Conclusion
Our study demonstrates for the first time, to our knowledge, that a deficiency of the main innate immunity markers in typical HS sites may explain the development of chronic inflammatory nodules in this disease.
Objective
To evaluate the expression of innate immunity markers at the site of nodules caused by hidradenitis suppurativa (HS). Design: Prospective analysis of 12 patients with HS. Setting: Unité de Cancéro-Dermatologie, Nantes Hospital, Nantes; Service de Dermatologie, Poitiers Hospital, Poitiers; and Service de Dermatologie, Clinique de Courlancy, Reims, France Patients: Twelve patients (Hurley stage I or II) in whom the disease had progressed for at least 6 months and who had a minimum of 2 closed nodules in typical sites. Main outcome measures: Two biopsies were performed at baseline: one in a closed inflammatory nodule and one in healthy adjoining skin. Patients were treated for 3 months with zinc gluconate at a dosage of 90 mg/d. A new biopsy was then performed in the same nodule. Innate immunity markers (toll-like receptors 2, 3, 4, 7, and 9; intercellular adhesion molecule 1; interleukin [IL] 6 and 10; tumor necrosis factor; α melanocyte stimulating hormone; transforming growth factor β; β-defensin 2 and 4; and insulinlike growth factor 1) were studied by immunohistochemical analysis.
Results
We observed significantly decreased expression (P < .001) of all the innate immunity markers studied except IL-10 in nonlesional and lesional HS skin. The downregulation of innate markers was significantly stronger in lesional HS skin compared with normal skin except for tumor necrosis factor. Three months of zinc treatment induced a significant increase in the expression of all the markers involved in innate immunity.