Abstract

Abstract Since the beginning of the Covid-19 pandemic in December 2019, much has been written about its bidirectional prognostic association with newly diagnosed diabetes, which can either be precipitated new-onset or unmasked previously undiagnosed diabetes, both often presenting as diabetic ketoacidosis. Various mechanisms have been proposed, including stress- or drug-induced hyperglycemia, proinflammatory direct and indirect effects on insulin secretion and activity, as well as direct viral cytolytic effect on the pancreatic β cells via action on the ACE2 receptor integral to islet cell homeostasis. We present a case of a 51-year-old normosthenic male with no known comorbidities, who came in with 2-day history of nausea and epigastric discomfort along with progressively worsening dyspnea and nonproductive cough. He tested positive for Covid-19 by TMA, with elevated acute-phase reactants (CRP and ferritin), and had received his first dose of Covid vaccine 10 days prior. Further evaluation was consistent with diabetic ketoacidosis (glucose 487 mg/dL, pH 7.22, anion gap 27, HCO3 10 mmol/L, beta-hydroxybutyrate 9.71 mmol/L) with concurrent pancreatitis (lipase 2327 U/L, no leukocytosis, lactate 1.41 mmol/L) and acute kidney injury (EGFR 58). His BMI at presentation was 26 kg/m2 with a hemoglobin A1c of 16.9, and no personal history of diabetes. His father and paternal grandmother both had type 2 diabetes. He was managed with hydration and insulin drip titrated as per protocol, with subsequent resolution of DKA and transition to subcutaneous basal-bolus insulin on the second hospital day. Mild-moderate respiratory Covid symptoms improved with dexamethasone, remdesivir, and oxygen supplementation via nasal cannula. Glucose was controlled throughout the hospital stay, and he was discharged improved on the fifth hospital day with twice-daily basal insulin. When he presented to the DKA clinic for follow-up five months post-hospital discharge, his HbA1c was remarkably down to 7.1. There was no evidence of any macrovascular or microvascular complications. GAD-65 and islet cell antibodies were negative. Given good glucose control and adequate β cell function as confirmed by C-peptide level of 3.50 ng/mL, we were hence able to further decrease his basal insulin to once daily and start metformin. With an increasing number of reports of patients with new-onset DKA following Covid-19 infection, without a typical phenotype of type 1 diabetes, it is possible that Covid-19 is associated with a unique form of provoked A- β+ Ketosis Prone Diabetes (KPD). Identical to our case, patients belonging to this subgroup resemble type 2 diabetes patients in that they have adult-onset diabetes, are overweight or obese, lack islet autoantibodies and have substantial β cell functional reserve measured shortly after the index episode of DKA. Awareness of this phenomenon is important as it can help guide a unique treatment path for these patients and avoid injudicious use of insulin moving forward. Presentation: Sunday, June 12, 2022 12:30 p.m. - 2:30 p.m.

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