Definition and research guide
This page combines a MeSH definition, publication statistics and selected research abstracts. It is a starting point for reading the literature, not a medical textbook or a systematic evidence review.
Content available: 4 complete abstracts (947 words), 10 references. Full article text is not stored or reproduced here; follow the PMID, DOI or PMC links to read the original sources and their access terms.
Definition
The inflammation of a sweat gland (usually of the apocrine type). The condition can be idiopathic or occur as a result of or in association with another underlying condition. Neutrophilic eccrine hidradenitis is a relatively rare variant that has been reported in patients undergoing chemotherapy, usually for non-Hodgkin lymphomas or leukemic conditions.
Definition: NLM Medical Subject Headings (MeSH) scope note (Public domain (U.S. National Library of Medicine); attribution requested). View the MeSH record.
Also known as: Hidradenitides; Hidrosadenitis; Hidrosadenitides; Hydradenitis; Hydradenitides; Neutrophilic Eccrine Hidradenitis; Eccrine Hidradenitides, Neutrophilic; Eccrine Hidradenitis, Neutrophilic.
Where it fits in the MeSH classification
- Broader topics
- Sweat Gland Diseases
- Narrower topics
- Hidradenitis Suppurativa
Research landscape
PubMed indexes 4,399 records tagged with the MeSH heading “Hidradenitis” (counts retrieved 2026-11-04). 2,381 of them (54.1%) were published from 2020 onward, and the busiest period so far is 2020 onward with 2,381 records.
Reviews account for 903 records (20.5%) and meta-analyses for 76. Randomized controlled trials number 67 (1.5%) as a share of all records on the topic. Randomized trials make up only a small share of this literature, so much of what is known comes from laboratory, observational or descriptive work.
Show the data
| Period | Records |
|---|---|
| through 1999 | 91 |
| 2000-2009 | 356 |
| 2010-2019 | 1,571 |
| 2020 onward | 2,381 |
Publication-type chart data
| Type | Records | Share |
|---|---|---|
| Reviews | 903 | 20.5% |
| Meta-analyses | 76 | 1.7% |
| Randomized controlled trials | 67 | 1.5% |
Method: PubMed query "Hidradenitis"[MeSH Terms] with publication-type and date filters, retrieved 2026-11-04.
Reading the evidence in bones, joints, muscles and skin
Joint, bone, muscle and skin conditions are often judged by pain scores, function questionnaires, imaging or photographs, and symptoms can fluctuate, so placebo response and natural improvement matter. Imaging changes are common in people without symptoms. Nothing on this page is advice about treatment. Check how outcomes were measured, whether the comparison group received a placebo or usual care, and how long the benefit lasted.
Evidence from open-access studies
These open-access studies come from PubMed’s best-match results for this heading (papers whose main topic it is), ranked here by citation count, with one recent addition. Each abstract is reproduced in full under its recorded open licence so that you can read the authors’ own words. They illustrate the literature; they are not a systematic summary of it. Citation counts measure attention, not reliability or clinical benefit.
| Study / authors | Year | Source label / design | Europe PMC citations | Licence / source |
|---|---|---|---|---|
| IRAK4 degrader in hidradenitis suppurativa and atopic dermatitis: a phase 1 trial | 2023 | Randomized controlled trial Design not recorded in structured metadata | 102 | cc by PMID 37957373 · DOI · PMC10719089 |
| The paradigm of IL-23-independent production of IL-17F and IL-17A and their role in chronic inflammatory diseases | 2023 | Review article Design not recorded in structured metadata | 78 | cc by PMID 37600764 · DOI · PMC10437113 |
| The Role of Hormones in Hidradenitis Suppurativa: A Systematic Review | 2022 | Systematic review Design not recorded in structured metadata | 56 | cc by PMID 36499573 · DOI · PMC9736970 |
| Efficacy and safety of biologics for hidradenitis suppurativa: A network meta-analysis of phase III trials | 2026 | Meta-analysis Design not recorded in structured metadata | 13 | cc by PMID 40062409 · DOI · PMC13014433 |
IRAK4 degrader in hidradenitis suppurativa and atopic dermatitis: a phase 1 trial [1]
Abstract reading summary — source excerpts
- Opening excerpt
- Toll-like receptor-driven and interleukin-1 (IL-1) receptor-driven inflammation mediated by IL-1 receptor-associated kinase 4 (IRAK4) is involved in the pathophysiology of hidradenitis suppurativa (HS) and atopic dermatitis (AD).
- Closing excerpt
- gov identifier: NCT04772885 .
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (231 words)
Toll-like receptor-driven and interleukin-1 (IL-1) receptor-driven inflammation mediated by IL-1 receptor-associated kinase 4 (IRAK4) is involved in the pathophysiology of hidradenitis suppurativa (HS) and atopic dermatitis (AD). KT-474 (SAR444656), an IRAK4 degrader, was studied in a randomized, double-blind, placebo-controlled phase 1 trial where the primary objective was safety and tolerability. Secondary objectives included pharmacokinetics, pharmacodynamics and clinical activity in patients with moderate to severe HS and in patients with moderate to severe AD. KT-474 was administered as a single dose and then daily for 14 d in 105 healthy volunteers (HVs), followed by dosing for 28 d in an open-label cohort of 21 patients. Degradation of IRAK4 was observed in HV blood, with mean reductions after a single dose of ≥93% at 600-1,600 mg and after 14 daily doses of ≥95% at 50-200 mg. In patients, similar IRAK4 degradation was achieved in blood, and IRAK4 was normalized in skin lesions where it was overexpressed relative to HVs. Reduction of disease-relevant inflammatory biomarkers was demonstrated in the blood and skin of patients with HS and patients with AD and was associated with improvement in skin lesions and symptoms. There were no drug-related infections. These results, from what, to our knowledge, is the first published clinical trial using a heterobifunctional degrader, provide initial proof of concept for KT-474 in HS and AD to be further confirmed in larger trials. ClinicalTrials.gov identifier: NCT04772885 .
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37957373 · DOI · PMC10719089
The paradigm of IL-23-independent production of IL-17F and IL-17A and their role in chronic inflammatory diseases [2]
Abstract reading summary — source excerpts
- Opening excerpt
- Interleukin-17 family (IL-17s) comprises six structurally related members (IL-17A to IL-17F); sequence homology is highest between IL-17A and IL-17F, displaying certain overlapping functions.
- Closing excerpt
- Therefore, dual inhibition of IL-17A and IL-17F could provide better outcomes than IL-23 or IL-17A blockade.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (245 words)
Interleukin-17 family (IL-17s) comprises six structurally related members (IL-17A to IL-17F); sequence homology is highest between IL-17A and IL-17F, displaying certain overlapping functions. In general, IL-17A and IL-17F play important roles in chronic inflammation and autoimmunity, controlling bacterial and fungal infections, and signaling mainly through activation of the nuclear factor-kappa B (NF-κB) pathway. The role of IL-17A and IL-17F has been established in chronic immune-mediated inflammatory diseases (IMIDs), such as psoriasis (PsO), psoriatic arthritis (PsA), axial spondylarthritis (axSpA), hidradenitis suppurativa (HS), inflammatory bowel disease (IBD), multiple sclerosis (MS), and asthma. CD4+ helper T cells (Th17) activated by IL-23 are well-studied sources of IL-17A and IL-17F. However, other cellular subtypes can also produce IL-17A and IL-17F, including gamma delta (γδ) T cells, alpha beta (αβ) T cells, type 3 innate lymphoid cells (ILC3), natural killer T cells (NKT), or mucosal associated invariant T cells (MAIT). Interestingly, the production of IL-17A and IL-17F by innate and innate-like lymphocytes can take place in an IL-23 independent manner in addition to IL-23 classical pathway. This would explain the limitations of the inhibition of IL-23 in the treatment of patients with certain rheumatic immune-mediated conditions such as axSpA. Despite their coincident functions, IL-17A and IL-17F contribute independently to chronic tissue inflammation having somehow non-redundant roles. Although IL-17A has been more widely studied, both IL-17A and IL-17F are overexpressed in PsO, PsA, axSpA and HS. Therefore, dual inhibition of IL-17A and IL-17F could provide better outcomes than IL-23 or IL-17A blockade.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 37600764 · DOI · PMC10437113
The Role of Hormones in Hidradenitis Suppurativa: A Systematic Review [3]
Abstract reading summary — source excerpts
- Opening excerpt
- Hidradenitis suppurativa (HS) is a chronic inflammatory disease manifesting in inverse body regions.
- Closing excerpt
- However, further studies are needed to better understand the hormonal relationship in HS.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (191 words)
Hidradenitis suppurativa (HS) is a chronic inflammatory disease manifesting in inverse body regions. In a systematic review, the role of hormones in HS will be presented to better understand the pathomechanisms of HS. The review is based on the PRISMA criteria. Systematic research was carried out using keywords. Subsequently, the data were analyzed based on the clinical response and other relevant information. The main focus of our systematic review was on HS manifestation, exacerbation, sex hormones, antiandrogen therapy, thyroid function, polycystic ovary syndrome, insulin resistance, and adipokines. In HS, there appears to be a dysregulated adipokine release that is shifted towards pro-inflammatory adipokines. Insulin resistance is significantly more common in HS than in healthy patients regardless of BMI, age, and gender. Insulin resistance in HS patients leads to further cardiovascular disease. The mechanism of insulin resistance and role of adipokines should be investigated in future studies to better provide the pathomechanisms of HS. The role of androgens seems to be important in a certain subgroup of female patients. Anti-androgenic therapy can be useful and helpful in some patients. However, further studies are needed to better understand the hormonal relationship in HS.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 36499573 · DOI · PMC9736970
Efficacy and safety of biologics for hidradenitis suppurativa: A network meta-analysis of phase III trials [4]
Abstract reading summary — source excerpts
- Opening excerpt
- BackgroundPhase III clinical trials are designed to evaluate the therapeutic effect of drugs and their superiority over other treatment methods, but biologics for hidradenitis suppurativa (HS) have not been compared head-to-head in phase III studies.
- Closing excerpt
- ConclusionsAmong currently approved biologic agents for moderate-to-severe HS, adalimumab demonstrated the highest efficacy and safety in the first 12-16 weeks of treatment.
- Interpretation limits
- Verbatim excerpts from the authors’ abstract; the closing excerpt may describe a finding, limitation or recommendation. Design, population, effect size and uncertainty have not been independently extracted or appraised. Read the complete abstract and linked paper before interpreting the findings.
Read complete abstract (280 words)
BackgroundPhase III clinical trials are designed to evaluate the therapeutic effect of drugs and their superiority over other treatment methods, but biologics for hidradenitis suppurativa (HS) have not been compared head-to-head in phase III studies.ObjectivesTo evaluate the relative efficacy and safety of biologics for HS in a network meta-analysis including available data from phase III trials.MethodsMEDLINE and Embase were searched for phase III trials investigating the efficacy and/or safety of at least one biologic for moderate-to-severe HS. The odds ratios for reaching an HS Clinical Response 50 (HiSCR50) and for the occurrence of adverse events after 12-16 weeks were compared between treatments.ResultsPIONEER I and II (adalimumab 40 mg weekly vs. placebo), SUNSHINE and SUNRISE (secukinumab 300 mg every 2 vs. 4 weeks vs. placebo) as well as BE HEARD I and II (bimekizumab 320 mg every 2 vs. 4 weeks vs. placebo) with 2731 patients were included. Adalimumab weekly was ranked most effective in reaching a HiSCR50 with significant superiority over secukinumab every 2 weeks (OR = 1.74; 95% confidence interval [CI]: 1.11-2.73) and 4 weeks (OR = 1.72; 95% CI: 1.09-2.7) and insignificant superiority over bimekizumab every 2 weeks (OR = 1.23; 95% CI: 0.74-2.06) and 4 weeks (OR = 1.25; 95% CI: 0.73-2.14). Adalimumab showed the fewest adverse events with significant superiority over bimekizumab every 2 weeks (OR = 0.52; 95% CI: 0.32-0.86) and insignificant superiority over bimekizumab every 4 weeks (OR = 0.79; 95% CI: 0.47-1.33) and secukinumab every 2 weeks (OR = 0.69; 95% CI: 0.45-1.07) and 4 weeks (OR = 0.71; 95% CI: 0.46-1.1).ConclusionsAmong currently approved biologic agents for moderate-to-severe HS, adalimumab demonstrated the highest efficacy and safety in the first 12-16 weeks of treatment.
Abstract reproduced from the open-access article under the recorded cc by licence; © the authors. PMID 40062409 · DOI · PMC13014433
Key reviews and meta-analyses
The most cited review-type papers among PubMed’s best-match results for this heading, listed with bibliographic details only. Follow the links for the full text and access terms.
- Research article Hidradenitis suppurativa: Epidemiology, clinical presentation, and pathogenesis [5]
- Research article Hidradenitis suppurativa: an update on epidemiology, phenotypes, diagnosis, pathogenesis, comorbidities and quality of life [6]
- Research article Comorbidity screening in hidradenitis suppurativa: Evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations [7]
- Research article Prevalence of Hidradenitis Suppurativa: A Systematic Review and Meta-regression Analysis [8]
- Research article Aetiology and pathogenesis of hidradenitis suppurativa [9]
- Research article What causes hidradenitis suppurativa ?-15 years after [10]
Full-text reviews on EvidenceLib
Open-access review articles about this topic, reproduced in full with authors, licence and references.
Hidradenitis suppurativa and its association with obesity, smoking, and diabetes mellitus: A systematic review and meta‐analysis
Khaled E. Elzawawi, Ibrahim Elmakaty, Mohammad Habibullah et al. · International Wound Journal 2024 · CC BY 4.0
Paradoxical Hidradenitis Suppurativa during Biologic Therapy, an Emerging Challenge: A Systematic Review
Angelo Ruggiero, Fabrizio Martora, Vincenzo Picone et al. · Biomedicines 2022 · CC BY 4.0
A systematic review on shared biological mechanisms of depression and anxiety in comorbidity with psoriasis, atopic dermatitis, and hidradenitis suppurativa
Michele Fabrazzo, Salvatore Cipolla, Simona Signoriello et al. · European Psychiatry 2021 · CC BY 4.0
Lipid Alterations and Metabolism Disturbances in Selected Inflammatory Skin Diseases
Julia Nowowiejska, Anna Baran, Iwona Flisiak · International Journal of Molecular Sciences 2023 · CC BY 4.0
References
- Ackerman L, Acloque G, Bacchelli S, Schwartz H, Feinstein BJ, La Stella P, et al.. IRAK4 degrader in hidradenitis suppurativa and atopic dermatitis: a phase 1 trial. . 2023. PMID 37957373 · DOI · PMC10719089
- Navarro-Compán V, Puig L, Vidal S, Ramírez J, Llamas-Velasco M, Fernández-Carballido C, et al.. The paradigm of IL-23-independent production of IL-17F and IL-17A and their role in chronic inflammatory diseases. . 2023. PMID 37600764 · DOI · PMC10437113
- Abu Rached N, Gambichler T, Dietrich JW, Ocker L, Seifert C, Stockfleth E, et al.. The Role of Hormones in Hidradenitis Suppurativa: A Systematic Review. . 2022. PMID 36499573 · DOI · PMC9736970
- Calabrese L, Cartocci A, Rubegni P, French LE, Kendziora B. Efficacy and safety of biologics for hidradenitis suppurativa: A network meta-analysis of phase III trials. . 2026. PMID 40062409 · DOI · PMC13014433
- Goldburg SR, Strober BE, Payette MJ. Hidradenitis suppurativa: Epidemiology, clinical presentation, and pathogenesis. J Am Acad Dermatol. 2020. PMID 31604104 · DOI
- Nguyen TV, Damiani G, Orenstein LAV, Hamzavi I, Jemec GB. Hidradenitis suppurativa: an update on epidemiology, phenotypes, diagnosis, pathogenesis, comorbidities and quality of life. J Eur Acad Dermatol Venereol. 2021. PMID 32460374 · DOI
- Garg A, Malviya N, Strunk A, Wright S, Alavi A, Alhusayen R, et al.. Comorbidity screening in hidradenitis suppurativa: Evidence-based recommendations from the US and Canadian Hidradenitis Suppurativa Foundations. J Am Acad Dermatol. 2022. PMID 33493574 · DOI · PMC8298595
- Jfri A, Nassim D, O'Brien E, Gulliver W, Nikolakis G, Zouboulis CC. Prevalence of Hidradenitis Suppurativa: A Systematic Review and Meta-regression Analysis. JAMA Dermatol. 2021. PMID 34037678 · DOI · PMC8156162
- Wolk K, Join-Lambert O, Sabat R. Aetiology and pathogenesis of hidradenitis suppurativa. Br J Dermatol. 2020. PMID 33048349 · DOI
- Zouboulis CC, Benhadou F, Byrd AS, Chandran NS, Giamarellos-Bourboulis EJ, Fabbrocini G, et al.. What causes hidradenitis suppurativa ?-15 years after. Exp Dermatol. 2020. PMID 33058306 · DOI
About this article
- Sources
- NLM Medical Subject Headings (definition, synonyms); NCBI PubMed (counts, identifiers); Europe PMC (open-access abstracts and citation counts).
- Verification
- Every reference was resolved against PubMed on 2026-11-04; title, year and DOI matched.
- Review state
- automated source verified; no human expert review has been recorded yet.
- Version
- 1, last updated 2026-11-04.
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Evidence strength
EvidenceHelix's computed view of the study designs behind this topic: how common meta-analyses, randomized trials and reviews are, how recent the literature is, and a plain-language reading. It describes the design mix of the literature. It is not a quality appraisal of any study, and it is not medical advice.