The potential role of Helicobacter pylori infection in the pathogenesis and exacerbation of psoriasis, with emphasis on E-selectin levels and specific histochemical features; a cross-sectional study

Introduction: Several studies have suggested a potential link between Helicobacter pylori infection and psoriasis; however, the underlying mechanisms remain unclear. One proposed pathway is mediated through endothelial activation and inflammatory responses, potentially indicated by changes in E-selectin expression and related histochemical features. Objectives: To assess the role of H. pylori infection in the expression of E-selectin in psoriasis patients and to evaluate related histological and immunohistochemical changes, aiming to provide insights into psoriasis pathogenesis and potential therapeutic targets. Patients and Methods: A cross-sectional study was conducted on 93 patients with psoriasis, who were evaluated using the Psoriasis Area and Severity Index (PASI), H. pylori IgG antibodies, serum E-selectin levels, histopathological examination, special staining (Masson trichrome), and Ki-67 immunostaining. Patients were categorized into H. pylori-positive (n = 35) and H. pylori-negative (n = 58) groups. Results: H. pylori-positive patients had significantly higher PASI scores (p = 0.007) and elevated E-selectin levels, particularly in severe cases (P < 0.001). Masson trichrome staining showed increased collagen in H. pylori-positive patients (64.3 ± 5%) compared to negative group (53.1 ± 2%), though not statistically significant (P = 0.152). Additionally, Ki-67 expression was significantly lower in H. pylori-positive individuals (0.51 ± 0.01%) than in H. pylori-negative ones (0.92 ± 0.01%, P = 0.04). Conclusion: H. pylori infection may contribute to the development and exacerbation of psoriasis by promoting endothelial activation and inflammation, suggesting its potential role in disease pathogenesis.