The arguments of Aspirin for COVID-19 complications | ||||
| Microbes and Infectious Diseases | ||||
| Article 4, Volume 2, Issue 1, February 2021, Page 7-8 PDF (207.52 K) | ||||
| Document Type: Letter to the Editor | ||||
| DOI: 10.21608/mid.2020.55406.1102 | ||||
 View on SCiNiTO | ||||
| Authors | ||||
Siukan Law   1; Albert Wingnang Leung2; Chuanshan Xu3
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| 1Department of Science, School of Science and Technology, The Open University of Hong Kong, Ho Man Tin, Kowloon, Hong Kong | ||||
| 2School of Graduate Studies, Lingnan University, Tuen Mun, Hong Kong | ||||
| 3Key Laboratory of Molecular Target and Clinical Pharmacology, State Key Laboratory of Respiratory Disease, School of Pharmaceutical Sciences and Fifth Affiliated Hospital, Guangzhou Medical University, Guangzhou 511436, China | ||||
| Abstract | ||||
| Recently, a research team from the School of Medicine at the University of Maryland reported that the usage of aspirin was associated with decreased mechanical ventilation, ICU admission, reduced lung injury, and in-hospital mortality in hospitalized patients with COVID-19. 412 patients participated in this study within three months from March to July. Patients were given a low dosage of aspirin (75-81 mg/day), only 44% of patients required to have ventilator and 43% of patients admitted to ICU, also 47% of patients decreased the death rate after COVID-19 infection. However, these investigations weren’t a randomized, double-blind, placebo-controlled trial. Up to the present, an important complication of COVID-19 was increased risk of blood clotting for the patients. This was an inflammatory response of at least 30% or 70% of patients in ICU for the lining of blood vessels in the cardiovascular and alveoli in the lungs. Aspirin was an anti-platelet agent which inhibited the formation of platelet by deactivating the activity of cyclooxygenase (COX) and making the irreversible reaction of acetylate serine 530 to generate the thromboxane A2, called “antithrombotic effect”. It also prohibited the virus replication by suppressing prostaglandin E2 (PGE2) in macrophages and up-regulated the production of type I interferon. (To be continued)... | ||||
| Keywords | ||||
| Aspirin; COVID-19 complications; Inflammatory response | ||||
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