LAUSR

EJD, vol. 32, n◦ 6, November-December 2022 features compatible with lichenoid drug eruption [3, 6]. The time from initiation of IL-17 blockade to the appearance of a lichenoid eruption varied from less than one week to 21 months, although onset within the first 12 months of therapy occurred in six of seven cases [2–6]. In all cases, secukinumab or ixekizumab was stopped, leading to complete regression of lichenoid lesions with no recurrence in six cases [3–6] and a substantial improvement in one case [2]. In one case, LP did not recur after replacing secukinumab with ixekizumab [5]. Although spontaneously occurring LP cannot be completely ruled out, the association between IL17A inhibitors and lichenoid lesions was supported by the temporal link between LP manifestations and IL-17A inhibitor introduction as well as LP regression after treatment discontinuation. The underlying mechanism of these eruptions remains unknown. It may be similar to that proposed for TNFinhibitors, given that TNFor IL-17 blockade might lead to the activation of plasmacytoid dendritic cells and interferonupregulation, which play a crucial role in LP pathogenesis [4]. In some cases, it is conceivable that anti-IL-17 drugs may have contributed to the development of oral LP by inducing oral candidiasis [3]. To conclude, a growing body of evidence suggests that IL-17 inhibitors can trigger severe mucosal and cutaneous LP. Clinicians should be aware of this rare but serious possible side effect which may warrant drug discontinuation.