Table 1.

Potential areas of investigation related to DM and COVID-19 infection

Investigative area of interest	Studies/therapies for further evaluation
Confirmation of SARS-CoV-2 diagnosis	PCR or other acute tests (antigen once available) during the acute phase, antibody testing postrecovery [102]
Insulin resistance	Plasma level of human insulin and insulin analogue, response to exogenous insulin, calculated HOMA-IR, c-peptide
Diabetic ketoacidosis	Beta hydroxybutyrate, acetone, acetoacetate
Inflammation	CRP, cytokines, acute phase reactants, triglycerides, free fatty acids [33, 103–106]
Therapies altering insulin resistance/sensitivity	Hydroxychloroquine/chloroquine, azithromycin, remdesivir, DPPIV Inhibitors, ACE-inhibitors/ARBs, catecholamines, corticosteroids, immune modulators (i.e., sarilumab and others) [33–35, 65, 66, 107]
Beta cell function (all disease phases)	C-peptide and plasma glucose (acute and recovery phase)
Autoimmune diabetes (all disease phases)	Glutamic acid decarboxylase antibodies (GAD-65), Islet cell antibodies, tyrosine phosphatase antibodies (IA-2), ZnT8 antibodies (acute and recovery phase) [108] genotyping for T1DM associated HLA genotypes [109, 110],
Beta cell injury*	Beta cell specific cell free DNA, or differentially methylated INS DNA [111–113]
Genetic modulators of glycemic response**	Genotyping for known T2DM predisposing SNPs and monogenic diabetes [114], whole-genome sequencing or SNP Array

*Occurring via direct islet infection facilitated by islet ACE-2/TMPRSS2 or inflammatory destruction

**Including monogenic diabetes, type 1 diabetes, and type 2 diabetes