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二甲双胍相关乳酸酸中毒与正常血糖性酮症酸中毒合并症

Combined metformin-associated lactic acidosis and euglycemic ketoacidosis.

作者信息

Schwetz Verena, Eisner Florian, Schilcher Gernot, Eller Kathrin, Plank Johannes, Lind Alice, Pieber Thomas R, Mader Julia K, Eller Philipp

机构信息

Department of Internal Medicine, Division of Endocrinology and Diabetology, Medical University of Graz, Auenbruggerplatz 15, 8036, Graz, Austria.

Department of Internal Medicine, Intensive Care Unit, Medical University of Graz, Graz, Austria.

出版信息

Wien Klin Wochenschr. 2017 Sep;129(17-18):646-649. doi: 10.1007/s00508-017-1251-6. Epub 2017 Sep 1.

Abstract

BACKGROUND

In renal failure metformin can lead to lactic acidosis. Additional inhibition of hepatic gluconeogenesis by accumulation of the drug may aggravate fasting-induced ketoacidosis. We report the occurrence of metformin-associated lactic acidosis (MALA) with concurrent euglycemic ketoacidosis (MALKA) in three patients with renal failure.

CASE PRESENTATIONS

Patient 1: a 78-year-old woman (pH = 6.89, lactic acid 22 mmol/l, serum ketoacids 7.4 mmol/l and blood glucose 63 mg/dl) on metformin and insulin treatment. Patient 2: a 79-year-old woman on metformin treatment (pH = 6.80, lactic acid 14.7 mmol/l, serum ketoacids 6.4 mmol/l and blood glucose 76 mg/dl). Patient 3: a 71-year-old man on metformin, canagliflozin and liraglutide treatment (pH = 7.21, lactic acid 5.9 mmol/l, serum ketoacids 16 mmol/l and blood glucose 150 mg/dl). In all patients, ketoacidosis receded on glucose infusion and renal replacement therapy.

CONCLUSION

This case series highlights the parallel occurrence of MALA and euglycemic ketoacidosis, the latter exceeding ketosis due to starvation, suggesting a metformin-triggered inhibition of gluconeogenesis. Affected patients benefit from glucose infusion counteracting suppressed hepatic gluconeogenesis.

摘要

背景

在肾衰竭患者中,二甲双胍可导致乳酸酸中毒。药物蓄积对肝糖异生的额外抑制作用可能会加重禁食诱导的酮症酸中毒。我们报告了3例肾衰竭患者发生二甲双胍相关性乳酸酸中毒(MALA)并伴有正常血糖性酮症酸中毒(MALKA)的情况。

病例报告

患者1:一名78岁女性(pH = 6.89,乳酸22 mmol/L,血清酮酸7.4 mmol/L,血糖63 mg/dl),正在接受二甲双胍和胰岛素治疗。患者2:一名79岁女性,正在接受二甲双胍治疗(pH = 6.80,乳酸14.7 mmol/L,血清酮酸6.4 mmol/L,血糖76 mg/dl)。患者3:一名71岁男性,正在接受二甲双胍、卡格列净和利拉鲁肽治疗(pH = 7.21,乳酸5.9 mmol/L,血清酮酸16 mmol/L,血糖150 mg/dl)。所有患者在输注葡萄糖和进行肾脏替代治疗后,酮症酸中毒均有所缓解。

结论

该病例系列突出了MALA与正常血糖性酮症酸中毒的同时发生,后者超过了饥饿所致的酮症,提示二甲双胍引发了对糖异生的抑制。受影响的患者可通过输注葡萄糖获益,以对抗肝糖异生受抑制的情况。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2151/5599436/8b5caf330215/508_2017_1251_Fig1_HTML.jpg

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