Author: Brufsky, Adam
Title: Hyperglycemia, hydroxychloroquine, and the COVIDâ€19 pandemic Cord-id: ub7s6yz6 Document date: 2020_4_27
ID: ub7s6yz6
Snippet: Coronavirus diseaseâ€2019 (COVIDâ€19) infection and its severity can be explained by the concentration of glycosylated severe acute respiratory syndromeâ€coronavirus 2 (SARSâ€CoVâ€2) viral particles in the lung epithelium, the concentration of glycosylated angiotensinâ€converting enzyme receptor 2 (ACE2) in the lung epithelium, and the degree and control of the pulmonary immune response to the SARSâ€CoVâ€2 spike protein at approximately day 8 to 10 after symptom onset, which may be relat
Document: Coronavirus diseaseâ€2019 (COVIDâ€19) infection and its severity can be explained by the concentration of glycosylated severe acute respiratory syndromeâ€coronavirus 2 (SARSâ€CoVâ€2) viral particles in the lung epithelium, the concentration of glycosylated angiotensinâ€converting enzyme receptor 2 (ACE2) in the lung epithelium, and the degree and control of the pulmonary immune response to the SARSâ€CoVâ€2 spike protein at approximately day 8 to 10 after symptom onset, which may be related to both. Binding of ACE2 by SARSâ€CoVâ€2 in COVIDâ€19 also suggests that prolonged uncontrolled hyperglycemia, and not just a history of diabetes mellitus, may be important in the pathogenesis of the disease. It is tempting to consider that the same mechanism acts in COVIDâ€19 as in SARS, where an overactive macrophage M1 inflammatory response, as neutralizing antibodies to the SARSâ€CoVâ€2 spike protein form at day 7 to 10, results in acute respiratory distress syndrome (ARDS) in susceptible patients. It also allows consideration of agents, such as hydroxychloroquine, which may interfere with this overly brisk macrophage inflammatory response and perhaps influence the course of the disease, in particular, those that blunt but do not completely abrogate the M1 to M2 balance in macrophage polarization, as well as viral load, which in SARS appears to be temporally related to the onset of ARDS.
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