700 Vascularization in the deep dermis of hidradenitis suppurativa lesions

Abstract

Hidradenitis Suppurativa (HS) is a chronic inflammatory disease with presentation ranging from nodules and abscesses to draining tunnels. Dermal tunnels are unique to HS, and are marked by keratinocyte hyperproliferation and differentiation, raising the question of whether the tunnels are akin to neoplastic structures. Recent data by our lab demonstrated elevated levels of CXCL8 (IL-8), a potent mediator of angiogenesis. CXCL8 staining was especially prominent around HS tunnels. We hypothesized that high levels of CXCL8 and cellular proliferation could lead to neovascularization in the dermis and deep dermis. In this study, we aimed to characterize the angiogenic changes relating to HS and dermal tunnels. Following Institutional Review Board approval, we enrolled untreated Hurley Stage II and III HS patients. Biopsies were taken from lesional, perilesional and nonlesional skin, and control skin was obtained from healthy volunteers. Samples were stratified based on the presence or absence of histologically confirmed dermal tunnels. Neovascularization was assessed via immunohistochemistry. Chemokine levels were analyzed by RT-qPCR from HS biopsies. HS samples showed significantly elevated vascularization compared to control samples. Vessel development was concentrated in the dermis. Neovascularization was extensive but was especially prominent around dermal tunnels and primarily composed of blood vessels. ICAM-1 confirmed widespread inflammatory activation of blood vessels. The association between CXCL8, dermal tunnels and neovascularization supports a model of extensive remodeling in HS tunnels. Positive ICAM-1 staining suggests leukocyte transmigration into HS lesions from new vessels. This suggests vascularization may be instrumental in supporting the continuous immune infiltration in HS and may contribute to the chronicity of lesions. Treatments targeting angiogenetic pathways may be explored to target HS progression.