Giris ve Amaç: Hepatit C virüsü enfeksiyonunda steatoza yol açan mekanizma karmasiktir. Bizim çalismamizin amaci hepatit C virüsü ile ilgili steatozda adipositokinlerin rolünü arastirmaktir. Gereç & Yöntem: Tedavi edilmemis genotip 1 kronik hepatit C virüslü 65 hasta adipositokinler, beden kitle indeksi, yas, ve insulin direncinin karaciger yaglanmasi ndaki etkilerini degerlendirmek için çalismaya alindi. Bulgular: Yaglanma 31 (%47.7) hastada gözlendi. Fibroza göre adiponektin ve leptin gruplandirildiginda, adiponektin ve leptin arasinda bir fark gözlemlemedik (p sirasiyla 0.597 ve 0.159). Leptin için anlamli bir fark (p=0.021) varken, steatozlu hastalarda adiponektin düzeyleri arasinda bir fark saptamadik (p=0.674). Sonuç: Hiperleptinemi kronik hepatit C virüslü hastalarda steatozun gelisimiyle iliskilidir.
Background and Aims: The mechanism that leads to steatosis in hepatitis C virus infection is complex. The aim of our study was to search the role of adipocytokines in hepatitis C virus-related steatosis. Materials and Methods: Sixty-five untreated genotype 1 chronic hepatitis C virus patients were included in the study to evaluate the effects of adipocytokines, body mass index, age, and insulin resistance on hepatic steatosis. Results: Steatosis was observed in 31 patients (47.7%). When adiponectin and leptin were grouped according to fibrosis, we did not determine a difference between adiponectin and leptin (p values 0.597 and 0.159, respectively). We did not determine a difference in adiponectin levels in patients with different degrees of steatosis (p=0.674), while there was a significant difference for leptin (p=0.021). Conclusions: Hyperleptinemia is related to the development of steatosis in patients with chronic hepatitis C virus.