Irsigler K, Brändle J, Kaspar L, Kritz H, Lageder H, Regal H
Arzneimittelforschung. 1979;29(3):555-9.
The administration of dichloroacetate (DCA) in cases of biguanide-induced lactic acidosis (LA) improves pyruvate oxidation and therefore increases energy production from glucose. Preliminary results of treatment of LA in humans are reported. A continuous fall in pyruvate was observed in all 3 cases after administration of at least 20 g of DCA (4 g i.v. bolus, then continuously 12 g/h). In Case 1, in which no supplementary measures for controlling the acidosis were applied, the acidosis did not improve and the patient died. In Case 2, despite administration of tris-buffer and dialysis, pH-values could not be raised sufficiently. The production of hydrogen ions persisted and lactate continued to rise. This patient also died. Case 3 was admitted in the beginning stages of a phenformin-induced LA, and in this case therapy was successful. The decline in pyruvate was accompanied by a slow fall in lactate, and a further fall in pH was averted. The clinical condition of the patient improved markedly after i.v. administration of a total of 34 g of DCA.
在双胍类药物引起的乳酸性酸中毒(LA)病例中,给予二氯乙酸(DCA)可改善丙酮酸氧化,从而增加葡萄糖的能量生成。本文报告了人类LA治疗的初步结果。在给予至少20 g DCA(静脉推注4 g,然后持续以12 g/h给药)后,所有3例患者的丙酮酸均持续下降。病例1未采取控制酸中毒的补充措施,酸中毒未改善,患者死亡。病例2尽管给予了三羟甲基氨基甲烷缓冲液和透析治疗,pH值仍未能充分升高。氢离子持续产生,乳酸持续上升。该患者也死亡。病例3在苯乙双胍引起的LA早期入院,此例治疗成功。丙酮酸下降的同时乳酸缓慢下降,避免了pH值进一步下降。静脉内总共给予34 g DCA后,患者的临床状况明显改善。