Abstract

Vitamin D exerts functions in skin physiology by modulating keratinocyte proliferation and different immunoregulatory processes.¹ In several dermatoses, vitamin D correlates to disease severity and is significantly lower if compared to healthy subjects.² Hidradenitis suppurativa (HS) is a chronic inflammatory disease characterized by painful suppurating lesions mainly localized in the folds.³ Kelly et al.⁴ conducted the first study assessing vitamin D status in HS, concluding that 75% of patients had vitamin D levels of less than 50 nmol/L compared to 40% of the general population. Subsequently, Guillet et al.⁵ described an association between vitamin D deficiency and HS severity, also reporting a significant decrease of the inflammatory nodules in patients supplemented with vitamin D. The same authors found a correlation between the response to HS therapies and increased vitamin D levels upon supplementation. Likewise, Fabbrocini et al.⁶ found an inverse correlation between vitamin D levels and disease severity in refractory HS and reported the improvement of clinical responsiveness to therapies as directly proportional to the increase of vitamin D level following supplementation. A recent study demonstrated through whole exome sequencing the role of vitamin D metabolism dysfunction in syndromic HS pathogenesis, molecularly reinforcing the clinical observations of the above‐mentioned studies.⁷