LAUSR

EJD, vol. 30, n◦ 4, July-August 2020 areas affected by seborrheic dermatitis or psoriasis of the scalp [6]. Several reports described the coexistence of AA and psoriasis, with psoriatic lesions that tended to be spared from hair loss, suggesting that patches of clinically active psoriatic lesions involving the scalp could prevent hair loss or induce hair regrowth [7, 8]. The Renbök phenomenon has been hypothesised to result from activation of different T-helper cell (Th) pathways (Th1, Th2, and Th17) with the amplification of an inflammatory pathway and concomitant suppression of other subsets. In HS, as in psoriasis, the interaction between cytokines may play a key role in the competition between the two concomitant immune responses, a phenomenon also known as “duelling cytokines” (described for the first time by Happle in 1980 to explain the therapeutic efficacy of immunomodulatory therapy in the management of AA). Specifically, the Th17 pathway may polarize and recruit T cells, excluding the Th1 subset primarily involved in AA, and exert a nonspecific inhibitory effect on the immune response against hair follicles [9, 10]. Thus, we postulate that in our patient, two events may explain the presence of HS lesions in areas with healthy scalp hair. First, HS inflammatory lesions primarily involved areas with normal hair follicles and second, the HS inflammation antagonized the inflammatory mechanisms involved in AA, inducing hair regrowth. Our case is the first description of the Renbök phenomenon in association with HS. Further investigation into the nature of the relationship between these two disorders is warranted.