Polyclonal hyperglobulinemia and elevated acute phase reactants in hidradenitis suppurativa

Abstract

Hidradenitis suppurativa (HS) is a chronic, painful inflammatory skin disease characterized by recurrent nodules and abscesses affecting intertriginous areas including the axilla, inframammary, and anogenital regions. Hurley staging (I-III) is commonly used to classify patients, with mild disease limited to inflammatory cystic nodules (stage I), that may be connected by isolated tunnels/sinuses (stage II), or form a network of bridging tunnels/sinuses (stage III) associated with odiferous, purulent drainage. The cause of HS is unknown but it is generally considered to be multifactorial. It appears that an aberrant innate immune response initiates cutaneous inflammation in early lesions and recruitment of the adaptive immune system may be involved in maintaining HS chronicity.¹ Only a few published studies have focused on the humoral immune system in HS. The sera of patients with advanced HS revealed elevations of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IgE.^2-4 Significantly increased levels of C-reactive protein (CRP) have been found across all three Hurley stages.⁵

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