Department of General Surgery and Transplantology, Pomeranian Medical University in Szczecin, Szczecin, Poland.
Department of Pharmacology and Phytochemistry, Institute of Natural Fibers and Medicinal Plants, Poznan, Poland.
Clin Interv Aging. 2020 Jul 21;15:1231-1240. doi: 10.2147/CIA.S261516. eCollection 2020.
Since the beginning of 2020, the whole world has been struggling with the pandemic of Coronavirus Disease 2019 (COVID-19) caused by a novel coronavirus SARS-CoV-2. The SARS-CoV-2 infection depends on ACE2, TMPRSS2, and CD147, which are expressed on host cells. Several studies suggest that some single nucleotide polymorphisms (SNPs) of ACE2 might be a risk factor of COVID-19 infection. Genotypes affect ACE2 structure, its serum concentration, and levels of circulating angiotensin (1-7). Moreover, there is evidence that ACE genotype affects the outcomes of acute respiratory distress syndrome (ARDS) treatment, the most severe consequence of SARS-CoV-2 infection. COVID-19 morbidity, infection course, and mortality might depend on ACE D allele frequency. The aim of this narrative review was to analyze and identify the mechanisms of ACE-I and ARBs with particular emphasis on angiotensin receptors and their polymorphism in the light of COVID-19 pandemic as these medications are commonly prescribed to elderly patients. There is no direct evidence yet for ACE-I or ARBs in the treatment of COVID-19. However, for those already taking these medications, both the European Society of Cardiology and the American College of Cardiology recommend continuing the treatment, because at present, there is no clear clinical or scientific evidence to justify the discontinuation of ACE-I or ARBs. Individualized treatment decisions should be based on the clinical condition and co-morbidities of each patient.
自 2020 年初以来，全世界一直在与由新型冠状病毒 SARS-CoV-2 引起的 2019 年冠状病毒病（COVID-19）大流行作斗争。SARS-CoV-2 感染依赖于 ACE2、TMPRSS2 和 CD147，这些物质在宿主细胞上表达。一些研究表明，ACE2 的一些单核苷酸多态性（SNP）可能是 COVID-19 感染的危险因素。基因型影响 ACE2 的结构、其血清浓度和循环血管紧张素（1-7）水平。此外，有证据表明 ACE 基因型影响急性呼吸窘迫综合征（ARDS）治疗的结果，这是 SARS-CoV-2 感染的最严重后果。COVID-19 的发病率、感染过程和死亡率可能取决于 ACE D 等位基因频率。本综述的目的是分析和确定 ACE-I 和 ARB 的机制，特别强调血管紧张素受体及其在 COVID-19 大流行中的多态性，因为这些药物通常开给老年患者。目前尚无 ACE-I 或 ARB 治疗 COVID-19 的直接证据。然而，对于那些已经服用这些药物的患者，欧洲心脏病学会和美国心脏病学会都建议继续治疗，因为目前没有明确的临床或科学证据证明停止 ACE-I 或 ARB 的合理性。个体化治疗决策应基于每位患者的临床状况和合并症。
