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腺苷能对抗新冠病毒急性呼吸窘迫综合征吗?

Can Adenosine Fight COVID-19 Acute Respiratory Distress Syndrome?

作者信息

Falcone Carmela, Caracciolo Massimo, Correale Pierpaolo, Macheda Sebastiano, Vadalà Eugenio Giuseppe, La Scala Stefano, Tescione Marco, Danieli Roberta, Ferrarelli Anna, Tarsitano Maria Grazia, Romano Lorenzo, De Lorenzo Antonino

机构信息

Unit of Radiology, Grande Ospedale Metropolitano Bianchi Melacrino Morelli, 89124 Reggio Calabria, Italy.

Unit of Intensive Postoperative Therapy, Grande Ospedale Metropolitano Bianchi Melacrino Morelli, 89124 Reggio Calabria, Italy.

出版信息

J Clin Med. 2020 Sep 21;9(9):3045. doi: 10.3390/jcm9093045.

Abstract

Coronavirus disease 2019 (COVID-19) patients can develop interstitial pneumonia, which, in turn, can evolve into acute respiratory distress syndrome (ARDS). This is accompanied by an inflammatory cytokine storm. severe acute respiratory syndrome coronavirus type 2 (SARS-CoV-2) has proteins capable of promoting the cytokine storm, especially in patients with comorbidities, including obesity. Since currently no resolutive therapy for ARDS has been found and given the scientific literature regarding the use of adenosine, its application has been hypothesized. Through its receptors, adenosine is able to inhibit the acute inflammatory process, increase the protection capacity of the epithelial barrier, and reduce the damage due to an overactivation of the immune system, such as that occurring in cytokine storms. These features are known in ischemia/reperfusion models and could also be exploited in acute lung injury with hypoxia. Considering these hypotheses, a COVID-19 patient with unresponsive respiratory failure was treated with adenosine for compassionate use. The results showed a rapid improvement of clinical conditions, with negativity of SARS-CoV2 detection.

摘要

2019冠状病毒病(COVID-19)患者可发展为间质性肺炎,进而可演变为急性呼吸窘迫综合征(ARDS)。这伴随着炎症细胞因子风暴。严重急性呼吸综合征冠状病毒2型(SARS-CoV-2)具有能够引发细胞因子风暴的蛋白质,尤其是在包括肥胖症患者在内的合并症患者中。由于目前尚未找到针对ARDS的决定性治疗方法,且鉴于有关腺苷使用的科学文献,有人提出了腺苷的应用。通过其受体,腺苷能够抑制急性炎症过程,增强上皮屏障的保护能力,并减少由于免疫系统过度激活(如细胞因子风暴中发生的情况)而造成的损害。这些特性在缺血/再灌注模型中是已知的,也可用于缺氧性急性肺损伤。考虑到这些假设,一名对治疗无反应的呼吸衰竭COVID-19患者接受了腺苷的同情用药治疗。结果显示临床状况迅速改善,SARS-CoV2检测呈阴性。

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