Biologic Therapy May Reshape Blood Clot Risk in Hidradenitis Suppurativa Over Time

Hidradenitis suppurativa has long been understood as a disease of the skin, but researchers increasingly view it as a systemic inflammatory condition with consequences that reach far beyond painful nodules and abscesses in the armpits, groin, and beneath the breasts. A new research letter published in the Archives of Dermatological Research adds an important dimension to that evolving picture by examining how the risk of venous thromboembolism, a category that includes deep vein thrombosis and pulmonary embolism, changes over time in patients with hidradenitis suppurativa who are treated with biologic therapy. The work, led by Seo Won Cho and Jennifer Yoon of Texas A&M University Naresh K. Vashisht College of Medicine together with colleagues at Baylor University Medical Center and Clarity Dermatology in Dallas, arrives at a moment when clinicians are under growing pressure to understand not just whether biologics clear skin, but what they do to the rest of the body.

The study is a retrospective analysis built on TriNetX, a large federated database of deidentified electronic health records drawn from participating health care organizations. Because the platform is compliant with HIPAA and contains only deidentified information, the authors note that institutional review board approval was not required for their analysis. Retrospective database studies of this kind have become a workhorse of dermatologic outcomes research, allowing investigators to assemble cohorts far larger than any single medical center could provide. In this case, the scale matters because venous thromboembolism is a relatively uncommon event in any given year, and detecting how its risk shifts across the timeline of biologic treatment requires thousands of patient records followed over months and years.

The clinical stakes are grounded in a decade of accumulating evidence that patients with hidradenitis suppurativa carry an elevated baseline risk of cardiovascular and thrombotic disease. A large-scale, propensity-matched global retrospective cohort study published in 2024 in the International Journal of Dermatology by Krajewski and colleagues documented increased rates of cardiovascular disorders among patients with the condition. Separately, a multicenter retrospective cohort study published in the Journal of the American Academy of Dermatology in 2024, led by Garate and colleagues, found an association between hidradenitis suppurativa and an increased risk of venous thromboembolism. The Lancet’s comprehensive 2025 review of the disease, authored by Sabat, Alavi, Wolk and colleagues, cemented the framing of hidradenitis suppurativa as a chronic inflammatory disorder with systemic comorbidities rather than a purely cutaneous one.

The biological plausibility of a link between chronic inflammation and clotting is one of the more compelling threads in modern vascular medicine. Tumor necrosis factor alpha, a pro-inflammatory cytokine that sits at the center of hidradenitis suppurativa’s inflammatory cascade, is known to act on the endothelial cells that line blood vessels. Research published in Thrombosis and Haemostasis in 2014 by Lee and colleagues demonstrated that tumor necrosis factor receptor-1 signaling and the nuclear factor kappa B pathway drive the production of pro-inflammatory microparticles in endothelial cells exposed to tumor necrosis factor alpha. These microparticles are small membrane-bound vesicles that can promote coagulation, providing a mechanistic route by which a chronically inflamed state could translate into a hypercoagulable bloodstream. In other words, the same molecular signals that produce the disease’s characteristic inflammatory lesions may also tilt the hemostatic system toward clot formation.

This mechanistic backdrop is precisely why biologic therapy introduces such an interesting question. Tumor necrosis factor inhibitors such as adalimumab, which is approved for moderate to severe hidradenitis suppurativa, neutralize the cytokine that fuels both the skin disease and, potentially, the prothrombotic endothelial state. If tumor necrosis factor drives microparticle release and endothelial activation, then blocking it might be expected to lower thrombotic risk over time. Yet the picture is unlikely to be static. Drug-tolerant assays have revealed that circulating tumor necrosis factor levels change dynamically during adalimumab treatment, as Berkhout and colleagues reported in Science Translational Medicine in 2019, and the trajectory of inflammation during the first months of therapy may differ substantially from the state achieved after a year or more of sustained disease control. Risk, in other words, is not a fixed number but a curve.

That temporal framing is the distinguishing feature of the new research letter. Rather than asking simply whether patients on biologics experience more or fewer venous thromboembolic events than untreated patients, the Dallas-based team set out to characterize how risk changes across the course of therapy. The distinction is more than academic. A treatment that carries an early signal of thrombotic events but becomes protective with sustained use would demand a very different monitoring strategy than one whose risk accumulates steadily with duration of exposure. Conversely, if biologic therapy suppresses the inflammatory driver of hypercoagulability, the expected pattern would be a gradual decline in thromboembolic events as patients achieve and maintain disease control. The answer has direct implications for how dermatologists counsel patients starting biologics, how long clinicians should remain vigilant for warning symptoms, and whether concomitant measures to reduce thrombotic risk are ever warranted.

The methodological choices in the study reflect both the strengths and the inherent constraints of large-scale retrospective research. TriNetX allows investigators to define cohorts by diagnosis codes, medication exposures, and outcome codes, then compare event rates across defined windows of follow-up. The deidentified nature of the data protects patient privacy and enables the assembly of cohorts that would be impossible to recruit prospectively for a rare outcome like pulmonary embolism. At the same time, retrospective designs cannot fully eliminate confounding by indication, since patients selected for biologic therapy tend to have more severe disease, longer inflammatory histories, and greater exposure to other risk factors, including smoking, obesity, and prior systemic therapies, all of which themselves influence thrombotic risk. The authors report that the study was conducted without external funding and that all authors disclose no conflicts of interest, and the manuscript followed the principles of the Declaration of Helsinki.

For patients, the practical message is one of awareness rather than alarm. Venous thromboembolism typically announces itself through swelling, pain, or warmth in a leg when a clot forms in a deep vein, or through sudden shortness of breath and chest pain when a clot travels to the lungs. Recognizing that hidradenitis suppurativa itself elevates the baseline risk of these events, independent of treatment, is a crucial piece of patient education that has often lagged behind the field’s understanding of the disease’s systemic nature. The new analysis suggests that the conversation between dermatologist and patient should also include time as a variable: the risk profile of a patient in the first weeks of biologic therapy may not resemble that of the same patient two years later with well-controlled disease.

The research letter also lands in a broader moment of reassessment for dermatologic biologics. As tumor necrosis factor inhibitors, interleukin-17 blockers, and interleukin-23 pathway agents accumulate years of real-world postmarketing experience, the field is moving from questions of efficacy, which have been largely settled by randomized trials, toward questions of long-term safety and comorbidity modification. Whether suppressing key inflammatory cytokines ultimately reduces the excess cardiovascular and thrombotic burden carried by patients with chronic inflammatory skin disease is one of the defining questions of the next decade of dermatology. Studies that dissect risk over time, rather than collapsing it into a single averaged estimate, are the raw material from which that answer will be built.

The full research letter by Cho, Yoon, Malick, Jaros, and Kivelevitch was published in the Archives of Dermatological Research on 30 August 2026, in volume 318 of the journal, and is available under the identifier 10.1007/s00403-026-04823-0. The authors state that the data supporting the findings are available from the corresponding author upon reasonable request. As with all database-driven analyses, the findings will benefit from confirmation in independent cohorts and, ultimately, from prospective studies designed specifically to track thrombotic outcomes in patients initiating biologic therapy. What the study makes unmistakably clear, however, is that the relationship between hidradenitis suppurativa, its treatment, and the clotting system is dynamic, and that understanding that dynamism may prove as important to patient longevity as clearing the skin itself.

Subject of Research: Temporal changes in venous thromboembolism risk during biologic therapy for hidradenitis suppurativa

Article Title: Temporal changes in venous thromboembolism risk with biologic therapy in hidradenitis suppurativa

Article References: Cho, S. W., Yoon, J., Malick, H., Jaros, S., & Kivelevitch, D. (2026). Temporal changes in venous thromboembolism risk with biologic therapy in hidradenitis suppurativa. Archives of Dermatological Research, 318(1), Article 386. https://doi.org/10.1007/s00403-026-04823-0

Image Credits: AI Generated

DOI: 10.1007/s00403-026-04823-0

Keywords: hidradenitis suppurativa, venous thromboembolism, biologic therapy, TNF inhibitors, deep vein thrombosis, pulmonary embolism, inflammation, endothelial dysfunction, TriNetX, retrospective cohort study, dermatology, cardiovascular risk