Covid-19 and New Onset Diabetes: A Case Series

Background: During the SARS CoV1 pandemic in 2003, there was much literature published about newly diagnosed diabetes mellitus (DM) in the patient population infected. This phenomenon has not been well established during this SARS CoV2 pandemic. In this case series, we aim to evaluate patients admitted to our facility with new onset DM who had a history of COVID-19 infection. Method: This was a single center case series that included adult patients who presented to our facility with new onset DM during June-October 2020 who had a history of SARS CoV2 positive PCR and/or positive IgG antibody to SARS CoV2. Pregnant patients were excluded. Data was collected from the hospital electronic medical records. Diagnosis of diabetes was determined in these patients via hemoglobin A1C (HbA1C) level greater than 6.5%. Results: Six patients fulfilled our diagnostic criteria. All patients were male with a median age of 54 years. The median BMI is 33.9, with 5 patients considered to be obese and 1 overweight. Other than the increased BMI, 2 patients with pre-DM and 3 patients who had a family history of DM, no other identifiable risk factors for DM were noted in this cohort. Five patients required hospitalization for HHS or DKA and 1 patient was managed as an outpatient. Median random serum glucose on presentation was 761.5 mg/dl and median HbA1C on presentation was 11.5%. Significant dosages of parenteral insulin (0.45 U/Kg) was required for hospitalized patients during their inpatient stay along with immediately after discharge to control their hyperglycemia. Glutamic Acid Decarboxylase and Islet Cell antibodies were done for 2 of the patients and were negative. Three of the patients who had follow up in 2 months showed improvement in their HbA1C (median of 7.1% [5.4–10.7]) and considerably diminished subcutaneous insulin requirement (0.2U/Kg). Two of these patients continued to follow up, and at 4 months from onset of DM, median HbA1C was 5.85% with insulin ceased. Of note, the patient who was lost to follow up was found to have an HbA1C improvement from 11.4% to 5.4% at the 2 month mark. Discussion: Both SARS CoV1 and SARS CoV2 activates the RAAS, causing insulin resistance by altering insulin signaling and increasing oxidative stress leading to dysfunction of pancreatic beta calls. The inflammatory cytokine storm response seen in COVID-19 can also decrease skeletal muscle sensitivity to insulin and decrease peripheral glucose uptake. These mechanisms may be leading to the new-onset DM noticed in our COVID-19 patients. In addition, there may be a possible immune-mediated mechanism given the matched time line between the COVID-19 antibody life span and the duration of DM. It is unknown whether this effect is permanent or temporary, although our results do support the latter. More studies that utilize a larger cohort and longer follow up are needed in order to get a better understanding of the mechanism of DM in COVID-19 infection.