Apsner R, Schwarzenhofer M, Derfler K, Zauner C, Ratheiser K, Kranz A
Akutdialyse Klinik für Innere Medizin III, Universitätskliniken Allgemeines Krankenhaus Wien, Osterreich.
Wien Klin Wochenschr. 1997 Feb 28;109(4):123-7.
To compare the utilization of citrate employed as anticoagulant in patients with acute hepatic failure and subjects with normal liver function.
Three patients in acute hepatic failure and normal renal function were studied during therapeutic plasma exchange with citrate containing fresh frozen plasma. Six patients receiving immunapheresis or LDL-apheresis anticoagulated with citrate served as controls. Determinations of serum citrate concentrations, of ionized calcium and blood pH were performed before, during, and after the extracorporeal treatment. Total body clearance and elimination half life were calculated in a two compartment model.
Preinfusion citrate levels were higher in the patients with acute hepatic failure than in the controls (n.s.). The citrate level rose to 1.73 +/- 0.2 mmol/l in the liver patients versus 0.99 +/- 0.1 mmol/l in the healthy subjects (p < 0.03). Total body clearance was markedly reduced in patients with acute hepatic failure (3.31 +/- 0.03 ml/kg/min) as compared with the controls (6.34 +/- 0.16 ml/kg/min) (p < 0.02), the elimination half life (t/2 k1e) was prolonged (49.7 +/- 5.4 vs. 32.9 +/- 1.02 min, p < 0.05). In the controls blood pH rose from 7.4 +/- 0.01 to 7.45 +/- 0.01 (p < 0.05) after citrate infusion, whereas in the liver patients no rise in pH was observed, again reflecting the impairment of citrate metabolism. Ionized calcium was lower in the patients with acute hepatic failure at the beginning (1.01 +/- 0.05 vs. 1.21 +/- 0.04 mmol/l, p < 0.05) and the end (0.68 +/- 0.02 vs. 0.93 +/- 0.04 mmol/l, p < 0.05) of the citrate infusion.
Citrate metabolism is severely impaired and the plasmatic calcium stores are reduced in acute hepatic failure and, thus, the risk of adverse effects is high. Therapeutic infusions of citrate should be restricted in patients with acute hepatic failure and, if necessary, therapy should be closely monitored by repeated measurements of ionized calcium to avoid the development of potentially hazardous hypocalcemia.
比较急性肝衰竭患者与肝功能正常者使用枸橼酸盐作为抗凝剂的情况。
对3例急性肝衰竭且肾功能正常的患者在使用含枸橼酸盐的新鲜冰冻血浆进行治疗性血浆置换期间进行研究。6例接受免疫吸附或低密度脂蛋白吸附且用枸橼酸盐抗凝的患者作为对照。在体外治疗前、治疗期间和治疗后测定血清枸橼酸盐浓度、离子钙和血液pH值。采用二室模型计算全身清除率和消除半衰期。
急性肝衰竭患者输注前的枸橼酸盐水平高于对照组（无统计学差异）。肝衰竭患者的枸橼酸盐水平升至1.73±0.2 mmol/L，而健康受试者为0.99±0.1 mmol/L（p<0.03）。与对照组（6.34±0.16 ml/kg/min）相比，急性肝衰竭患者的全身清除率显著降低（3.31±0.03 ml/kg/min）（p<0.02），消除半衰期（t/2 k1e）延长（49.7±5.4对32.9±1.02分钟，p<0.05）。在对照组中，输注枸橼酸盐后血液pH值从7.4±0.01升至7.45±0.01（p<0.05），而肝衰竭患者未观察到pH值升高，再次反映了枸橼酸盐代谢受损。急性肝衰竭患者在输注枸橼酸盐开始时（1.01±0.05对1.21±0.04 mmol/L，p<0.05）和结束时（0.68±0.02对0.93±0.04 mmol/L，p<0.05）离子钙较低。
急性肝衰竭时枸橼酸盐代谢严重受损，血浆钙储备减少，因此不良反应风险高。急性肝衰竭患者应限制枸橼酸盐的治疗性输注，如有必要，应通过反复测量离子钙密切监测治疗，以避免发生潜在危险的低钙血症。
