Randa Youssef1, Ola Abu-Zeid1, Khadiga Sayed1, Shaimaa Osman1, Dalia Omran2, Arwa El Shafei3, Doaa Ghaith4. 1. Dept. of Dermatology, Faculty of Medicine, Cairo University, Cairo, Egypt. 2. Dept. of Tropical, Faculty of Medicine, Cairo University, Cairo, Egypt. 3. Dept. of Community Medicine, Faculty of Medicine, Cairo University, Cairo, Egypt. 4. Dept. of Clinical and Chemical Pathology, Faculty of Medicine, Cairo University, Cairo, Egypt.
Egypt is one of the highest hepatitis C virus (HCV) prevalent areas worldwide (10–20% of the general population) (1) and some investigators have reported an association between psoriasis and HCV infection (2). Based on these facts, we set to estimate the prevalence of HCV infection and its genetic diversity among Egyptian psoriaticpatients in comparison to the normal population.One hundred psoriaticpatients and 200 healthy volunteers were screened for HCV by detection of anti HCV antibodies using enzyme-linked immunosorbent assay (ELISA); further real time-polymerase chain reaction analysis was performed for HCV seropositive patients for detection of HCV Genotype. The prevalence of HCV infection was significantly higher among psoriaticpatients compared to controls (19% vs 8.5% respectively) (P<0.05). HCV seropositive psoriaticpatients had exhibited more severe degrees of psoriasis, as measured by PASI score, with significant longer duration of systemic treatment for psoriasis (P<0.05), in addition to significantly higher liver enzyme levels than the seronegative psoriaticpatients(P<0.05). HCV genotype IV was the commonest genotype in both groups.Our findings together with those of other researches (2, 3), support the suggestion that HCV infection can be an inducing factor for psoriasis in genetically predisposed individuals. We as well as other investigators point to the impact of HCV infection upon the severity of psoriasis (3, 4) which may be due the effect of HCV infection on the immune system. The significant higher levels of liver enzymes among HCV seropositive psoriaticpatients in our work may be due to the hepatotoxic systemic drugs used to treat psoriasis, or the high levels of interferons in psoriaticpatients (5); which maintain the survival of activated T cells at sites of chronic inflammation, including the liver (6).
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