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.
Hidradenitis suppurativa (HS) is a skin disorder of unknown etiology and pathogenesis. Its prevalence is reported to range from 1:300 to 4:100 in the general population.1 It is characterized by the development of nodular inflammatory lesions with a secondary evolution toward abscesses that are mainly localized near the apocrine glands. Recently, 4 mutations were identified in the gene coding for γ-secretase, a transmembrane protease composed of 4 essential protein subunits: 1 catalytic presenilin subunit and 3 cofactor subunits (presenilin enhancer 2, nicastrin, and anterior pharynx defective 1). The 4 mutations have been identified in the genes encoding presenilin 1 (1 deletion) and nicastrin.2
Current theories about HS pathogenesis implicate hyperkeratosis of the follicular epithelium as the hallmark pathogenetic process that leads to the occlusion of the apocrine glands with subsequent follicular rupture, inflammation, and a possible secondary infection by corynebacteria.3 The clinical improvement that results from therapies targeting the tumor necrosis factor (TNF) agrees with this theory of inflammatory pathogenesis because TNF is a major proinflammatory cytokine. The innate immune system plays an important role because it is the first line of defense or the first barrier against foreign organisms and substances. It also plays a role in acute and chronic inflammation. The inflammatory response is a major component or barrier created as part of innate immunity. Therefore, it is highly probable that skin affected by HS has abnormal innate immunity. The present study sought to evaluate the characteristics of various cutaneous innate immunity markers in skin that appeared to be clinically normal and in closed inflammatory nodules in patients with HS before and after 3 months of treatment with zinc gluconate.Case Study Dermatology Genetics Pathology Treatment