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一例罕见的二甲双胍诱发乳酸性酸中毒合并正常血糖性酮症酸中毒病例。

A Rare Case of Metformin-Induced Lactic Acidosis and Concomitant Euglycemic Ketoacidosis.

作者信息

Shiplett Alex, Mathias Jay

机构信息

Internal Medicine, Wright State University, Dayton, USA.

出版信息

Cureus. 2024 Nov 14;16(11):e73708. doi: 10.7759/cureus.73708. eCollection 2024 Nov.

DOI:10.7759/cureus.73708
PMID:39677160
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11646140/
Abstract

Acidemia arises primarily from the accumulation of carbon dioxide or the loss of bicarbonate, leading to a pH decrease within the body, which can be fatal if severe and not promptly addressed. Metabolic acidemia occurs due to a loss of bicarbonate and can manifest through direct losses of bicarbonate via renal or gastrointestinal routes, or through the accumulation of anions such as lactic acid or ketoacids, leading to an anion gap metabolic acidosis. Many common etiologies for lactic acid and ketoacid generation exist, including medication-induced causes. Metformin-induced lactic acidemia is a well-known, yet rare, complication of metformin usage, but metformin-induced ketoacidemia is not well described. This report presents a case involving a patient with end-stage renal disease (ESRD) who, while taking metformin, developed severe anion gap metabolic acidosis with undetectably high levels of lactic acid and ketones, supporting the potential role of metformin in inducing severe lactic acidosis and ketoacidosis.

摘要

酸血症主要源于二氧化碳的蓄积或碳酸氢盐的丢失,导致体内pH值下降,如果情况严重且未及时处理,可能会致命。代谢性酸血症是由于碳酸氢盐丢失所致,可通过肾脏或胃肠道途径直接丢失碳酸氢盐,或通过乳酸或酮酸等阴离子的蓄积表现出来,从而导致阴离子间隙代谢性酸中毒。乳酸和酮酸生成有许多常见病因,包括药物诱导的原因。二甲双胍诱导的乳酸性血症是二甲双胍使用中一种众所周知但罕见的并发症,但二甲双胍诱导的酮血症尚未得到充分描述。本报告介绍了一例终末期肾病(ESRD)患者的病例,该患者在服用二甲双胍时,出现了严重的阴离子间隙代谢性酸中毒,乳酸和酮水平高得无法检测,这支持了二甲双胍在诱导严重乳酸酸中毒和酮酸中毒中的潜在作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbde/11646140/13f1c5fb0646/cureus-0016-00000073708-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbde/11646140/13f1c5fb0646/cureus-0016-00000073708-i01.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/bbde/11646140/13f1c5fb0646/cureus-0016-00000073708-i01.jpg

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