³27 vücut kitle indeksi, diabetes mellitus, alkol kullanımı, serum trigliserid düzeyi >170 mg/dL) olan hastalar hariç tutulduğunda geriye kalan 50 hastadan 29 (%58)'unda steatoz mevcuttu. Steatozu olmayan ve olan grupta, kombine tedaviye (interferon + ribavirin) kalıcı cevap oranı benzerken (sırasıyla %50 ve %54), monoterapiye (interferon) cevap oranı steatozu olan grupta daha düşüktü (%38.4'e karşı %25, p< 0.05). Tartışma: Kronik C hepatiti yüksek oranda steatozla birlikte seyretmektedir. Konakçıya ait çeşitli metabolik faktörlerin steatozda rolü olduğu gibi virüsün direkt etkisine bağlı olarak da steatoz gelişebilmektedir. Steatoz kombine tedaviye cevap oranlarını değiştirmemektedir.">

Turkiye Klinikleri Journal of Medical Sciences

.: ORIGINAL RESEARCH
Kronik Hepatit C Virüsü Enfeksiyonuna Eşlik Eden Karaciğer Yağlanmasının Konakçı ve Virüse Ait Nedenleri ve Tedavi Cevabına Etkisi
VIRAL AND HOST FACTORS OF LIVER STEATOSIS ASSOCIATED WITH CHRONIC C HEPATITIS AND EFFECT OF STEATOSIS ON ANTIVIRAL TREATMENT
Seyfettin KÖKLÜa, Bahattin ÇİÇEKa, Osman YÜKSELa, Zeki M.Y. KILIÇa
aGastroenteroloji Bölümü, Türkiye Yüksek İhtisas Hastanesi, ANKARA
Turkiye Klinikleri J Med Sci. 2006;26(1):9-14
Article Language: TR
Full Text
ÖZET
 Amaç: Hepatit C virüs enfeksiyonunda karaciğerdeki yağlanmanın, virüs ve konakçıya ait nedenlerini araştırma ve karaciğerdeki yağlanmanın tedavi cevabı üzerindeki etkisinin incelenmesi amaçlandı. Gereç ve Yöntemler: 1994 ve 2002 yılları arasında kronik C hepatiti tanısı almış ve daha önce hiç antiviral tedavi almamış 136 hasta retrospektif olarak değerlendirildi. Karaciğer biyopsisindeki yağlanma düzeyine göre hastalar steatoz olmayan (<%5), hafif steatozlu (%5-29) ve ağır steatozlu (>%30) olarak gruplara ayrıldı. Gruplar steatoz oluşumu ve konakçıya ait risk faktörleri (vücut kitle indeksi, alkol kullanımı, diabetes mellitus ve serum lipid düzeyleri) ve virüse ait faktörler (genotip ve virüs yükü miktarı) yönünden karşılaştırıldı. Steatoz ve karaciğer histopatoloji bulguları (fibrozis ve nekroinflamatuar aktivite) arasındaki ilişki değerlendirildi. Steatozun tedavi cevabına etkisi incelendi. Sonuçlar: Toplam 136 hastanın 85 (%62.5)'inde steatoz [57 (%41.9) hafif ve 28 (%20.6) ağır steatozlu] tespit edildi. Steatoz derecesi ve vücut kitle indeksi arasında anlamlı bir ilişki vardı (p< 0.05). Steatozlu hastalarda oral glukoz tolerans testi bozukluğu daha sıktı (p< 0.05). Steatoz derecesi ve cinsiyet, yaş, alkol kullanımı, diabetes mellitus, serum lipid düzeyleri, karaciğer biyokimyasal testleri, karaciğer histopatoloji bulguları arasında anlamlı bir ilişki kurulamadı. Steatoz derecesi ve virüs yük miktarı arasında ilişki mevcut değildi. Steatoza neden olabilecek konakçı faktörleri (³27 vücut kitle indeksi, diabetes mellitus, alkol kullanımı, serum trigliserid düzeyi >170 mg/dL) olan hastalar hariç tutulduğunda geriye kalan 50 hastadan 29 (%58)'unda steatoz mevcuttu. Steatozu olmayan ve olan grupta, kombine tedaviye (interferon + ribavirin) kalıcı cevap oranı benzerken (sırasıyla %50 ve %54), monoterapiye (interferon) cevap oranı steatozu olan grupta daha düşüktü (%38.4'e karşı %25, p< 0.05). Tartışma: Kronik C hepatiti yüksek oranda steatozla birlikte seyretmektedir. Konakçıya ait çeşitli metabolik faktörlerin steatozda rolü olduğu gibi virüsün direkt etkisine bağlı olarak da steatoz gelişebilmektedir. Steatoz kombine tedaviye cevap oranlarını değiştirmemektedir.

Anahtar Kelimeler: Kronik hepatit C virüs enfeksiyonu, karaciğer yağlanması
ABSTRACT
 Objective: To investigate the role of host and viral factors in the progression of liver steatosis in hepatitis C virus infection, and to evaluate the impact of steatosis on the response to antiviral therapy. Material and Methods: We retrospectively analyzed 136 treatment-naive patients who had received a diagnosis of chronic hepatitis C between 1994 and 2002. Patients were divided into three groups according to the grade of steatosis on liver biopsy: None (<5%), mild (5%-29%) and severe (>30%) steatosis. The groups were compared for host (body mass index, alcohol consumption, diabetes mellitus and serum lipid levels) and viral (genotype and load) factors. Biopsy specimens were assessed for steatosis, necroinflammatory activity and fibrosis. Influence of steatosis on the response to antiviral therapy was investigated. Results: Steatosis was present in 85 (62.5%) of the 136 subjects; 57 (41.9%) mild and 28 (20.6%) severe steatosis. Steatosis correlated with body mass index (p< 0.05). The prevalence of oral glucose intolerance was higher in patients with steatosis (p< 0.05). There was no association between steatosis and sex, age, alcohol consumption, diabetes mellitus, serum lipid levels, liver biochemical tests and histopathological findings. Grade of steatosis was not correlated with viral load. When patients with risk factors for hepatosteatosis (body mass index ³27, diabetes mellitus, alcohol consumption, serum triglycerides level >170 mg/dL) were excluded, 29 (58%) of the remaining 50 patients had steatosis. Prevalence of sustained response to combined therapy (interferon + ribavirin) was similar in groups with and without steatosis (50% and 54% respectively). However, the prevalence of sustained response to monotherapy (interferon) was lower in the steatosis group compared to the group without steatosis (25% versus 38.4%, p< 0.05). Conclusion: Steatosis is frequent in chronic C hepatitis. Viral factors may influence liver steatosis as well as host factors. Steatosis seems not to affect the treatment response to combined therapy.

Keywords: Hepacivirus, hepatitis C, fatty liver

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