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Cutaneous sarcoidosis after Hodgkin lymphoma

(Fig. 1b). No recurrence was noted after a 6-month follow-up. A dozen previously identified IL36RN mutations have been assessed in vitro in terms of their impact on the expression of IL-36Ra protein and inhibition of NFjB, in order to identify a genotype–phenotype association. Null mutations (no protein) were associated with only severe “systemic” conditions (GPP and acute generalized exanthematous pustulosis), whereas hypomorphic mutations (reduced protein expression) were also associated with less severe, localized pustular variants (pustular palmoplantar psoriasis and acrodermatitis continua of Hallopeau). In this context, such mutations may also affect response to treatment. In a few months, four cases of GPP in patients carrying IL36RN mutations with successful IL-17 inhibitor treatment were reported. Cases are described in Table 1. Two of these mutations had been described as null mutations, but the impact on protein expression had not been described for the two other cases. We describe the first case, to the best of our knowledge, of a marked response to secukinumab in a GPP patient carrying a mutation previously reported to be hypomorphic. These findings, although still sparse, suggest that IL-17 inhibitors are effective in the subset of GPP patients carrying IL36RN mutations, with no obvious impact of the type of mutation. However, the respective roles of genetic, epigenetic, and environmental factors that may affect clinical expression and response to treatment are still widely unknown and deserve further research.