COVID-19患者高血压和电解质紊乱

Pub Date : 2020-12-01 Epub Date: 2020-12-28 DOI:10.5049/EBP.2020.18.2.23
Jeong-Hoon Lim, Hee-Yeon Jung, Ji-Young Choi, Sun-Hee Park, Chan-Duck Kim, Yong-Lim Kim, Jang-Hee Cho
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引用次数: 16

摘要

2019年全球冠状病毒病(COVID-19)大流行仍在进行中,但对该疾病仍有许多未知之处。在本文中,我们综述了高血压或肾素血管紧张素系统(RAS)与COVID-19的关系以及电解质紊乱与疾病严重程度的相关性。潜在高血压可能与严重或危重型COVID-19相关,但由于混杂因素,这种关系尚不清楚。血管紧张素转换酶2 (Angiotensin-converting enzyme, ACE2)在非经典RAS通路中发挥重要作用,并与SARS-CoV-2的一个受体结合域结合。已知RAS阻断可增加ACE2水平,但关于RAS阻断治疗在COVID-19过程中的效果仍存在争议。一些报告表明RAS阻断剂对COVID-19具有保护作用,而另一些报告则表明RAS阻断剂治疗与急性肾损伤和入住重症监护病房等严重并发症的发生有关。电解质紊乱在COVID-19患者中并不罕见,严重的COVID-19经常表现为低钾血症、低钠血症和低钙血症。电解质失衡是由SARS-CoV-2入侵引起的RAS改变、胃肠功能丧失、促炎细胞因子的影响和肾小管功能障碍引起的。
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Hypertension and Electrolyte Disorders in Patients with COVID-19.

The worldwide coronavirus disease 2019 (COVID-19) pandemic is still in progress, but much remains unknown about the disease. In this article, we review the association of hypertension or the renin-angiotensin system (RAS) with COVID-19 and the correlation between electrolyte disorders and disease severity. Underlying hypertension is likely to be associated with severe or critical COVID-19, but the relationship is not clear owing to confounding factors. Angiotensin-converting enzyme 2 (ACE2) plays an important role in the non-classical RAS pathway and binds to a receptor binding domain of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2). The RAS blockade is known to increase ACE2 levels, but controversy remains regarding the effect of RAS blockade therapy in the course of COVID-19. Some reports have indicated a protective effect of RAS blockade on COVID-19, whereas others have reported an association of RAS blockade therapy with the occurrence of severe complications such as acute kidney injury and admission to the intensive care unit. Electrolyte disorders are not uncommon in patients with COVID-19, and severe COVID-19 has frequently shown hypokalemia, hyponatremia, and hypocalcemia. Electrolyte imbalances are caused by alteration of RAS, gastrointestinal loss, effects of proinflammatory cytokines, and renal tubular dysfunction by the invasion of SARS-CoV-2.

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