Hepatosteatosis is a significant independent risk factor for portal fibrosis in HCV infected patients with genotype 1B

Amaç: Kronik hepatit C infeksiyonlu olgularda karaciğer steatozu varlığı çalışıldı ve steatoz ile hasta faktörleri, viral faktörler ve portal fıbrozis ilişkisi incelendi. Metod: Kronik hepatit C virüs infeksiyon varlığı verifıye edilmiş 20 hasta çalışmaya dahil edildi. Alkol kullanım öyküsü, hepatit B virüs, human immunodeficiency virus varlığı yönünden pozitif seroloji, interferon veya immunsupresiftedavi öyküsü, obesite (vücut kitle indeksi >32 kg/m2), eşlik eden karaciğer hastalığı veya sistemik bir hastalığın olması çalışmadan dışlanma kriterleridir. Hastaya ait parametreler; yaş, cinsiyet, vücut kitle indeksi, serum kolesterol, trigliserid ve ferritin düzeyleridir. Biz ayrıca hepatit C virus genotip ve heaptit C viral yük gibi viral faktörleri de inceledik. Veriler, steatoz varlığına veya yokluğuna, yağlı dejenerasyon ve fıbrotik değişikliğin çeşitli derecelerine bağlı olarak değerlendirildi. Sonuçlar: Hastaların 12'si erkek olup, ortalama hasta yaşı 46.25 ± 11.34 (aralık, 20-61) yıldı. Bütün hastalarda heaptit C virus genotip lb saptandı. Histopatolojik inceleme ile 5 hastada (%20) karaciğerde yağlı değişim yokdu. Bu olguların tümü erkek cinsiyetinde idi. Steatozun derecesi 6 hastada grade 1, 4 hastada grade 2, 5 hastada grade 3 idi. Portal fıbroz 10 hastada grade 1, 5 hastada grade 2, 5 hastada grade 3 olarak bulundu. Steatoz kadın olgularda daha ciddi olarak saptandı (p

HCV genotip 1B ile infekte hastalarda hepatosteatoz portal fibrozis için bağımsız bir risk faktörüdür

Purpose: We studied patients with chronic hepatitis C virus (HCV) infection for the presence of liver steatosis, and examined relationships between steatosis and host factors, viral factors, and portal fibrosis. Methods: Twenty subjects with confirmed chronic HCV infection were enrolled in the study. The exclusion criteria included history of alcohol abuse, serological evidence of hepatitis B virus and/or human immunodeficiency virus, interferon or immunosuppressive treatment, obesity (body mass index >32 kg/m2), concommitant liver disease, or presence of systemic disease. The host parameters studied were age, gender, body mass index, and serum levels of cholesterol, triglyceride, and ferritin. We also investigated viral factors of HCV genotype and serum HCV viral load. Liver biopsy specimens were examined and graded for steatosis and portal fibrosis. Data were analyzed according to presence or absence of steatosis, and on the basis of the various grades of fatty degeneration and fibrotic change. Results: Twelve of the patients were men, and the mean patient age was 46.25 ± 11.34 years (range, 20-61 years). All patients were of HCV genotype lb. Histopathological examination revealed that five patients (20%) had no signs of fatty degeneration in the liver. All these individuals were men. The severity of steatosis was grade 1 in 6, grade 2 in 4, and grade 3 in 5 patients. Portal fibrosis was grade 1 in 10, grade 2 in 5 and grade 3 in 5 patients. Steatosis was more severe in the female subjects (p

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  • Yayın Aralığı: Yılda 4 Sayı
  • Yayıncı: Gazi Üniversitesi Tıp Fakültesi
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