Budris W A, Roxe D M, Duvel J M
Department of Pharmacy, Northwestern Memorial Hospital, Chicago, IL 60611, USA.
Ann Pharmacother. 1999 Mar;33(3):308-11. doi: 10.1345/aph.18029.
To report a case of high anion gap metabolic acidosis related to infusion of aminocaproic acid (ACA) that temporarily corrected during hemodialysis and resolved upon ACA discontinuation.
A 65-year-old white woman with staphylococcal sepsis complicated by acute renal failure was treated with ACA to control a hemorrhagic coagulopathy. After receiving an initial 5-g bolus of ACA, she received a continuous intravenous infusion of 500 mg/h for just over 5 days, then 250 mg/h for a final 12 hours. Immediately after beginning ACA therapy, she developed a severe anion gap metabolic acidosis that briefly improved after hemodialysis. The condition resolved completely only after the discontinuation of ACA and therapy with a systemic alkalinizer.
ACA is not among the previously identified causes of high anion gap metabolic acidosis. The temporal profile relating anion gap to ACA initiation, hemodialysis treatment, and ACA discontinuation supports causality in this case. The magnitude of increase in the anion gap appears to have been proportional to the dose of ACA.
In patients with renal impairment, ACA administration may produce a dose-related, high anion gap metabolic acidosis that might be reversible during hemodialysis. Insufficient data are available, but when ACA must be used in such patients, a more conservative dosing of ACA should be coupled with close monitoring.
报告一例与氨基己酸（ACA）输注相关的高阴离子间隙代谢性酸中毒病例，该病例在血液透析期间暂时得到纠正，停用ACA后酸中毒得以缓解。
一名65岁白人女性，患有葡萄球菌败血症并伴有急性肾衰竭，接受ACA治疗以控制出血性凝血病。在初始静脉推注5g ACA后，她接受了500mg/h的持续静脉输注，持续时间超过5天，最后12小时为250mg/h。在开始ACA治疗后不久，她出现了严重的阴离子间隙代谢性酸中毒，血液透析后短暂改善。仅在停用ACA并使用全身性碱化剂治疗后，病情才完全缓解。
ACA并非先前已确定的高阴离子间隙代谢性酸中毒的病因之一。阴离子间隙与ACA起始、血液透析治疗及ACA停用之间的时间关系支持本病例中的因果关系。阴离子间隙升高的幅度似乎与ACA剂量成正比。
在肾功能损害患者中，使用ACA可能会产生剂量相关的高阴离子间隙代谢性酸中毒，这种酸中毒在血液透析期间可能是可逆的。现有数据不足，但当必须在此类患者中使用ACA时，应采用更保守的ACA给药方案并密切监测。
