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疟疾乳酸酸中毒的病因。

Etiology of lactic acidosis in malaria.

机构信息

Laboratory of Immunoparasitology, Department of Microbiology and Immunology, Rega Institute for Medical Research, KU Leuven, University of Leuven, Belgium.

出版信息

PLoS Pathog. 2021 Jan 7;17(1):e1009122. doi: 10.1371/journal.ppat.1009122. eCollection 2021 Jan.

DOI:10.1371/journal.ppat.1009122
PMID:33411818
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC7790250/
Abstract

Lactic acidosis and hyperlactatemia are common metabolic disturbances in patients with severe malaria. Lactic acidosis causes physiological adverse effects, which can aggravate the outcome of malaria. Despite its clear association with mortality in malaria patients, the etiology of lactic acidosis is not completely understood. In this review, the possible contributors to lactic acidosis and hyperlactatemia in patients with malaria are discussed. Both increased lactate production and impaired lactate clearance may play a role in the pathogenesis of lactic acidosis. The increased lactate production is caused by several factors, including the metabolism of intraerythrocytic Plasmodium parasites, aerobic glycolysis by activated immune cells, and an increase in anaerobic glycolysis in hypoxic cells and tissues as a consequence of parasite sequestration and anemia. Impaired hepatic and renal lactate clearance, caused by underlying liver and kidney disease, might further aggravate hyperlactatemia. Multiple factors thus participate in the etiology of lactic acidosis in malaria, and further investigations are required to fully understand their relative contributions and the consequences of this major metabolic disturbance.

摘要

乳酸酸中毒和高乳酸血症是重症疟疾患者常见的代谢紊乱。乳酸酸中毒会引起生理不良反应,从而加重疟疾的预后。尽管乳酸酸中毒与疟疾患者的死亡率明显相关,但乳酸酸中毒的病因尚不完全清楚。在这篇综述中,讨论了疟疾患者乳酸酸中毒和高乳酸血症的可能病因。乳酸生成增加和乳酸清除受损可能在乳酸酸中毒的发病机制中起作用。乳酸生成增加是由多种因素引起的,包括红细胞内疟原虫的代谢、激活免疫细胞的有氧糖酵解以及寄生虫隔离和贫血导致缺氧细胞和组织中无氧糖酵解的增加。潜在的肝、肾功能障碍导致的肝、肾功能减退可能进一步加重高乳酸血症。因此,多种因素参与了疟疾中乳酸酸中毒的病因,需要进一步研究以充分了解其相对贡献以及这种主要代谢紊乱的后果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4614/7790250/df430f59350d/ppat.1009122.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4614/7790250/c7b9530e0160/ppat.1009122.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4614/7790250/df430f59350d/ppat.1009122.g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4614/7790250/c7b9530e0160/ppat.1009122.g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4614/7790250/df430f59350d/ppat.1009122.g002.jpg

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