About

Robert G Micheletti, MD, is an Associate Professor of Dermatology at the Hospital of the University of Pennsylvania. He serves as an Attending Physician at the same hospital and is the Director of the Cutaneous Vasculitis Clinic at the Penn Vasculitis Center. Additionally, he directs the Hidradenitis Suppurativa Specialty Clinic at the University of Pennsylvania and is an active member of the medical staff at Presbyterian Medical Center and Pennsylvania Hospital. Dr. Micheletti is also the Chief of Hospital Dermatology at the University of Pennsylvania and the Chief of Dermatology at Pennsylvania Hospital. He holds a BA from Stanford University and an MD from Duke University School of Medicine. His professional focus includes vasculitis, hidradenitis suppurativa, and dermatologic conditions, with contributions to clinical evaluation, management, and research in these areas.

Research topics

• Medicine
• Dermatology
• Immunology
• Pathology
• Internal medicine
• Intensive care medicine
• Psychiatry
• Surgery

Selected publications

• Cutaneous Manifestations of Vasculitis: A Cross‐Sectional Analysis From an International Cohort

  International Journal of Dermatology · 2026-05-21

  article1st authorCorresponding

  The data that support the findings of this study are available on request from the corresponding author. The data are not publicly available due to privacy or ethical restrictions.

  PublisherDOI

• Long-term morbidity and quality of life in survivors of Stevens-Johnson syndrome/toxic epidermal necrolysis spectrum

  British Journal of Dermatology · 2025-09-25

  articleOpen access

  This is one of the largest long-term studies following an SJS/TEN reaction that reports long-term survey-based sequelae and adds to the understanding of SJS/TEN as a condition with chronic complications long beyond the acute reaction. We report significant long-term life impacts among survivors of SJS/TEN in the USA. Additional follow-up and long-term care of this patient population is of the utmost importance.

  PublisherOA PDFDOI

• Managing Hidradenitis Suppurativa with Biologics and Small Molecule Inhibitors

  Dermatologic Clinics · 2025-01-21 · 2 citations

  reviewSenior authorCorresponding
  PublisherDOI

• Outcome measures in Stevens–Johnson syndrome/toxic epidermal necrolysis: a systematic review

  Archives of Dermatological Research · 2025-09-06

  articleSenior author
  PublisherDOI

• 0203 HS progress: Baseline characteristics and disease impact

  Journal of Investigative Dermatology · 2025-07-21

  articleOpen access
  PublisherOA PDFDOI

• HLA-B Alleles with Shared Peptide Binding Specificities Define Global Risk of Cotrimoxazole-induced SCAR

  medRxiv · 2025-05-28 · 1 citations

  preprintOpen access

  ABSTRACT Background Co-trimoxazole is a leading global cause of severe cutaneous adverse drug reactions (SCAR) including Stevens-Johnson syndrome/toxic epidermal necrolysis (SJS/TEN) and drug reaction with eosinophilia and systemic symptoms (DRESS). Co-trimoxazole-induced SCAR are associated with HLA class I alleles including HLA-B*13:01 and HLA-B*38:02 in Southeast Asian (SEA) populations. However, the global generalizability of these associations is unknown but critical for population-appropriate risk stratification and diagnosis. Objective To determine HLA risk factors associated with co-trimoxazole-induced SJS/TEN and DRESS in populations from the United States (US) and South Africa (SA). Methods We performed high-resolution HLA typing on dermatologist-adjudicated co-trimoxazole-induced SCAR patients in the US (n=63) and SA (n=26) compared to population controls. Peptide binding and docking analyses were performed using MHCcluster2.0 and CB-Dock2. Results In a multiple logistic regression model, HLA-B*44:03 (Pc<0.001, OR: 4.08), HLA-B*38:01 (Pc<0.001, OR: 5.66), and HLA-C*04:01 (Pc=0.003, OR: 2.50) were independently associated with co-trimoxazole-induced SJS/TEN in the US. HLA-B*44:03 was also associated with co-trimoxazole-induced DRESS in SA (Pc=0.019, OR: 10.69). Distinct HLA-B variants with shared peptide binding specificities (SPBS) and HLA-C*04:01 identified 94% and 78% of co-trimoxazole-induced SJS/TEN and DRESS in the US, respectively. The SEA risk allele HLA-B*13:01, with SPBS to HLA-B*44:03, was identified in just 1/63 US SCAR patients. Conclusion HLA alleles with SPBS to SEA-related risk alleles including HLA-B*44:03 (SPBS with HLA-B*13:01) and HLA-B*38:01 (SPBS with HLA-B*38:02) but also HLA-C*04:01 predisposed to co-trimoxazole-induced SCAR in the US and SA. These findings provide biological plausibility and strategies for global risk prediction and diagnosis of co-trimoxazole-induced SCAR. HIGHLIGHTS BOX What is already known about this topic? HLA alleles including HLA-B*13:01 and HLA-B*38:02 are risk factors for co-trimoxazole-induced SCAR in Asian populations. However, the generalizability of these associations to other global populations is unknown but critical for population-appropriate risk stratification and diagnosis. What does this article add to our knowledge? HLA alleles with shared peptide binding specificities (SPBS) to Asian-related risk alleles including HLA-B*44:03 (SPBS with HLA-B*13:01) and HLA-B*38:01 (SPBS with HLA-B*38:02) but also HLA-C*04:01 predisposed to co-trimoxazole-induced SCAR in the US and South Africa. How does this study impact current management guidelines? HLA alleles previously associated with co-trimoxazole-induced SCAR do not identify risk across populations. However, HLA alleles with SPBS provide biological plausibility and strategies for global and population-appropriate clinical risk stratification and diagnosis of cotrimoxazole-induced SCAR.

  PublisherOA PDFDOI

• Patient-reported outcomes of glucagon-like peptide-1 agonists on hidradenitis suppurativa severity

  JAAD International · 2025-05-29 · 2 citations

  articleOpen access
  PublisherDOI

• SAA1/FPR2 signaling between keratinocytes and neutrophils sustains chronic inflammation in Sweet syndrome

  Journal of Clinical Investigation · 2025-08-19 · 5 citations

  articleOpen access

  Sweet syndrome (also known as acute febrile neutrophilic dermatosis) is a rare inflammatory skin disorder characterized by erythematous plaques with a dense dermal neutrophilic infiltrate. The first-line therapy remains oral corticosteroids, which suppresses inflammation nonspecifically. Although neutrophils are typically short-lived, how they persist in Sweet syndrome skin and contribute to disease pathogenesis remains unclear. Here, we identify a previously unrecognized population of antigen-presenting cell-like (APC-like) neutrophils expressing MHC class II genes that are uniquely present in Sweet syndrome skin but absent in healthy tissue and the circulation. Keratinocytes extended neutrophil lifespan 10-fold in coculture experiments and drove the emergence of an APC-like phenotype in approximately 30% of neutrophils, mirroring observations in patients' lesions. Mechanistically, keratinocyte-derived serum amyloid A1 (SAA1) signals through the formyl peptide receptor 2 (FPR2) on neutrophils to promote their survival. These long-lived neutrophils actively orchestrate local immune responses by recruiting T cells and inducing cytokine production. Strikingly, dual blockade of SAA1/FPR2 signaling restores neutrophil turnover to baseline levels, with efficacy comparable to high-dose corticosteroids. These findings uncover a keratinocyte/neutrophil/T cell axis that sustains chronic inflammation in Sweet syndrome and highlight the SAA1/FPR2 pathway as a promising target for precision therapy.

  PublisherOA PDFDOI

• Development of a Skin-Directed Scoring System for Stevens-Johnson Syndrome and Epidermal Necrolysis

  UNC Libraries · 2025-07-26

  articleOpen access

  Importance: Scoring systems for Stevens-Johnson syndrome and epidermal necrolysis (EN) only estimate patient prognosis and are weighted toward comorbidities and systemic features; morphologic terminology for EN lesions is inconsistent. Objectives: To establish consensus among expert dermatologists on EN terminology, morphologic progression, and most-affected sites, and to build a framework for developing a skin-directed scoring system for EN. Evidence Review: A Delphi consensus using the RAND/UCLA appropriateness criteria was initiated with a core group from the Society of Dermatology Hospitalists to establish agreement on the optimal design for an EN cutaneous scoring instrument, terminology, morphologic traits, and sites of involvement. Findings: In round 1, the 54 participating dermatology hospitalists reached consensus on all 49 statements (30 appropriate, 3 inappropriate, 16 uncertain). In round 2, they agreed on another 15 statements (8 appropriate, 7 uncertain). There was consistent agreement on the need for a skin-specific instrument; on the most-often affected skin sites (head and neck, chest, upper back, ocular mucosa, oral mucosa); and that blanching erythema, dusky erythema, targetoid erythema, vesicles/bullae, desquamation, and erosions comprise the morphologic traits of EN and can be consistently differentiated. Conclusions and Relevance: This consensus exercise confirmed the need for an EN skin-directed scoring system, nomenclature, and differentiation of specific morphologic traits, and identified the sites most affected. It also established a baseline consensus for a standardized EN instrument with consistent terminology.

  PublisherDOI

• HLA-B Alleles With Shared Peptide Binding Specificities Define Global Risk of Co-trimoxazole-Induced Severe Cutaneous Adverse Drug Reactions

  The Journal of Allergy and Clinical Immunology In Practice · 2025-08-08 · 3 citations

  articleOpen access
  PublisherOA PDFDOI

Frequent coauthors

• Arash Mostaghimi

  Brigham and Women's Hospital

  51 shared

• Misha Rosenbach

  University of Pennsylvania

  38 shared

• Helena B. Pasieka

  Unifor

  23 shared

• Megan H. Noe

  Harvard University

  22 shared

• Kanade Shinkai

  University of California, San Francisco

  22 shared

• Daniela Kroshinsky

  Massachusetts General Hospital

  21 shared

• Haley B. Naik

  University of California, San Francisco

  20 shared

• Afsáneh Alavi

  WinnMed

  19 shared

Education

• MD

  Duke University

  2008

• BA

  Stanford University

  2004