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Serum leptin and ghrelin in chronic hepatitis C patients with steatosis

机译:慢性丙型肝炎脂肪变性患者的血清瘦素和生长素释放肽

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AIM: To determine the associations between leptin and ghrelin concentrations and sustained virological response (SVR) in chronic hepatitis C patients with steatosis. METHODS: We retrospectively assessed 56 patients infected with hepatitis C virus (HCV) genotype-1 and 40 with HCV genotype-3. Patients with decompensated cirrhosis, and those with other causes of chronic liver disease, were excluded. Serum HCV-RNA concentrations were measured before the initiation of treatment; at weeks 12 (for genotype 1 patients), 24 and 48 during treatment; and 24 wk after the end of treatment. Genotype was determined using INNO-LIPA HCV assays, and serum leptin and ghrelin concentrations were measured using enzyme-linked immunosorbent assay. Biopsy specimens were scored according to the Ishak system and steatosis was graded as mild, moderate, or severe, according to the Brunt classification. RESULTS: Overall, SVR was positively related to the presence of genotype-3, to biopsy-determined lower histological stage of liver disease, and lower grade of steatosis. Patients ≥ 40 years old tended to be less responsive to therapy. In genotype-1 infected patients, SVR was associated with a lower grade of liver steatosis, milder fibrosis, and an absence of insulin resistance. Genotype-1 infected patients who did not achieve SVR had significantly higher leptin concentrations at baseline, with significant increases as the severity of steatosis worsened, whereas those who achieved SVR had higher ghrelin concentrations. In genotype-3 infected patients, SVR was associated only with fibrosis stage and lower homeostasis model assessment insulin resistance at baseline, but not with the degree of steatosis or leptin concentrations. Genotype-3 infected patients who achieved SVR showed significant decreases in ghrelin concentration at end of treatment. Baseline ghrelin concentrations were elevated in responders of both genotypes who had moderate and severe steatosis. CONCLUSION: Increased serum leptin before treatment may predict non-SVR, especially in HCV genotype-1 infected patients, whereas increased ghrelin may predict SVR in genotype-1.
机译:目的:确定瘦素和生长素释放肽浓度与慢性丙型肝炎脂肪变性患者的持续病毒学应答(SVR)之间的关系。方法:我们回顾性评估了56例感染了HCV基因型1的患者和40例HCV基因型3的患者。失代偿性肝硬化和其他原因引起的慢性肝病的患者被排除在外。在开始治疗前测量血清HCV-RNA浓度;在治疗的第12周(对于基因型1的患者)为24和48;治疗结束后24周。使用INNO-LIPA HCV测定法确定基因型,并使用酶联免疫吸附测定法测定血清瘦素和生长素释放肽浓度。根据Ishak系统对活检标本进行评分,根据Brunt分类,将脂肪变性分为轻度,中度或重度。结果:总体而言,SVR与基因型3的存在,活检确定的肝脏疾病的较低组织学阶段和较低的脂肪变性呈正相关。 ≥40岁的患者往往对治疗反应较弱。在感染基因型1的患者中,SVR与较低级别的肝脂肪变性,轻度纤维化和缺乏胰岛素抵抗相关。未达到SVR的被基因型1感染的患者在基线时的瘦素浓度显着较高,随着脂肪变性严重程度的增加,瘦素浓度显着增加,而达到SVR的患者的生长素释放肽浓度更高。在基因型3感染的患者中,SVR仅与基线时的纤维化分期和较低的稳态模型评估胰岛素抵抗有关,而与脂肪变性或瘦素浓度无关。达到SVR的被基因型3感染的患者在治疗结束时显示生长素释放肽浓度显着降低。在患有中度和重度脂肪变性的两种基因型的应答者中,基线生长素释放肽浓度均升高。结论:治疗前血清瘦素水平升高可能预示着非SVR,尤其是在HCV基因型1感染的患者中,而生长素释放肽的升高可能预示了基因型1的SVR。

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