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Controversies in Hidradenitis Suppurativa: Bridging Gaps in Science and Practice
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Controversies in Hidradenitis Suppurativa: Bridging Gaps in Science and Practice

A Special Issue of Journal of Clinical Medicine (ISSN 2077-0383) belonging to the section "Dermatology".

Deadline for manuscript submissions: 25 October 2026 | Viewed by 3649

Editors

Dr. Hadar Lev-Tov

E-Mail Website
Guest Editor
Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami, Miami, FL, USA
Interests: dermatology; cutaneous surgery; wound healing; hidradenitis suppurativa (HS)
Dr. Tammy González

E-Mail Website
Guest Editor
Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, Miller School of Medicine, University of Miami, Miami, FL, USA
Interests: dermatology; hidradenitis suppurativa; chronic itch; inflammatory skin disease

Special Issue Information

Dear Colleagues,

Hidradenitis suppurativa (HS) is a chronic, debilitating inflammatory skin disorder marked by painful nodules, abscesses, and sinus tract formation. Despite growing awareness and recent advances, significant controversy persists regarding its underlying mechanisms, optimal treatment strategies, and classification as either a primarily infectious, inflammatory, genetic, or immune-driven disease.

This Special Issue aims to spotlight the most pressing and debated aspects of HS through point–counterpoint style contributions from leading experts across disciplines. Topics will explore key controversies including the following:

  • Infection vs. Inflammation: Revisiting the microbiome’s vs. immune cell role in HS pathogenesis;
  • Genetic vs. Sporadic Origins: Unpacking heritability and disease onset;
  • Medical vs. Surgical Management: Defining the standard of care in complex HS;
  • Innate vs. Adaptive Immunity: Interrogating immune dysregulation and therapeutic targets.

By fostering scientific dialogue across divergent viewpoints, this Special Issue seeks to stimulate research collaboration, inform clinical decision making, and guide the development of consensus in HS care.

Dr. Hadar Lev-Tov
Dr. Tammy González
Guest Editors

Manuscript Submission Information

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Submitted manuscripts should not have been published previously, nor be under consideration for publication elsewhere (except conference proceedings papers). All manuscripts are thoroughly refereed through a single-anonymized peer-review process. A guide for authors and other relevant information for submission of manuscripts is available on the Instructions for Authors page. Journal of Clinical Medicine is an international peer-reviewed open access semimonthly journal published by MDPI.

Please visit the Instructions for Authors page before submitting a manuscript. The Article Processing Charge (APC) for publication in this open access journal is 2600 CHF (Swiss Francs). Submitted papers should be well formatted and use good English. Authors may use MDPI's English editing service prior to publication or during author revisions.

Keywords

  • hidradenitis suppurativa (HS)
  • inflammatory skin disorder
  • controversies
  • treatment strategies
  • science and practice

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Published Papers (4 papers)

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Review

21 pages, 1041 KB  
Review
Intrinsic Dysregulation and Environmental Modifiers in Hidradenitis Suppurativa: Toward an Integrated Pathophysiologic Model
by Dorsa Moslehi, Lannika Johnson, Alexandra P. Charrow and Irena Pastar
J. Clin. Med. 2026, 15(16), 6256; https://doi.org/10.3390/jcm15166256 - 13 Aug 2026
Viewed by 429
Abstract
Hidradenitis suppurativa (HS) is increasingly recognized as a disorder of intrinsic dysregulation at the intersection of genetic susceptibility, host–microbial interactions, and hormonal signaling, with select environmental exposures acting as important secondary modifiers. This narrative review synthesizes mechanistic, clinical, and epidemiologic evidence on intrinsic [...] Read more.
Hidradenitis suppurativa (HS) is increasingly recognized as a disorder of intrinsic dysregulation at the intersection of genetic susceptibility, host–microbial interactions, and hormonal signaling, with select environmental exposures acting as important secondary modifiers. This narrative review synthesizes mechanistic, clinical, and epidemiologic evidence on intrinsic and extrinsic contributors to HS pathogenesis. Genetic susceptibility for HS involves pathways regulating keratinocyte differentiation, epidermal stem cell function, and follicular architecture, including Notch signaling and transcriptional regulators such as SOX9 and KLF5. Microbiome alterations in both lesional and non-lesional skin suggest that early dysbiosis may contribute to follicular occlusion, epithelial disruption, and immune activation. Hormonal signaling, particularly androgen signaling, promotes follicular dysfunction and inflammation during periods of hormonal fluctuation, frequently aligning with the time of disease onset and flares. Environmental exposures vary considerably in the strength of supporting evidence: tobacco use and elevated body mass index have the most robust epidemiologic and mechanistic data, heat and humidity are increasingly recognized as disease activity modifiers, and evidence for air pollution and microplastics is growing. Collectively, these findings support a model in which HS arises from intrinsic follicular dysregulation shaped by genetic, microbial, and hormonal factors, with environmental exposures influencing but unlikely to independently initiate disease. Full article
(This article belongs to the Special Issue Controversies in Hidradenitis Suppurativa: Bridging Gaps in Science and Practice)
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20 pages, 334 KB  
Review
Exposome Versus Genome in HS: How Do We Currently Explain Where Disease Arises from?
by Emily G. Summers, Olivia D. Perez, Christopher J. Sayed and Lynn Petukhova
J. Clin. Med. 2026, 15(14), 5332; https://doi.org/10.3390/jcm15145332 - 8 Jul 2026
Viewed by 683
Abstract
Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease with marked clinical heterogeneity and a multifactorial pathogenesis. Environmental and lifestyle factors, including obesity, tobacco exposure, microbiome dysbiosis, dietary patterns, and plastic-associated endocrine disruptors, have all been linked to HS risk or disease severity. [...] Read more.
Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease with marked clinical heterogeneity and a multifactorial pathogenesis. Environmental and lifestyle factors, including obesity, tobacco exposure, microbiome dysbiosis, dietary patterns, and plastic-associated endocrine disruptors, have all been linked to HS risk or disease severity. However, these exposures alone do not fully explain why only some individuals develop HS, why age at onset and severity vary substantially, or why disease occurs in patients without major identifiable environmental burden. In parallel, genetic studies have demonstrated that inherited susceptibility is a central component of HS pathogenesis. Rare loss-of-function variants in γ-secretase complex genes cause a small subset of familial, autosomal dominant HS, while genome-wide association studies have shown that population-level risk implicates pathways involved in epithelial differentiation, follicular biology, immune signaling, and cutaneous inflammation. Recent work further suggests that common and rare genetic risk may converge on shared biological mechanisms, including γ-secretase-related signaling. While nature vs. nurture arguments dichotomize genetic constitution and environmental exposures, current evidence supports a model in which genetic susceptibility interacts with environmental exposures to shape HS risk, clinical expression, and disease progression. In this review, we examine the evidence supporting both exposomic and genomic contributions to HS and argue that the disease is best understood as arising from their intersection rather than from either domain alone. Full article
(This article belongs to the Special Issue Controversies in Hidradenitis Suppurativa: Bridging Gaps in Science and Practice)
11 pages, 223 KB  
Review
Medical and Surgical Management of Hidradenitis Suppurativa
by John W. Frew and Falk G. Bechara
J. Clin. Med. 2026, 15(13), 5238; https://doi.org/10.3390/jcm15135238 - 4 Jul 2026
Viewed by 958
Abstract
Background: HS is a chronic inflammatory skin disease in which inflammatory nodules and abscesses coexist with tunnels, fibrosis, and scarring. This dual biology explains why medical therapy often improves inflammatory dissease activity without fully addressing fixed tissue damage, whereas surgery can achieve durable [...] Read more.
Background: HS is a chronic inflammatory skin disease in which inflammatory nodules and abscesses coexist with tunnels, fibrosis, and scarring. This dual biology explains why medical therapy often improves inflammatory dissease activity without fully addressing fixed tissue damage, whereas surgery can achieve durable local control but does not treat diffuse inflammatory burden. Contemporary international guidelines increasingly endorse multimodal and medicosurgical care. Objective: To critically compare the evidence supporting medical and surgical management of HS, with emphasis on outcomes, indications, limitations, and clinical decision-making relevant to contemporary practice. Methods: A structured review was undertaken using PubMed/MEDLINE, the Cochrane Library, and major dermatology guideline sources, with searches updated to 7 May 2026. Priority was given to clinical guidelines, systematic reviews and meta-analyses, randomized controlled trials, and higher-quality observational studies. Evidence was synthesized narratively because endpoints, populations, and follow-up intervals differed markedly across medical and surgical studies. Results: Medical evidence is strongest for biologic therapy in moderate-to-severe inflammatory HS. Weekly adalimumab improved week-12 HiSCR in the phase 3 PIONEER trials; secukinumab improved week-16 and week-52 outcomes in SUNSHINE/SUNRISE; and bimekizumab improved week-16 HiSCR50 in BE HEARD I/II. Surgical evidence is strongest for wide excision in structurally advanced disease, particularly when compared with local excision or incision and drainage. Meta-analytic data consistently show lower recurrence after wide excision than after local excision, and lower recurrence after flap or graft reconstruction than after primary closure. Combined therapy is increasingly supported: peri-operative adalimumab improved outcomes in SHARPS, and surgery plus adalimumab outperformed adalimumab alone in a pragmatic 12-month RCT. Conclusions: HS is best managed by matching treatment to disease phenotype. Medical therapy is essential for inflammatory control; surgery is essential for persistent tunnels, fibrosis, and scarred regional disease. The strongest overall clinical position is an integrated, multidisciplinary model in which systemic therapy reduces inflammatory load and surgery definitively treats irreversible tissue damage. Full article
(This article belongs to the Special Issue Controversies in Hidradenitis Suppurativa: Bridging Gaps in Science and Practice)
20 pages, 1350 KB  
Review
A Neuroendocrine–Immune Model of Hidradenitis Suppurativa: Mechanistic Insights into Pain, Pruritus, and Hormonal Triggers
by Sophie M. Bilik, Rebecca E. Kaiser, Jacob Jalal Shawwa, Benjamin Fleischmann, Sierra Simecek, Irena Pastar and Rivka C. Stone
J. Clin. Med. 2026, 15(10), 3820; https://doi.org/10.3390/jcm15103820 - 15 May 2026
Viewed by 955
Abstract
Background/Objectives: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease traditionally viewed through a purely dermatologic lens. However, this perspective fails to explain stress-induced flares, menstrual cycle-linked exacerbations, and severe pain and itch disproportionate to visible cutaneous inflammation. This narrative review synthesizes evidence [...] Read more.
Background/Objectives: Hidradenitis suppurativa (HS) is a chronic inflammatory skin disease traditionally viewed through a purely dermatologic lens. However, this perspective fails to explain stress-induced flares, menstrual cycle-linked exacerbations, and severe pain and itch disproportionate to visible cutaneous inflammation. This narrative review synthesizes evidence supporting a neuroendocrine–immune model of HS pathogenesis, with emphasis on mechanisms underlying pain and itch. Methods: A comprehensive literature search was conducted using PubMed, Scopus, and Web of Science databases (January 1990–September 2025) with terms including hidradenitis suppurativa, neuroendocrine mechanisms, HPA axis, sex hormones, neuropeptides, pain (including nociceptive and neuropathic pain, burning, and dysesthesia), and pruritus (itch). Eligible studies included peer-reviewed research examining hormonal, stress-related, or neuropeptide mechanisms in HS. Data were synthesized into thematic categories: endocrine influences, HPA axis function, neuropeptide signaling, immune crosstalk, and clinical implications. Results: Sex hormones promote follicular occlusion and modulate immune responses, explaining perimenstrual flares. Prolactin amplifies inflammation during stress through immune cell activation. Insulin resistance and adipokine imbalance create pro-inflammatory conditions. Chronic stress induces HPA axis dysfunction with cortisol resistance, exacerbating inflammation. Neuropeptides released from cutaneous nerves amplify immune activation and directly mediate pain and itch. These pathways establish self-perpetuating feedback loops wherein inflammation drives stress, and neuroendocrine dysfunction amplifies immune responses. Conclusions: HS represents a systemic disorder with a strong neuroendocrine–immune component, rather than a purely dermatologic condition. This framework supports multidisciplinary management integrating hormonal therapies, targeted immunomodulation, and stress reduction. Future research should characterize neuroendocrine biomarkers and test combination therapies targeting multiple system nodes. Full article
(This article belongs to the Special Issue Controversies in Hidradenitis Suppurativa: Bridging Gaps in Science and Practice)
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