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目的:了解单纯慢性乙型肝炎患者与慢性乙型肝炎合并脂肪变性者的肝脏病变特点及临床改变的差异,并寻找与肝纤维化程度改变相关的危险因素.方法:分析275例初治HBsAg阳性患者的肝组织病理情况,依据肝脏病理检查结果将病例分为单纯乙型肝炎组和乙型肝炎合并脂肪变性组,用t检验比较两组患者在年龄、腰围、尿酸、血脂方面的差异,利用多元线性回归法分析各危险因素对肝脏纤维化的影响.统计学处理采用SPSS Statistics17.0统计软件,P<0.05有统计学意义.结果:275例乙型肝炎患者中有脂肪变性者104例.慢性乙型肝炎合并脂肪肝组相比单纯慢性乙型肝炎组在腰围(84.2cm±9.9cm vs 80.1cm±7.8cm,P=0.03),尿酸(325.05μmol/L±98.32μmol/L vs 275.57μmol/L±74.00μmol/L,P=0.001),甘油三酯(1.68mmol/L±1.03mmol/L vs 1.13mmol/L±0.65mmol/L,P=0.001),低密度脂蛋白(2.70mmol/L±0.77mmol/L vs 2.29mmol/L±0.60mmol/L,P=0.001),胆固醇(4.30mmol/L±0.83mmol/L vs 3.97mmol/L±0.79mmol/L,P=0.02)水平上存在统计学意义,合并脂肪变性组相对于单纯慢性乙型肝炎组有着更大的体质量指数.而且单纯慢性乙型肝炎组与脂肪变性组在纤维化水平上存在差异(χ2=5.364,P=0.021).通过多元回归分析发现:年龄,炎症水平分级,饮酒以及HBeAg阴性状态是慢性乙型肝炎患者纤维化进展加重的独立危险因素(均P<0.05);脂肪沉积对肝脏纤维化的影响为负相关,即肝脏纤维化程度较重,脂肪沉积越轻(t=-2.689,P=0.008).结论:肝组织病理及临床资料显示:血脂紊乱,肥胖等代谢综合征是肝细胞脂肪变性的主要原因,而与酒精因素无关.年龄、炎症水平、e抗原阴性状态、饮酒是慢性乙型病毒性肝炎(hepatitis B virus infection,CHB)患者肝组织纤维化进展相关的独立危险因素,但随着纤维化程度的加重,肝细胞脂肪变程度反而减轻.
OBJECTIVE: To investigate the difference of liver lesion characteristics and clinical changes between patients with chronic hepatitis B and those with chronic hepatitis B and to find the risk factors related to the changes of liver fibrosis.Methods: 275 patients with newly diagnosed HBsAg positive According to the results of liver biopsy, the patients were divided into simple hepatitis B group and hepatitis B combined with steatosis group. The difference of age, waist circumference, uric acid and blood lipid between the two groups were compared by t test. Multivariate linear regression analysis of the risk factors of liver fibrosis.Statistical analysis using SPSS Statistics17.0 statistical software, P <0.05 was statistically significant.Results: Of the 275 cases of hepatitis B patients with fatty degeneration in 104 cases. Chronic hepatitis B with fatty liver group compared with chronic hepatitis group only in the waist circumference (84.2cm ± 9.9cm vs 80.1cm ± 7.8cm, P = 0.03), uric acid (325.05μmol / L ± 98.32μmol / L vs 275.57μmol /L ± 74.00μmol / L, P = 0.001), triglycerides (1.68mmol / L ± 1.03mmol / L vs 1.13mmol / L ± 0.65mmol / L, P = 0.001), low density lipoprotein L ± 0.77 mmol / L vs 2.29 mmol / L ± 0.60 mmol / L, P = 0.001), gallbladder (4.30mmol / L ± 0.83mmol / L vs 3.97mmol / L ± 0.79mmol / L, P = 0.02). There was a significant difference between the combined steatosis group and the chronic hepatitis B group Index.And simple chronic hepatitis B group and steatosis group in fibrosis level difference (χ2 = 5.364, P = 0.021) .Multivariate regression analysis found: age, grade of inflammation, drinking and HBeAg negative state is chronic B (All P <0.05). The effect of fat deposition on liver fibrosis was negatively correlated with the severity of hepatic fibrosis and fat deposition (t = -2.689, P = 0.008) .Conclusion: Liver histopathology and clinical data show that metabolic syndrome such as dyslipidemia and obesity are the main causes of fatty degeneration in hepatocytes, but have no relationship with alcoholic factors.Ages, levels of inflammation, negative e antigen and alcohol consumption are chronic B Hepatitis B virus infection (CHB) in patients with liver fibrosis progression-independent risk factors, but with the degree of fibrosis, hepatocellular steatosis but reduced.