Frequency of seropositivity against infectious agents amongst pemphigus vulgaris patients: a case-control study on Strongyloides stercoralis, Helicobacter pylori, Toxoplasma gondii, Leishmania major, and Epstein-Barr virus.

Abstract

Environmental and genetic factors may contribute to the pathogenesis of pemphigus vulgaris (PV) as an autoimmune disease. We aimed to determine rates of seropositivity for immunoglobulin G (IgG) antibodies against a number of infectious agents in untreated and treated PV patients and in healthy individuals. Eighty-two newly diagnosed untreated PV patients (34 men and 48 women; mean ± standard deviation [SD] age: 44.18 ± 14.43 years) and 36 previously diagnosed patients under immunosuppressive therapy (16 men and 20 women; mean ± SD age: 38.53 ± 9.96 years) were enrolled in the study. The clinical diagnosis of PV was confirmed by histopathology and direct immunofluorescence findings. As a control group, 131 healthy individuals (68 men and 63 women; mean ± SD age: 42.56 ± 19.69 years) were recruited. In all patients and controls, serum IgG antibodies against Strongyloides stercoralis, Helicobacter pylori, Epstein-Barr virus (EBV) capsid antigen, and Leishmania major were measured using enzyme-linked immunosorbent assays. The indirect immunofluorescence test was used to detect IgG antibodies against Toxoplasma gondii. Newly-diagnosed untreated PV patients had significantly higher rates of seropositivity of IgG antibodies against S. stercoralis and H. pylori compared with the control group (69.5% vs. 16.0% [P < 0.001] and 79.3% vs. 59.5% [P = 0.004], respectively). For the other agents, namely T. gondii, L. major, and EBV capsid antigen, the differences between groups in seropositivity for IgG antibodies were not statistically significant. Significant associations between S. stercoralis and H. pylori seropositivity rates and untreated disease led to the hypothesis that these pathogenic agents may contribute to the pathogenesis of PV.