Skin Disease, Silent Metabolism: Large Database Study Links Hidradenitis Suppurativa to Type 2 Diabetes

A chronic, painful skin condition that has long been dismissed as merely a dermatological nuisance may be sending a much louder signal about the state of a patient’s metabolism. A new real-world analysis published in the Archives of Dermatological Research suggests that people living with hidradenitis suppurativa, a debilitating inflammatory disease of the hair follicles, face an increased risk of developing type 2 diabetes compared with the general population. The finding, drawn from a large federated network of electronic health records, adds fresh weight to a growing body of evidence that this skin disease is not confined to the skin at all, but is instead intertwined with systemic metabolic dysfunction.

Hidradenitis suppurativa, often abbreviated as HS, is a chronic inflammatory condition that typically manifests after puberty and targets areas of the body rich in apocrine glands and hair follicles, most commonly the armpits, groin, and beneath the breasts. Patients experience recurrent, deeply painful nodules, abscesses, and draining tunnels beneath the skin known as sinus tracts. The disease is far more than a cosmetic concern: it causes scarring, limits mobility, and exacts a heavy psychological toll, with rates of depression and anxiety markedly elevated among those affected. Epidemiological studies suggest the condition affects somewhere between one and four percent of the population, though many cases likely go undiagnosed because patients are reluctant to seek care for lesions in intimate areas, and clinicians frequently mistake early disease for ordinary boils or acne.

The new research letter, led by Rahib K. Islam of the Louisiana State University Health Sciences Center School of Medicine in New Orleans, together with colleagues at LSU, Tulane University School of Medicine, and Central State University in Ohio, took advantage of TriNetX, a global health research network that aggregates de-identified electronic medical records from large numbers of healthcare organizations. Platforms of this kind allow investigators to identify cohorts of patients with a particular diagnosis, match them to controls with remarkable precision, and then track downstream outcomes across millions of records. In this case, the team queried the network for patients carrying a diagnosis of hidradenitis suppurativa and compared their subsequent rates of type 2 diabetes against carefully matched individuals without the skin disease.

The methodological strength of such real-world database studies lies in their matching strategy. Rather than simply comparing raw rates, which can be distorted by differences in age, sex, body weight, and other health conditions, researchers using TriNetX typically employ propensity score matching, a statistical technique that balances the two groups on dozens of demographic and clinical variables simultaneously. When the groups are balanced in this way, any difference in the rate of new diabetes diagnoses becomes far more suggestive of a genuine biological or clinical association rather than a statistical artifact of who happens to end up in a dermatology clinic. The technique cannot prove causation, but it substantially narrows the field of alternative explanations.

The result aligns with a pattern that dermatologists and endocrinologists have been assembling for more than a decade. A 2015 cross-sectional study of more than 3,200 patients with HS published in the British Journal of Dermatology found that the metabolic syndrome, the cluster of abdominal obesity, elevated blood pressure, dyslipidemia, and impaired glucose handling, was strikingly common in this population compared with matched controls. Three years later, a systematic review and meta-analysis in the Journal of the American Academy of Dermatology examined the relationship between hidradenitis suppurativa and diabetes mellitus specifically and reported a consistent positive association across available studies. A separate analysis of United States population data estimated that the prevalence of type 2 diabetes among HS patients was substantially higher than in the general population, even after accounting for body mass index.

What makes the accumulation of evidence compelling is its convergence from different directions: cross-sectional comparisons, meta-analyses of smaller studies, population prevalence estimates, and now a propensity-matched analysis of longitudinal electronic health records. Each study design has distinct weaknesses. Cross-sectional snapshots cannot establish which came first, the skin disease or the metabolic derangement. Meta-analyses inherit the biases of the studies they pool. Database studies depend on the accuracy of diagnostic coding and may miss undiagnosed disease. Yet when independent methods keep pointing in the same direction, the underlying signal becomes increasingly difficult to dismiss as statistical noise.

The biological plausibility of a skin-to-pancreas connection rests on the biology of chronic inflammation. Hidradenitis suppurativa is characterized by follicular occlusion and a dysregulated immune response in which pro-inflammatory signaling molecules, including tumor necrosis factor-alpha, interleukin-1 beta, and interleukin-17, are produced at elevated levels in affected tissue. These cytokines do not remain politely confined to the skin. Tumor necrosis factor-alpha in particular is well known to interfere with insulin signaling, promoting insulin resistance in muscle, liver, and adipose tissue by disrupting the phosphorylation cascades that allow the insulin receptor to do its work. Chronic systemic inflammation, even at low grade, is a recognized contributor to the development of type 2 diabetes, and patients with other chronic inflammatory diseases such as psoriasis and rheumatoid arthritis show similarly elevated cardiometabolic risk.

There is also the question of shared risk factors and treatment effects. Obesity is strongly associated with hidradenitis suppurativa, both as a potential aggravating factor for the skin disease and as the leading modifiable risk factor for type 2 diabetes. Smoking, another common exposure in the HS population, further compounds metabolic risk. Some therapies used for severe HS, including systemic corticosteroids used intermittently for flares, can transiently worsen glycemic control. Disentangling how much of the observed diabetes excess reflects shared lifestyle and anthropometric factors, how much reflects the inflammatory burden of the disease itself, and how much reflects treatment exposure remains one of the central challenges for the field, and precisely the kind of question that large matched cohorts are designed to address.

For clinicians, the practical implication is straightforward even if the causal picture remains incomplete. Patients diagnosed with hidradenitis suppurativa should not be managed as skin cases alone. The North American clinical management guidelines published by the United States and Canadian Hidradenitis Suppurativa Foundations already emphasize a comprehensive, multidisciplinary approach to the disease, acknowledging its systemic dimensions. The accumulating diabetes evidence strengthens the argument that dermatologists caring for HS patients should maintain a low threshold for screening fasting glucose or hemoglobin A1c, particularly in patients with additional risk factors, and that primary care physicians seeing a patient with recurrent boils in typical locations should recognize the diagnosis early rather than after years of misdirected treatment.

The researchers, who report no competing interests and no external funding for the work, note that all authors contributed to and reviewed the analysis, with the lead author performing the data analysis and drafting the manuscript. As with any records-based study, the authors’ findings describe associations in a real-world population rather than mechanisms in a laboratory, and further work will be needed to determine whether aggressive early control of skin inflammation translates into reduced metabolic risk downstream. But the message for the millions of people living with this often-hidden disease is increasingly clear: hidradenitis suppurativa deserves to be treated as a whole-body inflammatory condition, and its reach may extend well beyond the skin to the very systems that regulate blood sugar. Recognizing that connection sooner rather than later could mean catching prediabetes in time to change its course.

Subject of Research: Association between hidradenitis suppurativa and increased risk of type 2 diabetes

Article Title: Increased risk of type 2 diabetes in patients with hidradenitis suppurativa: a real-world analysis using TriNetX

Article References: Islam, R. K., Magharehabed, Y., Pirzadah, H. A., Islam, K. N., Prejean, R., Joseph, J. M., Haas, C. J., Falgout, L. M., & Hilton, D. (2026). Increased risk of type 2 diabetes in patients with hidradenitis suppurativa: a real-world analysis using TriNetX. Archives of Dermatological Research, 318(1), Article 418. https://doi.org/10.1007/s00403-026-04925-9

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04925-9

Keywords: hidradenitis suppurativa, type 2 diabetes, TriNetX, electronic health records, chronic inflammation, metabolic syndrome, insulin resistance, dermatology, endocrinology, propensity score matching, real-world evidence, epidemiology