期刊文献+

Hyperlactatemia in patients with non-acetaminophen-related acute liver failure 被引量:2

Hyperlactatemia in patients with non-acetaminophen-related acute liver failure
下载PDF
导出
摘要 AIM: To characterize hyperlactatemia in patients with non-acetaminophen acute liver failure (ALF) in an attempt to clarify the mechanisms implicated and the role as a prognosis factor. METHODS: In the setting of liver transplantation, 63 consecutive patients with non-acetaminophen acute liver failure were studied in relation to tissue oxygenation, hemodynamic and metabolic parameters. Before and after transplantation, the number of infected patients and outcome were registered. RESULTS: Acute ALF showed higher levels of lactate than subacute ALF (5.4 ± 1 mmol/L versus 2.2 ± 0.6 mmol/L, P= 0.01). Oxygenation parameters were within the normal range. Lactate levels showed good correlation with respiratory quotient (r=0.759, P〈 0.005), mean glucose administration (r= 0.664, P= 0.01) and encephalopathy (r= 0.698, P= 0.02), but not with splanchnic arteriovenous difference in PCO2, pH and the presence of infection (P=0.1). Portal vein lactate was higher (P〈0.05) than arterial and mixed venous lactate, suggesting its production of hyperlactatemia in the intestine and spleen. The presence of infection was an independent predictor of survival. CONCLUSION: Hyperlactatemia is not a prognosis factor due to byproduct of the overall acceleration in glycolysis. 瞄准:为了与 non-acetaminophen 在病人描绘 hyperlactatemia,在一次尝试的尖锐的肝失败(ALF ) 含有澄清机制并且角色作为一个预后因素。方法:在肝移植的背景,有 non-acetaminophen 的 63 个连续病人尖锐的肝失败在与织物氧化的关系被学习,血液动力学、新陈代谢的参数。在移植前后,感染的病人和结果的数字被登记。结果:尖锐 ALF 比稍尖的 ALF 显示出 lactate 的高水平(5.4+/- 1 mmol/L 对 2.2+/- 0.6 mmol/L, P=0.01 ) 。氧化参数在正常范围以内。Lactate 层次与呼吸商显示出好关联(r=0.759, P< 0.005 ) ,吝啬的葡萄糖管理(r=0.664, P=0.01 ) 并且脑病(r=0.698, P=0.02 ) ,然而并非与在 PCO2, pH 和感染(P=0.1 ) 的存在的内脏的动静脉的差别。门静脉 lactate 更高(P< 0.05 ) 比动脉、混合静脉 lactate,在肠和怒气建议它 hyperlactatemia 的生产。感染的存在是幸存的一个独立预言者。结论:Hyperlactatemia 不由于在糖酵解的全面加速的副产品是一个预后因素。
出处 《World Journal of Gastroenterology》 SCIE CAS CSCD 2006年第12期1949-1953,共5页 世界胃肠病学杂志(英文版)
关键词 Hyperlactatemia Non-acetaminophen acuteliver failure Splanchnic hypoperfusion Acute liverfailure 醋氨酚 肝功能障碍 病理机制 临床表现
  • 相关文献

参考文献25

  • 1[1]Makin AJ,Hughes RD,Williams R.Systemic and hepatic hemodynamic changes in acute liver injury.Am J Physiol 1997;272:G617-625
  • 2[2]Bihari D,Gimson AE,Lindridge J,Williams R.Lactic acidosis in fulminant hepatic failure.Some aspects of pathogenesis and prognosis.J Hepatol 1985; 1:405-416
  • 3[3]Bihari D,Gimson AE,Waterson M,Williams R.Tissue hypoxia during fulminant hepatic failure.Crit Care Med 1985;13:1034-1039
  • 4[4]Clemmesen JO,Gerbes AL,Gulberg V,Hansen BA,Larsen FS,Skak C,Tygstrup N,Ott P.Hepatic blood flow and splanchnic oxygen consumption in patients with liver failure.Effect of high-volume plasmapheresis.Hepatology 1999; 29:347-355
  • 5[5]Clemmesen JO,Hoy CE,Kondrup J,Ott P.Splanchnic metabolism of fuel substrates in acute liver failure.J Hepatol 2000; 33:941-948
  • 6[6]Gore DC,O'Grady JG,Schalm S,Williams R.Acute liver failure:redefining the syndromes.Lancet 1993; 342:273-275
  • 7[7]Castells A,Salmeron JM,Navasa M,Rimola A,Salo J,Andreu H,Mas A,Rodes J.Liver transplantation for acute liver failure:analysis of applicability.Gastroenterology 1993; 105:532-538
  • 8[8]Kropf J,Marx AM,Hildebrandt J,Gressner AM.Practical implications of coexistent different technologies in clinical chemical laboratories.Solid phase chemistry and conventional analysis.Eur J Clin Chem Clin Biochem 1991; 29:675-683
  • 9[9]Murphy ND,Kodakat SK,Wendon JA,Jooste CA,Muiesan P,Rela M,Heaton ND.Liver and intestinal lactate metabolism in patients with acute hepatic failure undergoing liver transplantation.Crit Care Med 2001; 29:2111-2118
  • 10[10]Ducey JP,Lamiell JM,Gueller GE.Arterial-venous carbon dioxide tension difference during severe hemorrhage and resuscitation.Crit Care Med 1992; 20:518-522

同被引文献9

引证文献2

二级引证文献5

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