Hidradenitis Suppurativa and Bipolar Disorders: A Role for Lithium Therapy?

ing a temporal association between lithium therapy and the initiation or an exacerbation of HS. It has been suggested that the pathophysiology of lithium-induced HS may be similar to that of lithium-induced acneiform and psoriatic lesions [7]. Lithium can inhibit adenyl cyclase and inositol monophosphatase, leading to a decreased intracellular level of cyclic adenosine monophosphate (cAMP) and inositol [8, 9]. It can also inhibit GSK3 (glycogen synthase kinase 3), a factor that activates the transcription factor HIF-1 (hypoxia-induced factor 1) [10]. This results in an increased neutrophilic mass (including neutrophilic infiltration of the epidermidis), the release of lysosomal enzymes, and a keratinocyte proliferation [7–10], leading to the inflammatory cascade and the follicular plugging reported in HS. This series is short and retrospective, making it difficult to draw reliable conclusions. It does, however, reinforce the possible role of lithium therapy in the association between bipolar disorders and HS. Further studies are needed to evaluate both the prevalence of HS among patients with bipolar disorders, and especially those with lithium therapy, and prospectively the temporal link between lithium initiation and HS course of occurrence. The diagnosis and the treatment of bipolar disorders must be considered as a crucial point in the therapeutic management of HS patients.