期刊文献+

慢性丙型肝炎患者能量代谢特点分析

Characteristics of energy metabolism in patients with chronic hepatitis C
下载PDF
导出
摘要 目的研究慢性丙型肝炎(CHC)患者能量代谢特点,为临床营养干预治疗提供依据。方法选取首都医科大学附属北京佑安医院2004年12月-2014年9月收治的70例CHC患者及30例健康对照(HC)者为研究对象,应用代谢车进行能量代谢指标测定,包括静息能量消耗(REE)、预测REE(p REE)、呼吸商(RQ),以及碳水化合物氧化率(CHO%)、脂肪氧化率(FAT%)和蛋白质氧化率(PRO%)。计数资料采用χ2检验,计量资料两组比较采用独立样本t检验,三组比较采用单因素方差分析。结果 CHC组REE、REE/p REE(%)分别为(1360.46±467.55)kcal/d、(99.07±32.92)%,与HC组比较差异均无统计学意义(P值分别为0.169、0.660)。CHC组RQ、CHO%分别为0.82±0.06、(35.80±19.56)%,低于HC组(P值均为0.000)。CHC组FAT%、PRO%分别为(46.64±22.76)%、(17.56±8.80)%,高于HC组(P值分别为0.011、0.000)。CHC轻度、中度、重度组REE/p REE(%)分为(93.47±26.57)%、(105.42±37.88)%、(116.09±46.24)%,3组比较差异无统计学意义(P=0.092);RQ分别为0.84±0.06、0.81±0.06、0.78±0.05,3组比较差异有统计学意义(P=0.001)。不同基因分型肝损伤程度差异无统计学意义(P=0.312),1b基因型组RQ为0.81±0.06、低于非1b基因型组0.85±0.06,差异有统计学意义(P=0.010)。结论 CHC患者REE总体呈正常代谢状态,随着肝损伤程度加重,REE增加;CHC患者存在营养物质代谢障碍,以FAT%及PRO%上升,CHO%降低为主,与肝功能损伤程度及基因分型有一定相关性。 Objective To characterize the energy metabolism in patients with chronic hepatitis C (CHC)and to provide a basis for clinical nutrition intervention.Methods This study included 70 cases of chronic hepatitis C (CHC)admitted to Beijing YouAn Hospital affiliated to Capital Medical University from December 2004 to September 2014,as well as 30 healthy controls (HCs).Energy metabolism indices were measured with the critical care management system,including resting energy expenditure (REE),predicted resting energy expenditure (pREE),respiratory quotient (RQ)and carbohydrate oxidation rate (CHO%),fat oxidation rate (FAT%),and protein oxidation rate (PRO%).Comparison of categorical data was made by chi -square test;for continuous data,comparison between two groups was made by independent -samples t test,while comparison between three groups by one -way analysis of variance.Results REE and REE /pREE (%)in the patients with CHC were 1360.46 ±467.55 kcal/d and 99.07% ±32.92%,respectively,without significant differences com-pared with those in HCs (P =0.169;P =0.660).RQ of 0.82 ±0.06 and CHO% of 35.80% ±19.56% in CHC patients were lower than those in HCs.(P =0.000;P =0.000).FAT% and PRO% in the participants with CHC were 46.64% ±22.76% and 17.56% ± 8.80%,respectively,significantly higher than those in HCs (P =0.011;P =0.000).REE /pREE (%)in the CHC patients with mild, moderate,and severe liver injury was 93.47% ±26.57%,105.42% ±37.88%,and 116.09% ±46.24%,respectively;there were no significant differences across the three groups (P =0.092).For the three groups,RQ was 0.84 ±0.06,0.81 ±0.06,and 0.78 ±0.05, respectively,and differed significantly (P =0.001).There were no significant differences in the severity of liver injury between patients with different genotypes (P =0.312).RQ was 0.81 ±0.06 for CHC patients with 1b genotype versus 0.85 ±0.06 for non -1b genotypes (P =0.010).Conclusion Generally,CHC patients show a normal metabolic st
出处 《临床肝胆病杂志》 CAS 2015年第5期716-720,共5页 Journal of Clinical Hepatology
基金 北京市科技计划重大项目(H020920020890) 国家卫计委2014重点建设专科项目(WJWYA-2014-001)
关键词 肝炎 丙型 慢性 能量代谢 hepatitis C,chronic energy metabolism
  • 相关文献

参考文献16

二级参考文献52

  • 1中华医学会肝病学分会,中华医学会感染病学分会.慢性乙型肝炎防治指南[J].传染病信息,2005,18(z1):1-12. 被引量:466
  • 2Fatty Liver and Alcoholic Liver Disease Study Group of the Chinese Liver Disease Association..非酒精性脂肪性肝病诊疗指南[J].中华肝脏病杂志,2006,14(3):161-163. 被引量:1512
  • 3Moucari R, Asselah T, Cazals-Hatem D, et al. Insulin Resistance in chronic hepatitis C: association with genotypes 1 and 4, serum HCV RNA level, and liver fibrosis[J]. Gastroenterology, 2008,134:416-423. 被引量:1
  • 4Zein C O, Levy C, Basu A, et al. Chronic hepatitis C and type II diabetes mellitus:a prospective cross-sectional study [ J ]. Am J Gastoenterology, 2005,100:48-55. 被引量:1
  • 5Grimbert S, Valensi P, Levy-Marchal C, et al. High prevalence of diabetes mellitus in patients with chronic hepatitis C. A case control study[ J]. Gastroenterol Clin Biol,1996, 20:544-548. 被引量:1
  • 6Laskus T, Radkowski M, Wang L F, et al. Search for hepatitis C virus extrahepatic replication sites in patients with acquired immunedeficiency syndrome:specific detection of negative-strand viral RNA in tissues [ J ]. Hepatology, 1998,28 : 1398- 1401. 被引量:1
  • 7Hotamisligil G S, Shargill N S, Spiegelman B M, et al. Adipose expression of tumor necrosis factor-alpha: direct role in obesity-linked insulin resistance[ J]. Science, 1993, 259:87-91. 被引量:1
  • 8Aguirre V, Werner E D, Giraud J, et al. Phosphorylation of Ser307 in insulin receptor substrate-1 blocks interactions with the insulin receptor and inhibits insulin action [ J ]. J Biol Chem, 2002, 277:1531-1537. 被引量:1
  • 9Hotamisligil G S, Peraldi P, Budavari A, et al. IRS-1-mediated inhibition of insulin receptor tyrosine kinase activity in TNF-alpha- and obesity-induced insulin resistance [J ]. Science, 1996,271:665-668. 被引量:1
  • 10Ueki K, Kondo T, Kahn C R, et al. Suppressor of cytokine signaling 1 ( SOCS-1 ) and SOCS-3 cause insulin resistance through Inhibition of tyrosine phosphorylation of insulin receptor substrate proteins by discrete mechanisms [ J ]. Mol Cell Biol, 2004,24:5434- 5446. 被引量:1

共引文献2589

相关作者

内容加载中请稍等...

相关机构

内容加载中请稍等...

相关主题

内容加载中请稍等...

浏览历史

内容加载中请稍等...
;
使用帮助 返回顶部