The average age of our cohort was 37.05 AE 13.97 years, and mean HS severity at initial presentation was 2.17 AE 1.17 using the 5-point HS-Physician Global Assessment (HS-PGA) scale. The mean serum 25-hydroxyvitamin D [25(OH)D] level at presentation was 23.51 AE 14.74 ng/ml. The mean body mass index (BMI) was 35.49 AE 9.11 kg/m 2 . The average time difference between dates of initial HS visit and 25(OH)D measurement was 127.95 AE 133.64 days. All patients were classified by disease severity (mild: HS-PGA 0-2, n = 135, 68.2%; severe: HS-PGA 3-5, n = 63, 31.8%) as patients with mild disease received similar but narrower treatment regimens while those with severe disease were targeted with more aggressive therapies.Among our variables of interest, numerical rating scale-pain scores (NRS-Pain), CRP, erythrocyte sedimentation rate (ESR), interleukin-6 (IL-6), vitamin D levels, and hypovitaminosis D (<20 ng/ml) were significantly different between mild and severe HS (Table 1). Using logistic regression, hypovitaminosis D was associated with severe HS (OR 5.11; 95% CI [2.60, 10.04]).After adjusting for NRS-Pain, BMI, and inflammatory markers (IL-6, CRP, ESR), hypovitaminosis D remained significantly associated with severe HS (OR 3.77; 95% CI [1.16, 12.28]).Our results suggest that hypovitaminosis D may serve as an indicator of severe HS at initial diagnosis, irrespective of patient race, ethnicity, vitamin D supplementation status, subjective pain scale, BMI, and traditional inflammatory markers. We recognize that the retrospective nature of our study, temporal variation in Vitamin D sampling, and the relatively small sample from a single institution are potential study limitations. Furthermore, unhealthy diet, which may result in both vitamin D deficiency and HS exacerbation, was not assessed. Future studies regarding vitamin D supplementation in the treatment of HS are warranted.