral LP. In contrast, in adalimumab-induced cutaneous LP, initial topical corticosteroid treatment led to progression of lesions, which mostly resolved after adalimumab cessation. In 1 patient with LPP in whom adalimumab therapy could not be discontinued, topical corticosteroid and methotrexate therapy reduced the perifollicular erythema and stabilized the alopecia without full remission.

Comment

Conventional treatment modalities for LP often include topical corticosteroids as first-line therapy, with systemic corticosteroids, phototherapy, retinoids, or immunosuppressants (eg, cyclosporine or methotrexate) reserved for more severe or widespread disease. Historically, these approaches primarily have aimed to control symptoms rather than achieve long-term resolution; however, novel therapies including biologics and targeted immunomodulators show potential to induce sustained remission and improve quality of life for patients with refractory or mucosal LP.

In all reports where adalimumab was used to treat LP, patients initially received topical corticosteroids. While corticosteroids and other immunosuppressive agents are standard therapies, they often provide only temporary relief and may have an unfavorable side effect profile. Our review highlights the emerging role of adalimumab, a TNF-α inhibitor, in off-label management of LP subtypes, including cutaneous, mucosal, and vulvar LP and LPP. In several small case series and reports, patients treated with adalimumab experienced clinical improvement, including symptom resolution and quality-of-life enhancement, as well as complete remission, indicating a durable response.

The potential benefit of adalimumab in treating LP must be balanced with its paradoxical risk for inducing lichenoid eruptions as well as LP and its variants, as identified in our narrative review that included reports of patients receiving this biologic for other indications.^17-29 Since adalimumab is a fully humanized antibody, the development of neutralizing antibodies may not account for drug-induced LP and lichenoid eruptions. Given that it blocks TNF-α, adalimumab may induce these lesions through a cytokine imbalance. This is supported by data demonstrating enhanced type I IFN-related proteins in plaques of patients with psoriasiform lesions treated with TNF-α inhibitors.²⁶ These drug-induced eruptions often resolved or improved with topical corticosteroids after discontinuation, but their occurrence underscores the complexity of therapeutically targeting TNF-α in the management of LP. Our literature review suggests that adalimumab may offer therapeutic benefit in select cases of LP refractory to conventional therapy, especially when systemic control is required. Nonetheless, the risk for LP and lichenoid reactions necessitates cautious use and further investigation.

Conclusion

While the current evidence is limited to case reports and series, adalimumab shows promise as an effective and tolerable off-label treatment for LP, particularly in patients who are unresponsive to conventional immunosuppressive therapies. Remission or clinically significant improvement was achieved in several cases; however, the potential for adalimumab to induce LP and lichenoid eruptions underscores the need for careful patient selection and monitoring. Further prospective studies and larger cohorts are warranted to better define the safety and efficacy of adalimumab in treating LP lesions.

Lichen planus (LP) is a chronic inflammatory condition affecting the skin (cutaneous LP), mucous membranes (oral, ocular, or vulvar LP), hair (lichen planopilaris [LPP]), and nails that predominantly occurs in middle-aged adults. Although the true etiology remains unknown, the pathogenesis of LP is thought to involve multiple factors. Several human leukocyte antigen (HLA) alleles have been associated with LP and its variants, including HLA-B27, HLA-B51, HLA-DR1 (cutaneous and oral LP), HLA-DRB1*11, and HLA-DQB1*03 (LPP). Additionally, HLA-Bw57 has been reported to be associated with oral LP in a cohort of British patients.¹ In addition to HLA alleles, genetic polymorphisms in cytokines including IL-4, IL-6, IL-18, interferon (IFN) γ, and tumor necrosis factor (TNF) α and its receptor have been found to be associated with LP.² Beyond genetics, chronic viral infection has been implicated in the development of LP. Systemic infection with the hepatitis C virus has been linked to the development of oral LP by promoting the recruitment of hepatitis C virus–specific CD8+ T cells from peripheral blood to the oral lesions, where they exhibit a terminally differentiated effector status.³ Another report found an association between human herpesvirus 7 (HHV-7) and cutaneous LP; in this study, HHV-7 RNA was detected in plasmacytoid dendritic cells but not T cells and diminished after treatment, providing evidence for dendritic cells being involved in the HHV-7–mediated pathogenesis of cutaneous LP.⁴ These findings were further corroborated by another study of oral LP patients that found enhanced infiltration of plasmacytoid and myeloid dendritic cells and upregulation in toll-like receptor and IFN-γ signaling.⁴

In addition to immune cell dysregulation, LP and its variants have been linked to neurogenic inflammation. In oral LP lesions, neurokinin 1 receptor and substance P were highly expressed and demonstrated a positive correlation with the expression of apoptotic marker caspase-3 and proliferation marker Ki-67.⁵ These results suggest that neuropeptides may be involved in cell proliferation and turnover in oral LP. Similarly, in patients with LPP, substance P was more abundant in affected areas, whereas another neuropeptide, calcitonin gene-related peptide, was more highly expressed in unaffected areas,⁶ further supporting the pathogenic role of neurogenic inflammation in LP.

A mucosal variant that often goes undiagnosed is vulvar LP. Although no distinct pathologic mechanism for vulvar LP has been established, prior reports found an association with autoantibodies.^7,8 In patients with erosive vulvar LP, epidermal-binding basement membrane zone antibodies were detected in epidermal skin biopsies and in circulation with reactivity to bullous pemphigoid antigens 180 (9/11 [81.8%] patients) and 230 (2/11 [18.2%] patients).⁷ A similar study in patients with vulvar lichen sclerosus found similar proportions of circulating antibodies reactive to bullous pemphigoid antigens 180 (6/7 [85.7%] patients) and 230 (1/7 [14.3%] patients).⁸ Erosive vulvar LP has been shown to be associated with autoimmune disease (eg, alopecia areata, celiac disease and pernicious anemia),⁹ which suggests that the previously reported autoreactive antibodies^7,8 are secondary to autoimmunity rather than primary drivers of vulvar LP pathogenesis.

Certain medications also have been reported to cause cutaneous lichenoid drug eruptions. Although they can clinically and histologically mimic classic LP, lichenoid drug eruptions are a distinct entity. Common inciting medications include thiazide diuretics, angiotensin-converting enzyme inhibitors, anti-inflammatory drugs, antimalarials, checkpoint inhibitors, antimicrobials, antihypertensives, antidiabetics, and psychiatric drugs. The exact pathologic mechanism of lichenoid drug eruptions currently is unclear but is thought to involve the binding of drug molecules to the cell-surface proteins of the epidermis, creating an antigenic hapten stimulus for CD8+T cells and triggering apoptosis of keratinocytes.¹

The clinical severity of LP can range from mild localized disease to widespread and debilitating involvement. Multiple treatment modalities have been developed for management of LP, including topical and intralesional corticosteroids, phototherapy, Janus kinase inhibitors, phosphodiesterase-4 inhibitors, and anti–TNF-α inhibitors. Herein, we provide a narrative review and summary of the use of the TNF-α inhibitor adalimumab as a potential effective treatment for patients with LP.

Methods

We conducted a PubMed search of articles indexed for MEDLINE from 2005 to 2025 using the terms adalimumab AND lichen planus or adalimumab AND lichen. Articles that reported cases of oral LP, cutaneous LP, LPP, or lichenoid eruptions and adalimumab therapy were included in our review. Articles that used non-adalimumab TNF-α inhibitors were excluded. Using the search terms, 2 independent reviewers (M.G. and N.E.) conducted the literature review then screened the articles based on the inclusion and exclusion criteria. Our literature search yielded 40 articles, of which 20 met the criteria for inclusion in our narrative review.

Results

Our literature search yielded 11 patients with LP who were treated with adalimumab across studies (Table 1).^10-16 Prior LP treatments included topical corticosteroids (11/11 [100%]), disease-modifying antirheumatic drugs (6/11 [54.5%]), retinoids (4/11 [36.4%]), and psoralen plus UVA (1/11 [36.4%]). Adalimumab was administered subcutaneously following 4 treatment regimens: (1) 160 mg in week 1, then 80 mg in week 2, then 40 mg weekly for a median duration of 36 weeks (6/11 [54.5%]); (2) 80 mg in week 1, then 40 mg in week 2, 40 mg every 2 weeks for 20 weeks (1/11 [9.1%]); (3) 80 mg in week 1, then 40 mg every 2 weeks for a median duration of 12 weeks (2/11 [18.2%]); and (4) 40 mg every 2 weeks (2/11 [18.2%]). Adalimumab generally was well tolerated, with only 1 (9.1%) patient experiencing minor stress-related mucocutaneous flares on the tongue and extremities that resolved spontaneously.¹² Remission was achieved in 5 (45.5%) patients, with time to remission ranging from 2 to 4 months after adalimumab therapy, with a median of 2.5 months. In 1 (9.1%) patient with bullous LP, adalimumab therapy led to remission after 10 weeks. In both cases of oral and cutaneous LP (2/11 [18.2%]), remission was achieved after 2 months of treatment. Of the 2 LPP patients reported, 1 had hair regrowth after 9 months, and the other experienced remission after 3 months of adalimumab therapy. In the 1 (9.1%) case of annular LP, adalimumab treatment led to remission after 4 months. Five (45.5%) patients with vulvar LP treated with adalimumab for at least 9 months demonstrated improved Vulvar Quality of Life Index scores without improvement in their mucosal LP lesions. In 4 of the 5 (80.0%) patients who experienced remission after adalimumab treatment, remission lasted at least 6 to 10 months, with a median of 6 months; remission duration was not reported in 1 (20.0%) patient.

Paradoxically, our review of the literature yielded 12 patients in whom adalimumab was associated with lichenoid-type eruptions across 9 studies (Table 2).^17-29 The conditions for which these patients were undergoing treatment with adalimumab included ulcerative colitis,¹⁷ psoriasis,^18,19 Crohn disease,^20,26 rheumatoid arthritis,^21-23,26 oligoarthritis,²⁴ and ankylosing spondylitis.²⁵ Lichenoid drug eruptions occurred on the legs (5/12 [41.7%]), arms (3/12 [25%]), oral mucosa (2/12 [16.7%]), and forehead or scalp (2/12 [16.7%]). Onset of time to these lichenoid eruptions ranged from 2 weeks to 17 months, with a median of 4 months. Adalimumab was discontinued in 9 (75.0%) patients and was continued in 3 (25.0%). One patient who had an onset of their lichenoid eruption after 17 months of treatment with adalimumab continued to receive adalimumab therapy with the addition of topical corticosteroids, which led to resolution of their oral lesions and partial remission of their cutaneous lesions. In 1 (8.3%) patient with localized buccal lichenoid eruptions, discontinuation of adalimumab on its own was sufficient to completely clear the lesions. Seven patients (7/12 [58.3%]) received topical corticosteroids with minimal (2/12 [16.7%]) or moderate (4/12 [33.3%]) improvement, and 1 (8.3%) patient did not have reported outcomes data. Eosinophils were detected within the adalimumab-associated lichenoid eruptions in 3 (25.0%) patients.^17,20,22

In addition to its association with lichenoid drug eruptions, adalimumab also was reported to induce LPP in a patient who was being treated for Behçet disease,²⁹ oral LP in a patient being treated for Crohn disease,²⁷ and cutaneous LP in a patient being treated for Crohn disease (Table 2).²⁸ Time to onset ranged from 4 to 10 months, with a median of 6 months. Adalimumab was discontinued in 2 of 3 (66.7%) patients and was continued in the other patient (33.3%). After cessation of adalimumab therapy, administration of topical steroids led to complete resolution in the case of associated oral LP. In contrast, in adalimumab-induced cutaneous LP, initial topical corticosteroid treatment led to progression of lesions, which mostly resolved after adalimumab cessation. In 1 patient with LPP in whom adalimumab therapy could not be discontinued, topical corticosteroid and methotrexate therapy reduced the perifollicular erythema and stabilized the alopecia without full remission.

Comment

Conventional treatment modalities for LP often include topical corticosteroids as first-line therapy, with systemic corticosteroids, phototherapy, retinoids, or immunosuppressants (eg, cyclosporine or methotrexate) reserved for more severe or widespread disease. Historically, these approaches primarily have aimed to control symptoms rather than achieve long-term resolution; however, novel therapies including biologics and targeted immunomodulators show potential to induce sustained remission and improve quality of life for patients with refractory or mucosal LP.

In all reports where adalimumab was used to treat LP, patients initially received topical corticosteroids. While corticosteroids and other immunosuppressive agents are standard therapies, they often provide only temporary relief and may have an unfavorable side effect profile. Our review highlights the emerging role of adalimumab, a TNF-α inhibitor, in off-label management of LP subtypes, including cutaneous, mucosal, and vulvar LP and LPP. In several small case series and reports, patients treated with adalimumab experienced clinical improvement, including symptom resolution and quality-of-life enhancement, as well as complete remission, indicating a durable response.

The potential benefit of adalimumab in treating LP must be balanced with its paradoxical risk for inducing lichenoid eruptions as well as LP and its variants, as identified in our narrative review that included reports of patients receiving this biologic for other indications.^17-29 Since adalimumab is a fully humanized antibody, the development of neutralizing antibodies may not account for drug-induced LP and lichenoid eruptions. Given that it blocks TNF-α, adalimumab may induce these lesions through a cytokine imbalance. This is supported by data demonstrating enhanced type I IFN-related proteins in plaques of patients with psoriasiform lesions treated with TNF-α inhibitors.²⁶ These drug-induced eruptions often resolved or improved with topical corticosteroids after discontinuation, but their occurrence underscores the complexity of therapeutically targeting TNF-α in the management of LP. Our literature review suggests that adalimumab may offer therapeutic benefit in select cases of LP refractory to conventional therapy, especially when systemic control is required. Nonetheless, the risk for LP and lichenoid reactions necessitates cautious use and further investigation.

Conclusion

While the current evidence is limited to case reports and series, adalimumab shows promise as an effective and tolerable off-label treatment for LP, particularly in patients who are unresponsive to conventional immunosuppressive therapies. Remission or clinically significant improvement was achieved in several cases; however, the potential for adalimumab to induce LP and lichenoid eruptions underscores the need for careful patient selection and monitoring. Further prospective studies and larger cohorts are warranted to better define the safety and efficacy of adalimumab in treating LP lesions.

Lichen planus (LP) is a chronic inflammatory condition affecting the skin (cutaneous LP), mucous membranes (oral, ocular, or vulvar LP), hair (lichen planopilaris [LPP]), and nails that predominantly occurs in middle-aged adults. Although the true etiology remains unknown, the pathogenesis of LP is thought to involve multiple factors. Several human leukocyte antigen (HLA) alleles have been associated with LP and its variants, including HLA-B27, HLA-B51, HLA-DR1 (cutaneous and oral LP), HLA-DRB1*11, and HLA-DQB1*03 (LPP). Additionally, HLA-Bw57 has been reported to be associated with oral LP in a cohort of British patients.¹ In addition to HLA alleles, genetic polymorphisms in cytokines including IL-4, IL-6, IL-18, interferon (IFN) γ, and tumor necrosis factor (TNF) α and its receptor have been found to be associated with LP.² Beyond genetics, chronic viral infection has been implicated in the development of LP. Systemic infection with the hepatitis C virus has been linked to the development of oral LP by promoting the recruitment of hepatitis C virus–specific CD8+ T cells from peripheral blood to the oral lesions, where they exhibit a terminally differentiated effector status.³ Another report found an association between human herpesvirus 7 (HHV-7) and cutaneous LP; in this study, HHV-7 RNA was detected in plasmacytoid dendritic cells but not T cells and diminished after treatment, providing evidence for dendritic cells being involved in the HHV-7–mediated pathogenesis of cutaneous LP.⁴ These findings were further corroborated by another study of oral LP patients that found enhanced infiltration of plasmacytoid and myeloid dendritic cells and upregulation in toll-like receptor and IFN-γ signaling.⁴

In addition to immune cell dysregulation, LP and its variants have been linked to neurogenic inflammation. In oral LP lesions, neurokinin 1 receptor and substance P were highly expressed and demonstrated a positive correlation with the expression of apoptotic marker caspase-3 and proliferation marker Ki-67.⁵ These results suggest that neuropeptides may be involved in cell proliferation and turnover in oral LP. Similarly, in patients with LPP, substance P was more abundant in affected areas, whereas another neuropeptide, calcitonin gene-related peptide, was more highly expressed in unaffected areas,⁶ further supporting the pathogenic role of neurogenic inflammation in LP.

A mucosal variant that often goes undiagnosed is vulvar LP. Although no distinct pathologic mechanism for vulvar LP has been established, prior reports found an association with autoantibodies.^7,8 In patients with erosive vulvar LP, epidermal-binding basement membrane zone antibodies were detected in epidermal skin biopsies and in circulation with reactivity to bullous pemphigoid antigens 180 (9/11 [81.8%] patients) and 230 (2/11 [18.2%] patients).⁷ A similar study in patients with vulvar lichen sclerosus found similar proportions of circulating antibodies reactive to bullous pemphigoid antigens 180 (6/7 [85.7%] patients) and 230 (1/7 [14.3%] patients).⁸ Erosive vulvar LP has been shown to be associated with autoimmune disease (eg, alopecia areata, celiac disease and pernicious anemia),⁹ which suggests that the previously reported autoreactive antibodies^7,8 are secondary to autoimmunity rather than primary drivers of vulvar LP pathogenesis.

Certain medications also have been reported to cause cutaneous lichenoid drug eruptions. Although they can clinically and histologically mimic classic LP, lichenoid drug eruptions are a distinct entity. Common inciting medications include thiazide diuretics, angiotensin-converting enzyme inhibitors, anti-inflammatory drugs, antimalarials, checkpoint inhibitors, antimicrobials, antihypertensives, antidiabetics, and psychiatric drugs. The exact pathologic mechanism of lichenoid drug eruptions currently is unclear but is thought to involve the binding of drug molecules to the cell-surface proteins of the epidermis, creating an antigenic hapten stimulus for CD8+T cells and triggering apoptosis of keratinocytes.¹

The clinical severity of LP can range from mild localized disease to widespread and debilitating involvement. Multiple treatment modalities have been developed for management of LP, including topical and intralesional corticosteroids, phototherapy, Janus kinase inhibitors, phosphodiesterase-4 inhibitors, and anti–TNF-α inhibitors. Herein, we provide a narrative review and summary of the use of the TNF-α inhibitor adalimumab as a potential effective treatment for patients with LP.

Methods

We conducted a PubMed search of articles indexed for MEDLINE from 2005 to 2025 using the terms adalimumab AND lichen planus or adalimumab AND lichen. Articles that reported cases of oral LP, cutaneous LP, LPP, or lichenoid eruptions and adalimumab therapy were included in our review. Articles that used non-adalimumab TNF-α inhibitors were excluded. Using the search terms, 2 independent reviewers (M.G. and N.E.) conducted the literature review then screened the articles based on the inclusion and exclusion criteria. Our literature search yielded 40 articles, of which 20 met the criteria for inclusion in our narrative review.

Results

Our literature search yielded 11 patients with LP who were treated with adalimumab across studies (Table 1).^10-16 Prior LP treatments included topical corticosteroids (11/11 [100%]), disease-modifying antirheumatic drugs (6/11 [54.5%]), retinoids (4/11 [36.4%]), and psoralen plus UVA (1/11 [36.4%]). Adalimumab was administered subcutaneously following 4 treatment regimens: (1) 160 mg in week 1, then 80 mg in week 2, then 40 mg weekly for a median duration of 36 weeks (6/11 [54.5%]); (2) 80 mg in week 1, then 40 mg in week 2, 40 mg every 2 weeks for 20 weeks (1/11 [9.1%]); (3) 80 mg in week 1, then 40 mg every 2 weeks for a median duration of 12 weeks (2/11 [18.2%]); and (4) 40 mg every 2 weeks (2/11 [18.2%]). Adalimumab generally was well tolerated, with only 1 (9.1%) patient experiencing minor stress-related mucocutaneous flares on the tongue and extremities that resolved spontaneously.¹² Remission was achieved in 5 (45.5%) patients, with time to remission ranging from 2 to 4 months after adalimumab therapy, with a median of 2.5 months. In 1 (9.1%) patient with bullous LP, adalimumab therapy led to remission after 10 weeks. In both cases of oral and cutaneous LP (2/11 [18.2%]), remission was achieved after 2 months of treatment. Of the 2 LPP patients reported, 1 had hair regrowth after 9 months, and the other experienced remission after 3 months of adalimumab therapy. In the 1 (9.1%) case of annular LP, adalimumab treatment led to remission after 4 months. Five (45.5%) patients with vulvar LP treated with adalimumab for at least 9 months demonstrated improved Vulvar Quality of Life Index scores without improvement in their mucosal LP lesions. In 4 of the 5 (80.0%) patients who experienced remission after adalimumab treatment, remission lasted at least 6 to 10 months, with a median of 6 months; remission duration was not reported in 1 (20.0%) patient.

Paradoxically, our review of the literature yielded 12 patients in whom adalimumab was associated with lichenoid-type eruptions across 9 studies (Table 2).^17-29 The conditions for which these patients were undergoing treatment with adalimumab included ulcerative colitis,¹⁷ psoriasis,^18,19 Crohn disease,^20,26 rheumatoid arthritis,^21-23,26 oligoarthritis,²⁴ and ankylosing spondylitis.²⁵ Lichenoid drug eruptions occurred on the legs (5/12 [41.7%]), arms (3/12 [25%]), oral mucosa (2/12 [16.7%]), and forehead or scalp (2/12 [16.7%]). Onset of time to these lichenoid eruptions ranged from 2 weeks to 17 months, with a median of 4 months. Adalimumab was discontinued in 9 (75.0%) patients and was continued in 3 (25.0%). One patient who had an onset of their lichenoid eruption after 17 months of treatment with adalimumab continued to receive adalimumab therapy with the addition of topical corticosteroids, which led to resolution of their oral lesions and partial remission of their cutaneous lesions. In 1 (8.3%) patient with localized buccal lichenoid eruptions, discontinuation of adalimumab on its own was sufficient to completely clear the lesions. Seven patients (7/12 [58.3%]) received topical corticosteroids with minimal (2/12 [16.7%]) or moderate (4/12 [33.3%]) improvement, and 1 (8.3%) patient did not have reported outcomes data. Eosinophils were detected within the adalimumab-associated lichenoid eruptions in 3 (25.0%) patients.^17,20,22

In addition to its association with lichenoid drug eruptions, adalimumab also was reported to induce LPP in a patient who was being treated for Behçet disease,²⁹ oral LP in a patient being treated for Crohn disease,²⁷ and cutaneous LP in a patient being treated for Crohn disease (Table 2).²⁸ Time to onset ranged from 4 to 10 months, with a median of 6 months. Adalimumab was discontinued in 2 of 3 (66.7%) patients and was continued in the other patient (33.3%). After cessation of adalimumab therapy, administration of topical steroids led to complete resolution in the case of associated oral LP. In contrast, in adalimumab-induced cutaneous LP, initial topical corticosteroid treatment led to progression of lesions, which mostly resolved after adalimumab cessation. In 1 patient with LPP in whom adalimumab therapy could not be discontinued, topical corticosteroid and methotrexate therapy reduced the perifollicular erythema and stabilized the alopecia without full remission.

Comment

Conventional treatment modalities for LP often include topical corticosteroids as first-line therapy, with systemic corticosteroids, phototherapy, retinoids, or immunosuppressants (eg, cyclosporine or methotrexate) reserved for more severe or widespread disease. Historically, these approaches primarily have aimed to control symptoms rather than achieve long-term resolution; however, novel therapies including biologics and targeted immunomodulators show potential to induce sustained remission and improve quality of life for patients with refractory or mucosal LP.

In all reports where adalimumab was used to treat LP, patients initially received topical corticosteroids. While corticosteroids and other immunosuppressive agents are standard therapies, they often provide only temporary relief and may have an unfavorable side effect profile. Our review highlights the emerging role of adalimumab, a TNF-α inhibitor, in off-label management of LP subtypes, including cutaneous, mucosal, and vulvar LP and LPP. In several small case series and reports, patients treated with adalimumab experienced clinical improvement, including symptom resolution and quality-of-life enhancement, as well as complete remission, indicating a durable response.

The potential benefit of adalimumab in treating LP must be balanced with its paradoxical risk for inducing lichenoid eruptions as well as LP and its variants, as identified in our narrative review that included reports of patients receiving this biologic for other indications.^17-29 Since adalimumab is a fully humanized antibody, the development of neutralizing antibodies may not account for drug-induced LP and lichenoid eruptions. Given that it blocks TNF-α, adalimumab may induce these lesions through a cytokine imbalance. This is supported by data demonstrating enhanced type I IFN-related proteins in plaques of patients with psoriasiform lesions treated with TNF-α inhibitors.²⁶ These drug-induced eruptions often resolved or improved with topical corticosteroids after discontinuation, but their occurrence underscores the complexity of therapeutically targeting TNF-α in the management of LP. Our literature review suggests that adalimumab may offer therapeutic benefit in select cases of LP refractory to conventional therapy, especially when systemic control is required. Nonetheless, the risk for LP and lichenoid reactions necessitates cautious use and further investigation.

Conclusion

While the current evidence is limited to case reports and series, adalimumab shows promise as an effective and tolerable off-label treatment for LP, particularly in patients who are unresponsive to conventional immunosuppressive therapies. Remission or clinically significant improvement was achieved in several cases; however, the potential for adalimumab to induce LP and lichenoid eruptions underscores the need for careful patient selection and monitoring. Further prospective studies and larger cohorts are warranted to better define the safety and efficacy of adalimumab in treating LP lesions.

To the Editor:

Severe cutaneous adverse reactions (SCARs) are rare, life-threatening reactions that include acute generalized exanthematous pustulosis (AGEP), drug reaction with eosinophilia and systemic symptoms (DRESS), and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN).¹ In addition to being associated with commonly implicated medications, SCARs also may occur in the setting of antineoplastic therapy.^2,3 Although ­antineoplastic-associated SCARs have been described, diagnosis can be difficult due to varying latency periods and atypical clinical features, such as those observed with BRAF inhibitor–related DRESS during immunotherapy.⁴ Severe cutaneous adverse reactions can increase morbidity and mortality in the oncologic patient population due to both the clinical sequelae from the cutaneous reaction and the potential to interrupt cancer treatment.

The aim of this study was to evaluate the clinical characteristics, outcomes, and impact on cancer treatment among patients diagnosed with a SCAR while receiving active therapy for malignancy. We conducted a retrospective chart review of electronic medical records at Yale New Haven Hospital (New Haven, Connecticut) from 2013 to 2023, identifying patients receiving antineoplastic therapy who were diagnosed with a SCAR. Cases were identified through a search of the electronic medical record performed by the joint data analytics team using the keywords DRESS, SJS, TEN, AGEP, and generalized bullous fixed drug eruption, along with spelling variations (both abbreviations and full terms), in addition to manual review by one of the authors (K.V.) of the inpatient dermatology consultation log and dermatopathology database. Only patients for whom an antineoplastic agent was identified as a high-probability culprit by the dermatology and/or oncology teams were included.

In total, 20 patients (11 female, 9 male) were identified as having an antineoplastic-associated SCAR. All patients had metastatic or advanced disease. We identified 2 (10%) cases of AGEP, 16 (80%) cases of DRESS, and 3 (15%) cases of SJS/TEN. One patient on immunotherapy had 2 distinct SCARs (AGEP, DRESS) at different time points. Table 1 describes patient and SCAR characteristics as well as impact on cancer treatment. The median (interquartile range [IQR]) latency period for AGEP was 7.5 (4-11) days. The median (IQR) latency period for 13 of the 16 (81%) DRESS cases was 14 (10-32) days. For 3 DRESS cases with a potential second-hit phenomenon in the setting of current or antecedent immunotherapy,⁵ the median (IQR) latency period was 122 (96-426) days for the immunotherapy drug and 28 (21-52) days for the drug culprit. The median (IQR) latency period for SJS/TEN was 23 (20-27) days.

Patients received treatment with combination systemic corticosteroids and topical corticosteroids in 13 (65%) cases, systemic corticosteroid monotherapy in 6 (30%) cases, or combination systemic corticosteroids and etanercept in 1 (5%) case. All patients experienced resolution of the SCAR and survived to hospital discharge. Most (17/20 [85%]) patients experienced interruption or discontinuation of cancer treatment. Table 2 describes the implicated antineoplastic therapies, which included chemotherapy (3 DRESS, 1 SJS/TEN), hormonal therapy (1 DRESS), immunotherapy (1 AGEP, 4 DRESS), and targeted therapy (1 AGEP, 8 DRESS, 2 SJS/TEN).

Limitations of this study include the retrospective study design, the small sample size, and the challenge of drug culprit identification in oncologic patients on multiple high-probability medications.

Though rare, SCARs can be encountered in patients on antineoplastic therapy with a wide range of drug culprits. In our cohort, SCARs occurred with various antineoplastic agents, including chemotherapy, hormonal therapy, immunotherapy, and targeted therapy. The most common antineoplastic-associated SCAR was DRESS, which had the widest latency period in the setting of a potential second-hit phenomenon with another drug culprit. Although we did not observe any cases of SJS/TEN in the immunotherapy category, it is important to consider progressive immunotherapy-related mucocutaneous eruption in the differential diagnosis. Fortunately, all patients survived to hospital discharge and experienced SCAR resolution with systemic treatment; however, most patients experienced interruption of cancer therapy, which has the potential to affect oncologic outcomes. This interruption is not uncommon, as rechallenge of an antineoplastic agent in patients with a therapy-related SCAR generally is not recommended. The awareness and prompt management of SCARs in a patient on treatment for malignancy are critical in order to minimize negative outcomes in this vulnerable patient population.

To the Editor:

Severe cutaneous adverse reactions (SCARs) are rare, life-threatening reactions that include acute generalized exanthematous pustulosis (AGEP), drug reaction with eosinophilia and systemic symptoms (DRESS), and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN).¹ In addition to being associated with commonly implicated medications, SCARs also may occur in the setting of antineoplastic therapy.^2,3 Although ­antineoplastic-associated SCARs have been described, diagnosis can be difficult due to varying latency periods and atypical clinical features, such as those observed with BRAF inhibitor–related DRESS during immunotherapy.⁴ Severe cutaneous adverse reactions can increase morbidity and mortality in the oncologic patient population due to both the clinical sequelae from the cutaneous reaction and the potential to interrupt cancer treatment.

The aim of this study was to evaluate the clinical characteristics, outcomes, and impact on cancer treatment among patients diagnosed with a SCAR while receiving active therapy for malignancy. We conducted a retrospective chart review of electronic medical records at Yale New Haven Hospital (New Haven, Connecticut) from 2013 to 2023, identifying patients receiving antineoplastic therapy who were diagnosed with a SCAR. Cases were identified through a search of the electronic medical record performed by the joint data analytics team using the keywords DRESS, SJS, TEN, AGEP, and generalized bullous fixed drug eruption, along with spelling variations (both abbreviations and full terms), in addition to manual review by one of the authors (K.V.) of the inpatient dermatology consultation log and dermatopathology database. Only patients for whom an antineoplastic agent was identified as a high-probability culprit by the dermatology and/or oncology teams were included.

In total, 20 patients (11 female, 9 male) were identified as having an antineoplastic-associated SCAR. All patients had metastatic or advanced disease. We identified 2 (10%) cases of AGEP, 16 (80%) cases of DRESS, and 3 (15%) cases of SJS/TEN. One patient on immunotherapy had 2 distinct SCARs (AGEP, DRESS) at different time points. Table 1 describes patient and SCAR characteristics as well as impact on cancer treatment. The median (interquartile range [IQR]) latency period for AGEP was 7.5 (4-11) days. The median (IQR) latency period for 13 of the 16 (81%) DRESS cases was 14 (10-32) days. For 3 DRESS cases with a potential second-hit phenomenon in the setting of current or antecedent immunotherapy,⁵ the median (IQR) latency period was 122 (96-426) days for the immunotherapy drug and 28 (21-52) days for the drug culprit. The median (IQR) latency period for SJS/TEN was 23 (20-27) days.

Patients received treatment with combination systemic corticosteroids and topical corticosteroids in 13 (65%) cases, systemic corticosteroid monotherapy in 6 (30%) cases, or combination systemic corticosteroids and etanercept in 1 (5%) case. All patients experienced resolution of the SCAR and survived to hospital discharge. Most (17/20 [85%]) patients experienced interruption or discontinuation of cancer treatment. Table 2 describes the implicated antineoplastic therapies, which included chemotherapy (3 DRESS, 1 SJS/TEN), hormonal therapy (1 DRESS), immunotherapy (1 AGEP, 4 DRESS), and targeted therapy (1 AGEP, 8 DRESS, 2 SJS/TEN).

Limitations of this study include the retrospective study design, the small sample size, and the challenge of drug culprit identification in oncologic patients on multiple high-probability medications.

Though rare, SCARs can be encountered in patients on antineoplastic therapy with a wide range of drug culprits. In our cohort, SCARs occurred with various antineoplastic agents, including chemotherapy, hormonal therapy, immunotherapy, and targeted therapy. The most common antineoplastic-associated SCAR was DRESS, which had the widest latency period in the setting of a potential second-hit phenomenon with another drug culprit. Although we did not observe any cases of SJS/TEN in the immunotherapy category, it is important to consider progressive immunotherapy-related mucocutaneous eruption in the differential diagnosis. Fortunately, all patients survived to hospital discharge and experienced SCAR resolution with systemic treatment; however, most patients experienced interruption of cancer therapy, which has the potential to affect oncologic outcomes. This interruption is not uncommon, as rechallenge of an antineoplastic agent in patients with a therapy-related SCAR generally is not recommended. The awareness and prompt management of SCARs in a patient on treatment for malignancy are critical in order to minimize negative outcomes in this vulnerable patient population.

To the Editor:

Severe cutaneous adverse reactions (SCARs) are rare, life-threatening reactions that include acute generalized exanthematous pustulosis (AGEP), drug reaction with eosinophilia and systemic symptoms (DRESS), and Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN).¹ In addition to being associated with commonly implicated medications, SCARs also may occur in the setting of antineoplastic therapy.^2,3 Although ­antineoplastic-associated SCARs have been described, diagnosis can be difficult due to varying latency periods and atypical clinical features, such as those observed with BRAF inhibitor–related DRESS during immunotherapy.⁴ Severe cutaneous adverse reactions can increase morbidity and mortality in the oncologic patient population due to both the clinical sequelae from the cutaneous reaction and the potential to interrupt cancer treatment.

The aim of this study was to evaluate the clinical characteristics, outcomes, and impact on cancer treatment among patients diagnosed with a SCAR while receiving active therapy for malignancy. We conducted a retrospective chart review of electronic medical records at Yale New Haven Hospital (New Haven, Connecticut) from 2013 to 2023, identifying patients receiving antineoplastic therapy who were diagnosed with a SCAR. Cases were identified through a search of the electronic medical record performed by the joint data analytics team using the keywords DRESS, SJS, TEN, AGEP, and generalized bullous fixed drug eruption, along with spelling variations (both abbreviations and full terms), in addition to manual review by one of the authors (K.V.) of the inpatient dermatology consultation log and dermatopathology database. Only patients for whom an antineoplastic agent was identified as a high-probability culprit by the dermatology and/or oncology teams were included.

In total, 20 patients (11 female, 9 male) were identified as having an antineoplastic-associated SCAR. All patients had metastatic or advanced disease. We identified 2 (10%) cases of AGEP, 16 (80%) cases of DRESS, and 3 (15%) cases of SJS/TEN. One patient on immunotherapy had 2 distinct SCARs (AGEP, DRESS) at different time points. Table 1 describes patient and SCAR characteristics as well as impact on cancer treatment. The median (interquartile range [IQR]) latency period for AGEP was 7.5 (4-11) days. The median (IQR) latency period for 13 of the 16 (81%) DRESS cases was 14 (10-32) days. For 3 DRESS cases with a potential second-hit phenomenon in the setting of current or antecedent immunotherapy,⁵ the median (IQR) latency period was 122 (96-426) days for the immunotherapy drug and 28 (21-52) days for the drug culprit. The median (IQR) latency period for SJS/TEN was 23 (20-27) days.

Patients received treatment with combination systemic corticosteroids and topical corticosteroids in 13 (65%) cases, systemic corticosteroid monotherapy in 6 (30%) cases, or combination systemic corticosteroids and etanercept in 1 (5%) case. All patients experienced resolution of the SCAR and survived to hospital discharge. Most (17/20 [85%]) patients experienced interruption or discontinuation of cancer treatment. Table 2 describes the implicated antineoplastic therapies, which included chemotherapy (3 DRESS, 1 SJS/TEN), hormonal therapy (1 DRESS), immunotherapy (1 AGEP, 4 DRESS), and targeted therapy (1 AGEP, 8 DRESS, 2 SJS/TEN).

Limitations of this study include the retrospective study design, the small sample size, and the challenge of drug culprit identification in oncologic patients on multiple high-probability medications.

Though rare, SCARs can be encountered in patients on antineoplastic therapy with a wide range of drug culprits. In our cohort, SCARs occurred with various antineoplastic agents, including chemotherapy, hormonal therapy, immunotherapy, and targeted therapy. The most common antineoplastic-associated SCAR was DRESS, which had the widest latency period in the setting of a potential second-hit phenomenon with another drug culprit. Although we did not observe any cases of SJS/TEN in the immunotherapy category, it is important to consider progressive immunotherapy-related mucocutaneous eruption in the differential diagnosis. Fortunately, all patients survived to hospital discharge and experienced SCAR resolution with systemic treatment; however, most patients experienced interruption of cancer therapy, which has the potential to affect oncologic outcomes. This interruption is not uncommon, as rechallenge of an antineoplastic agent in patients with a therapy-related SCAR generally is not recommended. The awareness and prompt management of SCARs in a patient on treatment for malignancy are critical in order to minimize negative outcomes in this vulnerable patient population.

To the Editor:

At-home microcurrent facial devices have gained rapid popularity for cosmetic rejuvenation, promising improvements in skin tone, contour, and collagen production.¹ In particular, the post–COVID-19 era has seen a surge in at-home beauty practices driven by social media influence, with the global microcurrent facial market estimated at $372.9 million in 2022 and projected to grow at a compound annual growth rate of 7.3% through 2030.¹ Microcurrent devices deliver low-level electrical currents to the skin and underlying muscles. Given the limited exploration of the long-term safety, we aimed to collate existing data and identify trends in reports of adverse events (AEs) associated with these microcurrent devices.

On April 15, 2025, the US Food and Drug Administration’s Manufacturer and User Facility Device Experience (MAUDE) database was queried for medical device reports from January 1, 2013, through March 31, 2025, using product names and keywords including NuFACE, TheraFace, FOREO, and microcurrent device. Search terms were limited to brands for which complaint data existed in the MAUDE database at the time of query. To ensure accuracy, reports were manually reviewed to eliminate duplicates and irrelevant entries.

A total of 28 unique AE reports associated with at-home microcurrent devices were identified (eTable). The majority involved NuFACE devices (ie, NuFACE Trinity, NuFACE Mini, and NuFACE Trinity+)(NuFACE)(n=25), followed by the TheraFace PRO (Therabody, Inc)(n=2) and the FOREO BEAR (FOREO)(n=1). The most frequently documented AEs associated with the NuFACE devices included arrhythmia (7/25 [28%]), pain (6/25 [24%]), dizziness (4/25 [16%]), headache (4/25 [16%]), and inflammation (4/25 [16%]). There was 1 (4%) case of retinal detachment. The TheraFace PRO was associated with device overheating (2/2 [100%]), and the FOREO BEAR was associated with facial deformity/disfigurement (1/1 [100%]).

While microcurrent therapy is widely marketed to consumers through social media influencers and at-home beauty platforms,¹ randomized controlled trials (RCTs) evaluating AEs related to use of this technology are lacking, possibly due to nonstringent regulation of nonprescription cosmetic devices.² Contrary to our findings, RCTs of microcurrent devices have reported minimal or no AEs; for instance, an RCT evaluating 56 participants treated 5 times weekly for 12 weeks with a microcurrent device that was not included in our analysis reported only mild erythema in all experimental group participants.² In another RCT of 30 participants, 15 of whom were treated with a microcurrent device and 15 with placebo for 30 minutes once daily over a period of 10 days, no AEs were reported.³ A cohort analysis of 34 patients also provided preliminary evidence supporting the use of microcurrent therapy for chronic back and neck pain, beyond its cosmetic applications.⁴ Despite the lack of reported AEs in the literature, there is a notable absence of large-scale, rigorous studies on this topic.

Our analysis was subject to the limitations of the MAUDE database, in which reports of severe AEs are more likely to be reported than transient ones. Additionally, the small sample size and lack of a known denominator make it difficult to compare frequencies of AEs among different microcurrent tools. The products chosen for this study were the select few that reported complaint data, but there is a large existing market of devices that may be associated with AEs that have yet to be reported, potentially because of their novelty.

Our findings suggest that, despite their over-the-counter availability, microcurrent facial devices may carry major risks—particularly in at-home settings. While short-term studies have highlighted potential benefits, the small sample sizes and limited follow-up make it difficult to comprehensively characterize long-term safety risks. Among available studies on microcurrent beauty treatments, the longest follow-up was only 12 weeks.² Our findings support the need for further large-scale and longitudinal studies to evaluate both the efficacy and safety of at-home microcurrent therapy, especially with increasing consumer interest. The diversity of the products available adds to the challenge of broad safety guidelines, in addition to the lack of long-term clinical studies.

To the Editor:

At-home microcurrent facial devices have gained rapid popularity for cosmetic rejuvenation, promising improvements in skin tone, contour, and collagen production.¹ In particular, the post–COVID-19 era has seen a surge in at-home beauty practices driven by social media influence, with the global microcurrent facial market estimated at $372.9 million in 2022 and projected to grow at a compound annual growth rate of 7.3% through 2030.¹ Microcurrent devices deliver low-level electrical currents to the skin and underlying muscles. Given the limited exploration of the long-term safety, we aimed to collate existing data and identify trends in reports of adverse events (AEs) associated with these microcurrent devices.

On April 15, 2025, the US Food and Drug Administration’s Manufacturer and User Facility Device Experience (MAUDE) database was queried for medical device reports from January 1, 2013, through March 31, 2025, using product names and keywords including NuFACE, TheraFace, FOREO, and microcurrent device. Search terms were limited to brands for which complaint data existed in the MAUDE database at the time of query. To ensure accuracy, reports were manually reviewed to eliminate duplicates and irrelevant entries.

A total of 28 unique AE reports associated with at-home microcurrent devices were identified (eTable). The majority involved NuFACE devices (ie, NuFACE Trinity, NuFACE Mini, and NuFACE Trinity+)(NuFACE)(n=25), followed by the TheraFace PRO (Therabody, Inc)(n=2) and the FOREO BEAR (FOREO)(n=1). The most frequently documented AEs associated with the NuFACE devices included arrhythmia (7/25 [28%]), pain (6/25 [24%]), dizziness (4/25 [16%]), headache (4/25 [16%]), and inflammation (4/25 [16%]). There was 1 (4%) case of retinal detachment. The TheraFace PRO was associated with device overheating (2/2 [100%]), and the FOREO BEAR was associated with facial deformity/disfigurement (1/1 [100%]).

While microcurrent therapy is widely marketed to consumers through social media influencers and at-home beauty platforms,¹ randomized controlled trials (RCTs) evaluating AEs related to use of this technology are lacking, possibly due to nonstringent regulation of nonprescription cosmetic devices.² Contrary to our findings, RCTs of microcurrent devices have reported minimal or no AEs; for instance, an RCT evaluating 56 participants treated 5 times weekly for 12 weeks with a microcurrent device that was not included in our analysis reported only mild erythema in all experimental group participants.² In another RCT of 30 participants, 15 of whom were treated with a microcurrent device and 15 with placebo for 30 minutes once daily over a period of 10 days, no AEs were reported.³ A cohort analysis of 34 patients also provided preliminary evidence supporting the use of microcurrent therapy for chronic back and neck pain, beyond its cosmetic applications.⁴ Despite the lack of reported AEs in the literature, there is a notable absence of large-scale, rigorous studies on this topic.

Our analysis was subject to the limitations of the MAUDE database, in which reports of severe AEs are more likely to be reported than transient ones. Additionally, the small sample size and lack of a known denominator make it difficult to compare frequencies of AEs among different microcurrent tools. The products chosen for this study were the select few that reported complaint data, but there is a large existing market of devices that may be associated with AEs that have yet to be reported, potentially because of their novelty.

Our findings suggest that, despite their over-the-counter availability, microcurrent facial devices may carry major risks—particularly in at-home settings. While short-term studies have highlighted potential benefits, the small sample sizes and limited follow-up make it difficult to comprehensively characterize long-term safety risks. Among available studies on microcurrent beauty treatments, the longest follow-up was only 12 weeks.² Our findings support the need for further large-scale and longitudinal studies to evaluate both the efficacy and safety of at-home microcurrent therapy, especially with increasing consumer interest. The diversity of the products available adds to the challenge of broad safety guidelines, in addition to the lack of long-term clinical studies.

To the Editor:

At-home microcurrent facial devices have gained rapid popularity for cosmetic rejuvenation, promising improvements in skin tone, contour, and collagen production.¹ In particular, the post–COVID-19 era has seen a surge in at-home beauty practices driven by social media influence, with the global microcurrent facial market estimated at $372.9 million in 2022 and projected to grow at a compound annual growth rate of 7.3% through 2030.¹ Microcurrent devices deliver low-level electrical currents to the skin and underlying muscles. Given the limited exploration of the long-term safety, we aimed to collate existing data and identify trends in reports of adverse events (AEs) associated with these microcurrent devices.

On April 15, 2025, the US Food and Drug Administration’s Manufacturer and User Facility Device Experience (MAUDE) database was queried for medical device reports from January 1, 2013, through March 31, 2025, using product names and keywords including NuFACE, TheraFace, FOREO, and microcurrent device. Search terms were limited to brands for which complaint data existed in the MAUDE database at the time of query. To ensure accuracy, reports were manually reviewed to eliminate duplicates and irrelevant entries.

A total of 28 unique AE reports associated with at-home microcurrent devices were identified (eTable). The majority involved NuFACE devices (ie, NuFACE Trinity, NuFACE Mini, and NuFACE Trinity+)(NuFACE)(n=25), followed by the TheraFace PRO (Therabody, Inc)(n=2) and the FOREO BEAR (FOREO)(n=1). The most frequently documented AEs associated with the NuFACE devices included arrhythmia (7/25 [28%]), pain (6/25 [24%]), dizziness (4/25 [16%]), headache (4/25 [16%]), and inflammation (4/25 [16%]). There was 1 (4%) case of retinal detachment. The TheraFace PRO was associated with device overheating (2/2 [100%]), and the FOREO BEAR was associated with facial deformity/disfigurement (1/1 [100%]).

While microcurrent therapy is widely marketed to consumers through social media influencers and at-home beauty platforms,¹ randomized controlled trials (RCTs) evaluating AEs related to use of this technology are lacking, possibly due to nonstringent regulation of nonprescription cosmetic devices.² Contrary to our findings, RCTs of microcurrent devices have reported minimal or no AEs; for instance, an RCT evaluating 56 participants treated 5 times weekly for 12 weeks with a microcurrent device that was not included in our analysis reported only mild erythema in all experimental group participants.² In another RCT of 30 participants, 15 of whom were treated with a microcurrent device and 15 with placebo for 30 minutes once daily over a period of 10 days, no AEs were reported.³ A cohort analysis of 34 patients also provided preliminary evidence supporting the use of microcurrent therapy for chronic back and neck pain, beyond its cosmetic applications.⁴ Despite the lack of reported AEs in the literature, there is a notable absence of large-scale, rigorous studies on this topic.

Our analysis was subject to the limitations of the MAUDE database, in which reports of severe AEs are more likely to be reported than transient ones. Additionally, the small sample size and lack of a known denominator make it difficult to compare frequencies of AEs among different microcurrent tools. The products chosen for this study were the select few that reported complaint data, but there is a large existing market of devices that may be associated with AEs that have yet to be reported, potentially because of their novelty.

Our findings suggest that, despite their over-the-counter availability, microcurrent facial devices may carry major risks—particularly in at-home settings. While short-term studies have highlighted potential benefits, the small sample sizes and limited follow-up make it difficult to comprehensively characterize long-term safety risks. Among available studies on microcurrent beauty treatments, the longest follow-up was only 12 weeks.² Our findings support the need for further large-scale and longitudinal studies to evaluate both the efficacy and safety of at-home microcurrent therapy, especially with increasing consumer interest. The diversity of the products available adds to the challenge of broad safety guidelines, in addition to the lack of long-term clinical studies.

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

THE DIAGNOSIS: Cutaneous Leiomyosarcoma

Based on the clinical and histopathologic findings, our patient was diagnosed with primary cutaneous leiomyosarcoma (LMS), a rare soft-tissue neoplasm that arises from smooth muscle and typically manifests as a firm pink nodule.¹ The neoplasm may occur in the area of a prior traumatic injury or develop spontaneously without an identifiable cause.^1-3 Cutaneous LMS represents 2% to 3% of all soft-tissue sarcomas worldwide, with an estimated incidence of 1 in 500,000 annually.^1,4 Men who are in their fifth to seventh decades of life are at the highest risk for LMS.¹

Histologically, cutaneous LMS can be subclassified as dermal, which has a low metastatic risk and excellent prognosis, or subcutaneous, which is associated with poorer outcomes and vascular muscle origin.¹ In our case, hematoxylin and eosin staining revealed fascicles of smooth muscle fibers with hypercellularity, atypia, and mitotic figures (Figure). The neoplasm stained positive for desmin, vimentin, and smooth muscle actin and negative for SOX10, Melan-A, PRAME (preferentially expressed antigen in melanoma), CD34, and Factor XIIIa.¹

Standard treatment for LMS is surgical excision.⁵ Poor prognostic factors include lesions with a diameter of 5 cm or larger, deep subcutaneous tumor invasion, and distant metastases.^2,5

The differential diagnosis may include dermatofibrosarcoma protuberans, which can have a similar pink nodular appearance and also may manifest after injury⁶; however, this lesion would stain positive for CD34 on histopathology.¹ Nodular melanoma also can manifest as a solitary red, raised lesion, but it would stain positive for SOX10, PRAME, and Melan-A on histopathology.⁷ Basal cell carcinoma, which also may have a similar clinical appearance, is associated with nests of basaloid cells and palisading nuclei histologically.⁸ Lastly, atypical fibroxanthoma also manifests as a red nodule or plaque and is associated with atypical mitotic figures on histology; however, it notably stains negative for desmin.⁹

In summary, cutaneous LMS should be included in the differential diagnosis for raised, pink nodules. Given its nonspecific clinical presentation, this rare and malignant neoplasm requires biopsy and immunohistochemical staining for accurate diagnosis.

Have you ever heard of the American Dermatological Association (ADA)? While many residents may not yet be familiar with this group, its members are among the most respected leaders in dermatology. They serve as current and past presidents of influential organizations including the American Academy of Dermatology (Susan C. Taylor, MD [Philadelphia, Pennsylvania]), the American Society for Dermatologic Surgery (M. Laurin Council, MD, MBA [Creve Coeur, Missouri]), and the Association of Professors of Dermatology (Sewon Kang, MD [Baltimore, Maryland]). Others lead certification boards or serve as editors of key journals like the Journal of the American Academy of Dermatology (Dirk Elston, MD [Charleston, South Carolina]), JAMA Dermatology (Kanade Shinkai, MD [San Francisco, California], and Cutis (Vincent A. DeLeo, MD [Los Angeles, California]).

The ADA is celebrating its 150th anniversary in 2026. What makes the organization so enduring is not just its history, but its culture. The members of the ADA foster deep, long-lasting relationships, and its meetings are purposefully designed to balance structured scientific sessions with unscheduled time for reflection, conversation, and connection. That intentional design cultivates learning, innovation, and wellness.

Steven Covey’s The 7 Habits of Highly Effective People¹ highlights the importance of renewal and relationship building, as does the Harvard Study of Adult Development, one of the longest-running research projects on well-being.^2-4 The key conclusion? Relationships are the strongest predictors of long, healthy, and fulfilling lives, not wealth or achievement. Medical training is intense, and the emphasis often falls squarely on achievement. But the friendships you form in medical school, residency, and early career are just as formative. Membership with the ADA continues this spirit of connection throughout one’s professional life, with meetings that welcome spouses and partners and encourage engagement across generations.

A hallmark of ADA culture is its commitment to mentoring and mutual support. Need advice about transitioning from private practice to academia? Navigating department leadership? Applying for a grant? Considering industry, editorial, or global health roles? Within the ADA, there’s someone who has done it and is eager to help. Recent meetings have addressed future-facing topics such as artificial intelligence, bedside diagnostics, workforce advocacy, and global health while also carving out time for rejuvenating activities: book clubs with best-selling authors, sessions on the arts, storytelling, wellness, and travel. This holistic programming reflects the ADA’s belief in supporting the whole physician.³ Members understand the value of relationships and appreciate these opportunities to learn about the passions and interests of their colleagues (Table).

Candidates are nominated by current members and must be board certified and at least 10 years beyond completion of their training. Members vote upon candidates in a rank voting system each year. If someone is nominated and not selected, they did not fail—they may be nominated again. The idea behind this membership process is to keep the organization small enough that members can get to know one another—there are currently 552 active members. Importantly, the ADA has embraced diversity and inclusion. While historically male- and White-dominated, recent inductee classes now reflect gender parity and a broader range of backgrounds, enriching the organization with fresh perspectives.^5-8

For residents and fellows, the lesson is clear: friendships, mentorship, and time for reflection are not luxuries—they are essential. Burnout stems from relentless output in isolation; however, in cultures that prioritize renewal, authenticity, and community, physicians can flourish.⁹ Membership in small professional organizations is an important step towards avoiding isolation. We encourage you to be active in your local, state, and national organizations.

The ADA stands as a powerful example of how professional societies can help you build the kind of life and career you want, not just a résumé. From informal beachside conversations to high-level scientific discussions, its enduring strength is this: leaders helping others lead.

Have you ever heard of the American Dermatological Association (ADA)? While many residents may not yet be familiar with this group, its members are among the most respected leaders in dermatology. They serve as current and past presidents of influential organizations including the American Academy of Dermatology (Susan C. Taylor, MD [Philadelphia, Pennsylvania]), the American Society for Dermatologic Surgery (M. Laurin Council, MD, MBA [Creve Coeur, Missouri]), and the Association of Professors of Dermatology (Sewon Kang, MD [Baltimore, Maryland]). Others lead certification boards or serve as editors of key journals like the Journal of the American Academy of Dermatology (Dirk Elston, MD [Charleston, South Carolina]), JAMA Dermatology (Kanade Shinkai, MD [San Francisco, California], and Cutis (Vincent A. DeLeo, MD [Los Angeles, California]).

The ADA is celebrating its 150th anniversary in 2026. What makes the organization so enduring is not just its history, but its culture. The members of the ADA foster deep, long-lasting relationships, and its meetings are purposefully designed to balance structured scientific sessions with unscheduled time for reflection, conversation, and connection. That intentional design cultivates learning, innovation, and wellness.

Steven Covey’s The 7 Habits of Highly Effective People¹ highlights the importance of renewal and relationship building, as does the Harvard Study of Adult Development, one of the longest-running research projects on well-being.^2-4 The key conclusion? Relationships are the strongest predictors of long, healthy, and fulfilling lives, not wealth or achievement. Medical training is intense, and the emphasis often falls squarely on achievement. But the friendships you form in medical school, residency, and early career are just as formative. Membership with the ADA continues this spirit of connection throughout one’s professional life, with meetings that welcome spouses and partners and encourage engagement across generations.

A hallmark of ADA culture is its commitment to mentoring and mutual support. Need advice about transitioning from private practice to academia? Navigating department leadership? Applying for a grant? Considering industry, editorial, or global health roles? Within the ADA, there’s someone who has done it and is eager to help. Recent meetings have addressed future-facing topics such as artificial intelligence, bedside diagnostics, workforce advocacy, and global health while also carving out time for rejuvenating activities: book clubs with best-selling authors, sessions on the arts, storytelling, wellness, and travel. This holistic programming reflects the ADA’s belief in supporting the whole physician.³ Members understand the value of relationships and appreciate these opportunities to learn about the passions and interests of their colleagues (Table).

Candidates are nominated by current members and must be board certified and at least 10 years beyond completion of their training. Members vote upon candidates in a rank voting system each year. If someone is nominated and not selected, they did not fail—they may be nominated again. The idea behind this membership process is to keep the organization small enough that members can get to know one another—there are currently 552 active members. Importantly, the ADA has embraced diversity and inclusion. While historically male- and White-dominated, recent inductee classes now reflect gender parity and a broader range of backgrounds, enriching the organization with fresh perspectives.^5-8

For residents and fellows, the lesson is clear: friendships, mentorship, and time for reflection are not luxuries—they are essential. Burnout stems from relentless output in isolation; however, in cultures that prioritize renewal, authenticity, and community, physicians can flourish.⁹ Membership in small professional organizations is an important step towards avoiding isolation. We encourage you to be active in your local, state, and national organizations.

The ADA stands as a powerful example of how professional societies can help you build the kind of life and career you want, not just a résumé. From informal beachside conversations to high-level scientific discussions, its enduring strength is this: leaders helping others lead.

Have you ever heard of the American Dermatological Association (ADA)? While many residents may not yet be familiar with this group, its members are among the most respected leaders in dermatology. They serve as current and past presidents of influential organizations including the American Academy of Dermatology (Susan C. Taylor, MD [Philadelphia, Pennsylvania]), the American Society for Dermatologic Surgery (M. Laurin Council, MD, MBA [Creve Coeur, Missouri]), and the Association of Professors of Dermatology (Sewon Kang, MD [Baltimore, Maryland]). Others lead certification boards or serve as editors of key journals like the Journal of the American Academy of Dermatology (Dirk Elston, MD [Charleston, South Carolina]), JAMA Dermatology (Kanade Shinkai, MD [San Francisco, California], and Cutis (Vincent A. DeLeo, MD [Los Angeles, California]).

The ADA is celebrating its 150th anniversary in 2026. What makes the organization so enduring is not just its history, but its culture. The members of the ADA foster deep, long-lasting relationships, and its meetings are purposefully designed to balance structured scientific sessions with unscheduled time for reflection, conversation, and connection. That intentional design cultivates learning, innovation, and wellness.

Steven Covey’s The 7 Habits of Highly Effective People¹ highlights the importance of renewal and relationship building, as does the Harvard Study of Adult Development, one of the longest-running research projects on well-being.^2-4 The key conclusion? Relationships are the strongest predictors of long, healthy, and fulfilling lives, not wealth or achievement. Medical training is intense, and the emphasis often falls squarely on achievement. But the friendships you form in medical school, residency, and early career are just as formative. Membership with the ADA continues this spirit of connection throughout one’s professional life, with meetings that welcome spouses and partners and encourage engagement across generations.

A hallmark of ADA culture is its commitment to mentoring and mutual support. Need advice about transitioning from private practice to academia? Navigating department leadership? Applying for a grant? Considering industry, editorial, or global health roles? Within the ADA, there’s someone who has done it and is eager to help. Recent meetings have addressed future-facing topics such as artificial intelligence, bedside diagnostics, workforce advocacy, and global health while also carving out time for rejuvenating activities: book clubs with best-selling authors, sessions on the arts, storytelling, wellness, and travel. This holistic programming reflects the ADA’s belief in supporting the whole physician.³ Members understand the value of relationships and appreciate these opportunities to learn about the passions and interests of their colleagues (Table).

Candidates are nominated by current members and must be board certified and at least 10 years beyond completion of their training. Members vote upon candidates in a rank voting system each year. If someone is nominated and not selected, they did not fail—they may be nominated again. The idea behind this membership process is to keep the organization small enough that members can get to know one another—there are currently 552 active members. Importantly, the ADA has embraced diversity and inclusion. While historically male- and White-dominated, recent inductee classes now reflect gender parity and a broader range of backgrounds, enriching the organization with fresh perspectives.^5-8

For residents and fellows, the lesson is clear: friendships, mentorship, and time for reflection are not luxuries—they are essential. Burnout stems from relentless output in isolation; however, in cultures that prioritize renewal, authenticity, and community, physicians can flourish.⁹ Membership in small professional organizations is an important step towards avoiding isolation. We encourage you to be active in your local, state, and national organizations.

The ADA stands as a powerful example of how professional societies can help you build the kind of life and career you want, not just a résumé. From informal beachside conversations to high-level scientific discussions, its enduring strength is this: leaders helping others lead.

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.

Dermatologists play a central role in the care of hospitalized patients with skin disease. This review summarizes research from January 2024 to December 2025 on severe cutaneous adverse drug reactions, emerging infectious diseases, hidradenitis suppurativa (HS), and inpatient dermatology workforce issues. Key developments include improved recognition and management of drug reactions; updated diagnostic and prognostic tools for Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN); and guidance for emerging infections such as measles, dengue, mpox, orthopoxviruses, and resistant dermatophytes. Evidence-based strategies for HS aim to reduce unnecessary admissions and optimize care. Workforce challenges, including limited access, high call burden, and potential for artificial intelligence (AI)–assisted diagnosis, are also highlighted. These findings emphasize the critical contributions of dermatologists to hospital-based care and provide emerging evidence to guide clinical practice.

Dermatologists play a critical role in the care of hospitalized patients. Herein, we review the research developments between January 2024 and December 2025 most relevant to the care of hospitalized patients with skin disease, including severe cutaneous adverse reactions (SCARs), emerging and re-emerging infectious diseases, hidradenitis suppurativa (HS), and access to inpatient dermatology services.

Severe Cutaneous Adverse Drug Reactions

Severe cutaneous adverse drug reactions are among the most frequent reasons for inpatient dermatology consultation. A National Inpatient Sample study identified more than 160,000 cases of drug rash with eosinophilia and systemic symptoms (DRESS syndrome) between January 2016 and December 2020.¹ The overall mortality rate was 2.0%, substantially lower than the rates of up to 10% reported in earlier studies.² Case burden and mortality peaked during the fall months, possibly due to either increased use of antibiotics or increased viral infection or reactivation during these months.¹

A retrospective cohort study of patients with probable or definite DRESS syndrome showed that, among 93 patients with at least 1 viral marker tested, human herpesvirus (HHV) reactivation was found in 42% (39/93), including HHV-6 (28%)(24/85), Epstein-Barr virus (17%)(15/87), and cytomegalovirus (20%)(18/89); furthermore, viral reactivation was associated with higher 1-year mortality (odds ratio, 3.9), dialysis initiation, flares of disease, and longer hospital stay (all P<.05).¹ Multiple reactivations were associated with higher inpatient mortality and 1-year mortality; however, despite apparent prognostic importance, the role of screening for viral reactivation in DRESS syndrome is undefined.³ A 2024 effort using the Delphi technique found consensus for obtaining HHV-6, Epstein-Barr virus, and cytomegalovirus viral load in all patients with suspected DRESS syndrome, but this topic was the subject of greatest uncertainty.⁴

A systematic review of 610 studies including 2122 patients with DRESS syndrome demonstrated that, among 193 causal agents identified, 14 drugs accounted for more than 1% of cases each and therefore were considered high risk. Seventy-eight percent of cases were attributed to these 14 drugs (Table).⁵ A TriNetX Query study analyzed antibiotic exposures across SCARs and reported that sulfonamides (hazard ratio [HR], 7.5), aminoglycosides (HR, 3.7), and tetracyclines (HR, 1.7) were associated with an elevated risk for SCARs. Sulfonamides had the highest absolute incidence of SCARs, followed by cephalosporins and penicillins.⁶

A multicenter randomized clinical trial⁷ compared high-potency topical corticosteroids (clobetasol 30 g/d) to systemic corticosteroids (prednisone 0.5 mg/kg/d) for treatment of moderate DRESS syndrome. On day 30, 53.8% (14/26) of patients in the topical group had achieved remission of visceral involvement, compared to 72.0% (18/25) in the systemic group. Before day 30, 23.1% (6/26) of patients in the topical group worsened, necessitating transition to high-dose systemic steroids. When inpatient monitoring is available, low-dose systemic corticosteroids or high-potency topical steroids may be reasonable management strategies for moderate DRESS syndrome⁷; however, the frequent need for treatment intensification suggests limitations to this strategy.

Since prolonged courses of systemic steroids generally are necessary for management of DRESS syndrome, steroid-sparing options are needed. A retrospective case series examined interleukin 5 inhibition in patients with possible DRESS syndrome (Registry of Severe Cutaneous Adverse Reactions score ≥3). All patients demonstrated rapid eosinophil reduction within 1 to 3 days (mean [SD] time to resolution, 1.4 [0.9] days) after treatment with mepolizumab or benralizumab, with clinical improvement occurring at a mean (SD) of 16 (3.7) days (range, 13-21 days).⁸

A French cohort study of 1221 adult patients with Stevens-Johnson syndrome (SJS)/toxic epidermal necrolysis (TEN) reported in-hospital mortality of 19% and a total mortality of 34% at 1 year.⁹ Risk factors contributing to in-hospital mortality included age, history of/current diagnosis of cancer, dementia, and liver disease, while postdischarge mortality was associated with acute kidney injury and sepsis. Long-term complications included ophthalmologic and mood disorders.⁹

A new set of diagnostic criteria for SJS/TEN, known as the Niigata criteria,¹⁰ includes 3 main items: severe mucosal lesions in cutaneous-mucosal transition zones (eg, eyes, lips, vulva) or generalized erythema with necrotic lesions; fever of 38.5 °C or higher; and necrosis of the epidermis seen on histopathology. Because epidermal detachment involving 10% of the body surface area (BSA) is an important mortality risk predicter, SJS is defined as less than 10% BSA involvement, and TEN has been redefined as 10% or more BSA involvement (not ≥30%). A new prognostic score—clinical risk score for TEN (CRISTEN)—can be tabulated at the point of care without laboratory values. It was developed based on the 10 most important risk factors for death in a retrospective study of 382 patients, which included age 65 years or older; epidermal detachment involving 10% BSA or higher; an antibiotic as causative agent; systemic corticosteroid therapy before the onset of SJS/TEN; involvement of all 3 mucosal surfaces; and medical comorbidities such as renal impairment, diabetes, cardiac disease, active cancer, and bacterial infection.¹¹

New potential therapeutic targets for SJS/TEN include PC111 (monoclonal antibody to Fas ligand), formyl peptide receptor 1 antagonists (which inhibit necroptosis induced by formyl peptide receptor 1–annexin A1 interaction), daratumumab (which depletes cytotoxic CD8-positive and CD38-positive T cells), and Janus kinase (JAK) inhibitors.¹⁰ Spatial proteomics showed marked enrichment of type I and type II interferon signatures as well as activation of signal transducer and activator of transcription 1. In vitro, tofacitinib reduced keratinocyte-directed cytotoxicity, and in vivo JAK inhibitors ameliorated disease severity in 2 TEN mouse models. Patients with TEN that was refractory to corticosteroid therapy received rescue treatment with JAK inhibitors and had re-epithelization within several days with marked reduction in levels of phosphorylated signal transducer and activator of transcription 1.¹² Controlled studies are needed to assess the potential role of JAK inhibitors for SJS/TEN.

Emerging and Re-emerging Infectious Diseases

Dermatologists may encounter emerging or re-emerging infections, performing an essential public health role in the process. In 2025, a total of 2281 confirmed cases of measles had been reported across 45 of the United States.¹³ During the COVID-19 pandemic, measles vaccine coverage in the United States dropped to 93%—down from 95% to 97% prepandemic. Worldwide, 2022 saw an increase of 1.4 million measles cases (18% increase) and 41,200 excess deaths (43% increase) compared to the previous year. Complications of measles include pneumonia, blindness, otitis media, and encephalitis, with 1 in 5 (20%) unvaccinated people with measles in the United States requiring hospitalization.¹⁴ A vaccine coverage rate higher than 95% is needed to prevent community spread of disease. Since efforts to detect and rapidly isolate cases of measles are critical, dermatologists should consider measles in the differential of morbilliform eruptions with viral symptoms and ask about vaccination status.

Since 2023, dengue infection rates have tripled in the Americas, representing the highest levels recorded since tracking began in 1980. In 2024, there were more than 12 million cases, with approximately 8000 deaths reported. Ninety percent of cases occur in Argentina, Brazil, Colombia, and Mexico, but local transmission has been reported in Arizona, California, Florida, Hawaii, and Texas.¹⁵ The characteristic exanthem of dengue is diffuse erythema with islands of sparing.<

Unlike during the 2022 outbreak of mpox clade II, which predominantly impacted men who have sex with men, there now is an ongoing outbreak of mpox clades 1a and 1b in the Democratic Republic of the Congo and surrounding countries that more commonly affects children and heterosexual adults. It is also more transmissible and virulent. Cases of mpox clade I have been reported in several European countries and across the United States, mostly among travelers from areas of active transmission. Vaccination of at-risk individuals is considered effective; however, tecovirimat is not.¹⁶

Outbreaks of 2 emerging zoonotic orthopoxviruses recently have been reported. Buffalopox virus (BPXV) is transmitted via direct contact with the skin of infected cattle and buffalo as well as fomites and has been responsible for human cases in South Asia. Characteristics of BPXV include macules, umbilicated papules, vesicles, pustules, and eschars that evolve over several weeks, with a predilection for the hands and face. It can manifest with prodromal symptoms of fever, malaise, and lymphadenopathy.¹⁷ Borealpox virus (formerly known as Alaskapox) has similar manifestations. Its reservoir includes small mammals such as voles and shrews, but it also has been found in cats and dogs and has been responsible for at least one human fatality. Cidofovir may be an effective therapy for both BPXV and borealpox virus, and prior smallpox vaccination may provide protection.¹⁸ These outbreaks demonstrate the continued importance of research for more effective vaccines and therapies against smallpox and other orthopoxviruses.¹⁹ A recent review provided a detailed overview of the epidemiology, transmission, dermatologic findings, and management strategies associated with smallpox and other bioweapons.²⁰

In 2023, a case was reported of a patient in a New York City hospital with tinea that was refractory to multiple rounds of topical antifungals, which called attention to the presence of Trichophyton indotineae in the United States.²¹ Since then, additional reports and case series have characterized the clinical presentation of T indotineae as widespread and atypical, refractory to traditional therapies, and most often encountered in travelers returning from Bangladesh or elsewhere in South Asia.²² The diagnosis should be confirmed via DNA testing of fungal culture. Itraconazole 100 to 200 mg/d is the antifungal therapy of choice.²³

Other series have reported cases of tinea genitalis caused by Trichophyton mentagrophytes type VII seen predominately in sex workers and others engaging in high-risk sexual contact, highlighting the spread of dermatophytes through sexual activity.^24-26 Lastly, it is important to culture pustules and consider atypical pathogens in patients with chronic folliculitis not responding to typical therapies such as tetracycline antibiotics. A case series reported the presence of pustules in the beard area of 7 men who have sex with men, with culture data showing Klebsiella aerogenes. Prolonged courses of fluoroquinolones were necessary for clearance.²⁷

Reducing HS Admissions Through Evidence-Based Management

Hidradenitis suppurativa is a frequent cause of emergency department visits and hospital admissions. In an analysis of the Nationwide Readmissions Database, 17.8% (392/2204) of patients admitted to the hospital with HS were readmitted within 30 days, a number comparable to that of heart failure.²⁸

Flaring HS can produce symptoms that mimic sepsis. A retrospective cohort study examining sepsislike features in HS showed that more than 50% (30/58) of those admitted to the hospital with an HS flare were misdiagnosed with sepsis, and more than 80% (53/64) of those patients received intravenous antibiotics.²⁹ A National Inpatient Sample (January 2016-December 2018) study demonstrated minimal rates of true infection in patients admitted with HS flares,³⁰ while patients with HS diagnosed as sepsis do not sustain the mortality expected from true sepsis. Improving recognition of HS and differentiation of the disease from true sepsis could decrease unnecessary antibiotic use, hospital admissions, and cost, underscoring the need for a framework to reliably and reproducibly distinguish sepsis from HS flare.³¹

While severe HS is difficult to manage, there may be a window of opportunity in which appropriate treatment of early disease may prevent progression and decrease inpatient utilization. A prospective cohort study of 335 biologic-naïve patients with mild to moderate HS (Hurley stages I and II) followed over a median of 2 years showed that active smoking, body mass index higher than 25, and the presence of disease in 2 or more anatomic areas were factors predictive of progression to severe disease.³²

Despite high utilization of emergency and inpatient care, there has been no consensus on inpatient management of HS. A Delphi consensus exercise including 26 expert dermatologists reached consensus on 40 statements.³³ Specific recommendations involve multidisciplinary care, including from a dermatologist; consideration of comorbid medical conditions; supportive care measures (wound care, pain control); evidence-based medical management, including initiation or adjustment of biologic therapies; targeted surgical intervention; nutritional support and maintenance of glycemic control; and attention to transitional care at discharge, including home health services, verification of insurance status, and timely outpatient dermatology follow-up.³⁴ A retrospective review of 98 patients treated with intravenous ertapenem for a mean duration of 13 weeks demonstrated improvement in clinical and inflammatory markers.³⁵ Patients with severe or treatment-refractory HS, including those admitted to the hospital, may benefit from initiation of this therapy in select circumstances.

Hospital Dermatology Workforce

Inpatient dermatology consultations are extremely valuable for improving diagnostic accuracy, reducing admissions for pseudocellulitis and inflammatory skin conditions, and keeping cancer patients on needed therapies.^36-38 Despite this clear value added, a cross-sectional analysis of inpatient Medicare claims data from January 2013 to December 2019 found that the number of dermatologists performing more than 10 inpatient consults per year decreased from 356 to 281.³⁹ Additionally, medical centers in which dermatology encounters occurred decreased from 239 to 157 during the same period. Ninety-eight percent of inpatient dermatologists were in metropolitan areas, with large regions lacking access to inpatient dermatology consultation altogether.³⁹

A survey of Society for Pediatric Dermatology members similarly characterized the state of the pediatric dermatology workforce performing hospital consultation.⁴⁰ Seventy-five percent reported a high call burden, defined as more than 11 days or nights per month, more than 1 weekend per month, and/or more than 5 hours per week seeing patients. Ninety-one percent of consultation services are based within academic institutions, reflecting disparities in access.⁴⁰ A prospective cohort study of academic pediatric dermatologists reported that 310 curbside consultations were performed over 24 weeks; of these calls, 17% occurred during weeknights and 23% on weekends. None of these curbside interactions was reimbursed.⁴¹ These findings underscore the burden of uncompensated time a subset of pediatric dermatologists dedicates to inpatient consultations, highlighting the need for improved financial and administrative support and an increased number of physicians performing this role.

A survey study⁴² suggested that unfamiliarity with the inpatient setting, rather than medical knowledge, is the most important barrier to inpatient work among clinical dermatologists. Proposed interventions include resource guides (eg, hospital maps, pager numbers for key individuals, and protocols for urgent specimens). Reference guides and refresher courses may decrease gaps in knowledge or awareness among dermatologists in ambulatory practice.⁴² Another way to bolster the inpatient dermatology workforce may be to provide more guidance to qualified advanced practice providers to triage and address dermatologic emergencies.⁴³

Artificial intelligence (AI) also has been explored as a tool for diagnosing complex dermatologic conditions. One study presented 15 published inpatient dermatology cases to 7 dermatologists. Participants were asked to formulate their top 3 differential diagnoses and were then shown AI-generated differentials and asked to submit a revised differential. Participants showed a diagnostic accuracy of 69% before seeing the AI-generated differential diagnosis and 79% after; however, in cases in which the AI differential was incorrect, diagnostic accuracy of the dermatologists decreased after being shown the AI model.⁴⁴

Final Thoughts

This January 2024 to December 2025 review of research relevant to hospital dermatology highlights important developments and ongoing challenges in SCARs, emerging and re-emerging infectious diseases, HS, and the inpatient dermatology workforce. Dermatologists continue to play a critical role in the care of hospitalized patients with skin disease.