NEW-ONSET HYPERGLYCEMIA AFTER SARS-COV-2 INFECTION

Abstract Patients who were hospitalized for coronavirus disease 2019 (COVID-19) have a higher prevalence of hyperglycemia. By altering glucose homeostasis, cytokine release brought on by The Severe Acute Respiratory Syndrome Coronavirus 2 (SARS-CoV-2) infection may hasten the onset of metabolic changes. Here, they are described different abnormalities, such as glycometabolic regulation, insulin resistance, and loss of beta cell function in COVID-19 patients. Most of those individuals had no prior history of diabetes or diabetes diagnosis. Additionally, it is reported the presence of glycaemic abnormalities in patients who were followed up several months after the onset of the illness. We discovered that 46% of patients in a sample of 551 patients hospitalized for COVID-19 in Milan were hyperglycemic, 27% were normoglycemic, while the remaining 27% were diabetic. Even in individuals with normoglycemia, we were able to identify altered glycometabolic regulation, insulin resistance, and an aberrant cytokine profile using clinical tests and continuous glucose monitoring in a sample of patients. Patients who healed from COVID-19 have been monitored for glycemic irregularities for at least two months. Moreover, in individuals who developed hyperglycemia following COVID-19, direct and indirect effect of SARS-CoV-2 on human pancreatic islets could possibly occur. The serum of these patients showed toxicity on human pancreatic islets despite the lack of peripheral anti-islet autoimmunity, which could be reversed by the administration of anti-interleukin-1 beta (anti IL-1B), anti-interleukin-6 (anti IL-6), and tumor necrosis factor-alpha (TNF-alpha), cytokines that are known to be significantly upregulated during COVID-19 infection. It's interesting to note that human pancreatic islets had high levels of expression of the cytokine receptors indicated above. Several COVID-19 patients showed an increase in peripheral unmethylated INS DNA, a sign of cell death. The pancreas of deceased COVID-19-positive hyperglycemic patients showed modest lymphocytic infiltration of the islets and pancreatic lymphonodes. Additionally, postmortem pancreatic tissues contained SARS-CoV-2-specific viral RNA and numerous immature insulin granules or proinsulin, suggesting altered proinsulin processing as well as beta-cell degeneration and hyperstimulation. Our findings show that COVID-19 is linked to poor glycometabolic regulation, and that these abnormalities can last even after recovery. In conclusion, SARS-CoV-2 may impair human pancreatic islet survival and function by inducing inflammatory conditions, possibly with a direct tropism, which may then result in metabolic abnormalities observed in COVID-19 patients.