T helper (Th)17 radiation-induced hidradenitis suppurativa.

To the Editor: We read with interest the case report describing the development of hidradenitis suppurativa (HS) lesions after radiation treatment in a patient with uterine adenocarcinoma. The authors provided several thoughts on the possible mechanism behind radiation-induced HS. The purpose of this letter is to provide additional insight about the likely immunologic mechanisms behind radiation-induced HS. The reported case is an example of an abscopal-like effect sharing adenocarcinoma antigens to antigens of apocrine glands of the groin. Abscopal effect is an immune-mediated phenomenon that has been heavily discussed in metastatic melanoma, whereby there is regression of nonirradiated metastatic lesions after irradiation of a distant melanoma tumor location.3, 4 Abscopal effects were also recently reported in advanced melanoma patients after immunotherapy, highlighting the therapeutic implications of this phenomenon.

As the authors point out, apoptosis can be induced by irradiation. It is likely that apoptotic uterine adenocarcinoma cells result in T-cell cross priming after radiation and activate Th17 subset. A recent article points out that Th17 is an important subset in the immunopathogenesis of HS,7, 8 like it is in psoriasis. This case and the article by Matusiak et al make a strong case that HS, like psoriasis, is an autoimmune disease with Th17 and the attendant polymorphonuclear leukocytes involved. Oppman et al identified the p19 third subunit of interleukin (IL)-12, and designated it as IL-23. This finding predicted the potential for treating psoriasis with anti–IL-12 ustekinumab and anti–IL-23 (guselkumab). This case of radiation-induced HS is likely to predict a positive outcome with clinical trials for HS with ustekinumab (IL-12 antagonist), secukinumab (IL-17 antagonist), and guselkumab (IL-23 antagonist).