GLP-1 Medications and Hidradenitis Suppurativa: The Evidence
GLP-1 drugs are showing up in hidradenitis suppurativa research with lower flare rates and fewer biologic escalations. Here's what the 2026 systematic reviews actually found.
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Reviewed by Dr. James Chen, MD, PhD, FACE on July 19, 2026
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Introduction
Hidradenitis suppurativa is one of the most painful conditions in dermatology and one of the least well served by existing treatment. Recurrent deep nodules, abscesses, and draining tunnels form in the armpits, groin, and under the breasts. Patients wait an average of seven to ten years for a diagnosis. Even after diagnosis, the therapeutic ladder is short: antibiotics, hormonal agents, two approved biologics, and surgery.
Against that backdrop, a pattern in the research literature has become hard to ignore. Patients who start GLP-1 medications for obesity or type 2 diabetes keep reporting that their hidradenitis suppurativa gets better — fewer flares, less drainage, less pain. Three separate systematic reviews published in 2026 have now examined whether the pattern holds up.
Evidence: "Treatment consistently resulted in reduced body mass index and disease activity, measured by Hurley-staging and the number of nodules and abscesses. Patients across studies experienced fewer flares and less pain." — Brogaard E, Nielsen VW, Pedersen NH, et al. Science Progress. 2026. DOI: 10.1177/00368504261464855
The evidence is real, but it is entirely observational. No randomized controlled trial of a GLP-1 medication in hidradenitis suppurativa has been completed. What follows is what the existing data supports, what it does not, and how dermatologists are currently using it.
Why Obesity and Hidradenitis Suppurativa Travel Together
The association between hidradenitis suppurativa and excess body weight is among the strongest in inflammatory skin disease. A systematic review and meta-analysis covering 23 studies and 29.6 million patients quantified it alongside the condition's other major risk factors.
Evidence: "Obesity (OR 2.48, 95% CI 1.64–3.74), type 2 diabetes (OR 2.78, 95% CI 2.23–3.47), and smoking (OR 3.10, 95% CI 2.60–3.69) were all significantly associated with hidradenitis suppurativa." — Elzawawi KE, Elmakaty I, Habibullah M, et al. International Wound Journal. 2024. DOI: 10.1111/iwj.70035
Association alone would not justify treating weight as a therapeutic target. Mendelian randomization work has pushed further, using genetic variants as a proxy for lifelong BMI to test causality. Each one-unit increase in BMI raised the odds of hidradenitis suppurativa by roughly 20 percent, a directional finding that observational confounding does not easily explain.
Three mechanisms plausibly connect the two. Mechanical friction and occlusion in skin folds worsen with body habitus. Adipose tissue behaves as an active endocrine organ, secreting IL-17, IL-1β, and TNF-α — the same cytokines that drive hidradenitis suppurativa lesions. And insulin resistance appears to amplify follicular hyperkeratinization, the initiating event in the disease.
That third mechanism matters for interpreting what follows, because it means a drug improving insulin sensitivity could affect the disease through a route independent of weight.
What the 2026 Systematic Reviews Found
Three reviews published this year converge on similar conclusions from overlapping but non-identical evidence bases.
The most detailed, in Science Progress, pooled 12 cohorts and 4 case-based reports. Beyond the clinical improvements, the authors emphasized a mechanistic argument: GLP-1 receptor activation inhibits NF-κB signaling, the master regulator of inflammatory gene transcription in hidradenitis suppurativa lesions. Reductions in systemic inflammatory markers accompanied the clinical gains.
A parallel systematic review in the Journal of Clinical Medicine reached the same clinical endpoint from a patient-reported angle.
Evidence: "HS patients using GLP-1 agonists showed improved clinical course with less pain and suppuration, improved quality of life and mental health, and reduced cardiovascular risk." — Caliezi A, Hosseini A, Wolf R, Seyed Jafari SM. Journal of Clinical Medicine. 2026;15:2909. DOI: 10.3390/jcm15082909
The American Journal of Clinical Dermatology published both a systematic review and a matched-pairs analysis, the latter comparing GLP-1 users against demographically matched hidradenitis suppurativa patients who were not treated.
The Consistency Is the Signal — and the Weakness
Every study points the same direction, which is reassuring. But uniformly positive results across a body of small, open-label, retrospective work is also the signature of publication bias. Case reports of patients whose disease did not improve on semaglutide rarely get written up.
The Population-Level Data
The strongest evidence comes from large database studies, which are less vulnerable to selective reporting than case series.
A retrospective cohort of 74,910 patients with type 2 diabetes examined whether GLP-1 exposure predicted the incidence of inflammatory skin disease. Of the cohort, 14,612 (19.6%) received a GLP-1 receptor agonist.
Evidence: "Patients treated with GLP-1 receptor agonists had significantly lower odds of hidradenitis suppurativa (OR 0.61, 95% CI 0.48–0.76, P < .001) and psoriasis (OR 0.41, 95% CI 0.35–0.48, P < .001)." — Ching LM, Guirguis CA, Iskandar NL, Tung JK. JAAD International. 2025;22:97–99. DOI: 10.1016/j.jdin.2025.07.003
The 39 percent reduction in odds persisted after adjustment for weight, glycemic control, and smoking status. That adjustment is the study's most interesting feature: if the protective effect survived controlling for weight, weight loss is not the whole explanation. The same signal appears in the psoriasis literature, where GLP-1 drugs show similar independent anti-inflammatory effects.
Separate TriNetX analyses have examined downstream treatment decisions rather than symptoms. Patients with hidradenitis suppurativa on GLP-1 medications initiated biologic therapy at lower rates than matched controls — a harder endpoint than a symptom score, since starting adalimumab or secukinumab reflects a clinician's judgment that disease is escalating.
How the Endpoints Compare
| Study design | Endpoint measured | Direction | Strength |
|---|---|---|---|
| Case series / cohorts (n=12–45) | Hurley stage, nodule count, DLQI | Improvement | Weak — open-label, no control |
| Matched-pairs analysis | Disease activity vs matched controls | Improvement | Moderate |
| Retrospective cohort (n=74,910) | New-onset HS incidence | 39% lower odds | Moderate–strong |
| TriNetX analyses | Biologic initiation, healthcare use | Reduced | Moderate — confounding by indication |
No cell in that table contains a randomized trial. Every row carries the same underlying vulnerability: patients who obtain and stay on GLP-1 medications differ systematically from those who do not, in insurance status, engagement with care, and baseline health behaviors.
Weight Loss or Direct Anti-Inflammatory Effect?
This is the central unresolved question, and it has practical consequences.
If the benefit runs entirely through weight loss, then any effective weight-loss intervention should work equally well, and the relevant clinical decision is simply whether a patient with hidradenitis suppurativa and obesity should be treated for the obesity. Bariatric surgery data partly supports this reading — surgical weight loss has long been associated with improvement in the condition, though a subset of patients paradoxically worsen, possibly due to rapid weight loss and redundant skin.
If GLP-1 receptor activation independently suppresses inflammation, the calculus shifts. Weight-neutral or lean patients with hidradenitis suppurativa — roughly a third of cases — might benefit, and the drug becomes a candidate therapy rather than a comorbidity management tool.
Three lines of evidence favor at least a partial direct effect: the persistence of the protective association after weight adjustment in the 74,910-patient cohort, the documented NF-κB inhibition in mechanistic work, and reductions in circulating inflammatory markers that track imperfectly with BMI change. This mirrors what has emerged in broader GLP-1 inflammation research.
None of this is conclusive. Statistical adjustment for weight in observational data is an imperfect instrument, and residual confounding is the default explanation until a trial says otherwise.
The Prescribing Gap
A 2025 analysis of 1,490 patients with psoriasis or hidradenitis suppurativa found that eligibility for GLP-1 therapy and access to it diverge sharply.
Evidence: "890 (59.7%) patients qualified for GLP-1RA therapy (54.9% psoriasis; 72.3% HS)... only 36.4% of eligible patients received counseling, and 22.1% were prescribed GLP-1RA medications." — Granovsky R, Bai A, Ponyatyshyn I, et al. JAAD International. 2025. DOI: 10.1016/j.jdin.2025.12.008
Nearly three-quarters of hidradenitis suppurativa patients in the cohort met eligibility criteria — a higher share than psoriasis patients, reflecting the tighter link with obesity. Dermatologists wrote 0.6 percent of the prescriptions. Primary care physicians handled 64.5 percent of both counseling and prescribing, and among eligible patients who were never counseled, 18 percent had no primary care provider at all and 23.5 percent saw dermatology exclusively.
The structural problem is visible in those numbers: the specialists who see these patients most often are not the ones prescribing, and a meaningful fraction of patients have no other physician to route the conversation to.
Among those who did receive a prescription, tirzepatide (42.7%), semaglutide (41.4%), and dulaglutide (14.4%) predominated. No comparative data exists on whether one outperforms another for skin outcomes.
What This Means Clinically
For a patient with hidradenitis suppurativa who independently qualifies for a GLP-1 medication on obesity or diabetes criteria, the evidence supports treatment. The metabolic indication stands on its own, the observational skin data points consistently in one direction, and the side effect profile is well characterized.
Several practical points follow from the current evidence:
- Timelines are slow. Reported improvement in the case literature accrues over months, tracking weight loss rather than preceding it. This is not a flare treatment.
- It is additive, not a replacement. Nothing in the data supports stopping a biologic. The TriNetX signal suggests GLP-1 use may reduce the need to escalate, which is a different claim.
- Rapid weight loss carries a theoretical risk. Redundant skin in intertriginous areas may increase friction. The bariatric surgery literature documents a paradoxical worsening subset, and whether that extends to pharmacologic weight loss is unstudied.
- Insurance is the practical barrier. Hidradenitis suppurativa is not an approved indication anywhere. Coverage depends entirely on meeting BMI or diabetes criteria.
For lean patients with hidradenitis suppurativa, there is currently no evidence base. The mechanistic argument is interesting; the clinical data does not exist.
Key Takeaways
GLP-1 medications are associated with meaningful improvement in hidradenitis suppurativa across three systematic reviews, a 74,910-patient cohort showing 39 percent lower odds of new-onset disease, and database analyses showing reduced biologic escalation. The consistency across study types is notable.
The evidence remains observational. The mechanism — weight loss versus direct NF-κB-mediated anti-inflammatory action — is unresolved, and the answer determines whether these drugs are a treatment for hidradenitis suppurativa or a treatment for the obesity that aggravates it. Randomized trials are needed and none have reported.
The most actionable finding may be the prescribing gap. Roughly 72 percent of hidradenitis suppurativa patients qualify for GLP-1 therapy on existing metabolic criteria, and fewer than a quarter receive it. Closing that gap requires no new evidence at all.
References
Brogaard E, Nielsen VW, Pedersen NH, Holgersen N, Thomsen SF. Clinical and mechanistic effects of GLP-1 receptor agonists in hidradenitis suppurativa and comorbidities. Science Progress. 2026;109(3). DOI: 10.1177/00368504261464855 PubMed
Caliezi A, Hosseini A, Wolf R, Seyed Jafari SM. Effects of GLP-1 agonists on patients with hidradenitis suppurativa: a systematic review. Journal of Clinical Medicine. 2026;15(8):2909. DOI: 10.3390/jcm15082909
Ching LM, Guirguis CA, Iskandar NL, Tung JK. Decreased incidence of hidradenitis suppurativa and psoriasis in diabetic patients treated with GLP-1 receptor agonists: a retrospective cohort study. JAAD International. 2025;22:97–99. DOI: 10.1016/j.jdin.2025.07.003 PubMed
Elzawawi KE, Elmakaty I, Habibullah M, et al. Hidradenitis suppurativa and its association with obesity, smoking, and diabetes mellitus: a systematic review and meta-analysis. International Wound Journal. 2024;21(9):e70035. DOI: 10.1111/iwj.70035 PubMed
Granovsky R, Bai A, Ponyatyshyn I, Gellatly ZS, Narang J, Cobos G. GLP-1 receptor agonist use in patients with psoriasis or hidradenitis suppurativa. JAAD International. 2025. DOI: 10.1016/j.jdin.2025.12.008
Lam T, Li JN, Lev-Tov H. A matched pairs analysis of GLP-1 receptor agonists in hidradenitis suppurativa. American Journal of Clinical Dermatology. 2026;27:411–413. DOI: 10.1007/s40257-026-01014-5
The impact of GLP-1 receptor agonists on clinical outcomes and healthcare utilization in hidradenitis suppurativa patients: a retrospective cohort study using TriNetX. Journal of the American Academy of Dermatology. 2026;94(3):972–974. DOI: 10.1016/j.jaad.2025.11.017
Last updated: 2026-07-19 Medical review: Dr. James Chen, MD, PhD, FACE
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Written By
Emily Rodriguez
Senior Medical Writer, MPH, RD
Emily Rodriguez is a registered dietitian and public health specialist. She translates complex medical research into accessible, actionable content for patients and healthcare providers.
Medical Reviewer
Dr. James Chen
Endocrinologist, MD, PhD, FACE
Dr. James Chen is a fellowship-trained endocrinologist with expertise in diabetes, metabolism, and hormone-related weight disorders. His research on GLP-1 receptor agonists has been published in leading medical journals.
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