{"title":"慢性乙型肝炎患者代谢综合征与肝脏疾病发生风险的关系","authors":"J. Dongsogo, Christopher Larbie","doi":"10.5897/AJBR2017.0956","DOIUrl":null,"url":null,"abstract":"Metabolic syndrome is a constellation of abnormal glucose and lipid metabolic parameter that increases ones risk of developing cardiovascular diseases. Metabolic profiles have been linked to progression of varying stages of liver disease in chronic hepatitis B infection. The main objective of this prospective cross sectional study was to establish a link between metabolic syndrome indicators and markers of progression of liver disease in chronic hepatitis B infection. This could provide data leading to an alternative to managing the complications of chronic hepatitis B infection by possibly targeting metabolic precursors and their pathways which will be more targeting, sensitive and has minimal treatment complications than the conventional treatment regimes. In all, 200 chronic hepatitis B patients were sampled of which 100 met the United State National Cholesterol Education Program –Adult Treatment Panel III (US NCEP ATP III) 2005 criterion for metabolic syndrome. Anthropometric data and biochemistry analysis were performed. Obesity and dyslipidemia markers except HDL were higher in metabolic syndrome while haematological makers except WBC were lower in metabolic syndrome. Markers of liver carcinogenesis were generally higher in metabolic syndrome and strongly associated (p=0.01) with initial hepatocellular necrosis and cirrhosis stages of liver carcinogenesis than the intermediary fibrosis stages suggesting virologic mechanism may be responsible more for the fibrosis than metabolic factors. Metabolic syndrome was associated with the developing of various hepatitis B related liver complications. A long term study to elucidate viral genomic and dietary contributions to liver complications due to hepatitis B is necessary. \n \n \n \n Key words: Metabolic syndrome, cardiovascular disease, carcinogenesis, anthropometry, chronic hepatitis, dyslipidemia, haematological, hepatocellular, fibrosis.","PeriodicalId":7631,"journal":{"name":"African Journal of Biochemistry Research","volume":"58 1","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2019-02-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Association of metabolic syndrome with the risk of developing liver disease in chronic hepatitis B patients\",\"authors\":\"J. Dongsogo, Christopher Larbie\",\"doi\":\"10.5897/AJBR2017.0956\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"Metabolic syndrome is a constellation of abnormal glucose and lipid metabolic parameter that increases ones risk of developing cardiovascular diseases. Metabolic profiles have been linked to progression of varying stages of liver disease in chronic hepatitis B infection. The main objective of this prospective cross sectional study was to establish a link between metabolic syndrome indicators and markers of progression of liver disease in chronic hepatitis B infection. This could provide data leading to an alternative to managing the complications of chronic hepatitis B infection by possibly targeting metabolic precursors and their pathways which will be more targeting, sensitive and has minimal treatment complications than the conventional treatment regimes. In all, 200 chronic hepatitis B patients were sampled of which 100 met the United State National Cholesterol Education Program –Adult Treatment Panel III (US NCEP ATP III) 2005 criterion for metabolic syndrome. Anthropometric data and biochemistry analysis were performed. Obesity and dyslipidemia markers except HDL were higher in metabolic syndrome while haematological makers except WBC were lower in metabolic syndrome. Markers of liver carcinogenesis were generally higher in metabolic syndrome and strongly associated (p=0.01) with initial hepatocellular necrosis and cirrhosis stages of liver carcinogenesis than the intermediary fibrosis stages suggesting virologic mechanism may be responsible more for the fibrosis than metabolic factors. Metabolic syndrome was associated with the developing of various hepatitis B related liver complications. A long term study to elucidate viral genomic and dietary contributions to liver complications due to hepatitis B is necessary. \\n \\n \\n \\n Key words: Metabolic syndrome, cardiovascular disease, carcinogenesis, anthropometry, chronic hepatitis, dyslipidemia, haematological, hepatocellular, fibrosis.\",\"PeriodicalId\":7631,\"journal\":{\"name\":\"African Journal of Biochemistry Research\",\"volume\":\"58 1\",\"pages\":\"\"},\"PeriodicalIF\":0.0000,\"publicationDate\":\"2019-02-28\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"African Journal of Biochemistry Research\",\"FirstCategoryId\":\"1085\",\"ListUrlMain\":\"https://doi.org/10.5897/AJBR2017.0956\",\"RegionNum\":0,\"RegionCategory\":null,\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"\",\"JCRName\":\"\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"African Journal of Biochemistry Research","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.5897/AJBR2017.0956","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
摘要
代谢综合征是一组糖脂代谢参数异常,可增加患心血管疾病的风险。代谢谱与慢性乙型肝炎感染中肝脏疾病不同阶段的进展有关。这项前瞻性横断面研究的主要目的是建立慢性乙型肝炎感染中代谢综合征指标与肝脏疾病进展标志物之间的联系。这可能会提供数据,导致通过可能靶向代谢前体及其途径来管理慢性乙型肝炎感染并发症的替代方案,这将比传统治疗方案更具针对性,敏感性和治疗并发症最小。总共有200名慢性乙型肝炎患者被抽样,其中100名符合美国国家胆固醇教育计划-成人治疗小组III (US NCEP ATP III) 2005年代谢综合征标准。进行了人体测量数据和生化分析。代谢综合征患者除HDL外肥胖和血脂异常标志物较高,而代谢综合征患者除白细胞外血液学标志物较低。代谢综合征的肝癌标志物普遍较高,且与肝癌的初始肝细胞坏死和肝硬化阶段的相关性强于中间纤维化阶段(p=0.01),提示病毒学机制可能比代谢因素对纤维化的作用更大。代谢综合征与各种乙型肝炎相关肝脏并发症的发生有关。有必要进行一项长期研究,以阐明病毒基因组和饮食对乙型肝炎肝脏并发症的影响。关键词:代谢综合征,心血管疾病,癌变,人体测量学,慢性肝炎,血脂异常,血液学,肝细胞,纤维化
Association of metabolic syndrome with the risk of developing liver disease in chronic hepatitis B patients
Metabolic syndrome is a constellation of abnormal glucose and lipid metabolic parameter that increases ones risk of developing cardiovascular diseases. Metabolic profiles have been linked to progression of varying stages of liver disease in chronic hepatitis B infection. The main objective of this prospective cross sectional study was to establish a link between metabolic syndrome indicators and markers of progression of liver disease in chronic hepatitis B infection. This could provide data leading to an alternative to managing the complications of chronic hepatitis B infection by possibly targeting metabolic precursors and their pathways which will be more targeting, sensitive and has minimal treatment complications than the conventional treatment regimes. In all, 200 chronic hepatitis B patients were sampled of which 100 met the United State National Cholesterol Education Program –Adult Treatment Panel III (US NCEP ATP III) 2005 criterion for metabolic syndrome. Anthropometric data and biochemistry analysis were performed. Obesity and dyslipidemia markers except HDL were higher in metabolic syndrome while haematological makers except WBC were lower in metabolic syndrome. Markers of liver carcinogenesis were generally higher in metabolic syndrome and strongly associated (p=0.01) with initial hepatocellular necrosis and cirrhosis stages of liver carcinogenesis than the intermediary fibrosis stages suggesting virologic mechanism may be responsible more for the fibrosis than metabolic factors. Metabolic syndrome was associated with the developing of various hepatitis B related liver complications. A long term study to elucidate viral genomic and dietary contributions to liver complications due to hepatitis B is necessary.
Key words: Metabolic syndrome, cardiovascular disease, carcinogenesis, anthropometry, chronic hepatitis, dyslipidemia, haematological, hepatocellular, fibrosis.