COVID-19: Too Sweet to Handle? A Case of New-Onset Diabetes Mellitus with Severe Diabetic Ketoacidosis Precipitated by Mild COVID-19 Pneumonia

Introduction: As further studies elucidate the extent of organ systems affected by COVID-19, extra-pulmonary involvement is emerging as an important contributor to its morbidity and lethality. Beta-islet cells in the pancreas have been shown to be affected by COVID-19 via ACE2 and TMPRSS2 receptors. Accordingly, diabetes mellitus (DM) has not only been described as an independent risk factor for severe COVID-19, but there is also an association between new-onset DM (NODM) and diabetic ketoacidosis (DKA) with COVID-19. This case report discusses a patient with NODM presenting with DKA precipitated by COVID-19. Case Summary: A 45-year-old male with no past medical history who emigrated from India in March 2020 presented to the emergency department with five days of dyspnea, chills, fatigue, polyuria, and polydipsia. He was COVID-19 PCR-positive while his labs were remarkable for WBC 14, sodium 126, bicarbonate 2, glucose 350, anion gap 33, pH 6.95, pCO2 26, lactate 4.4, D-dimer 479, LDH 350, Ferritin 2381, Procalcitonin 1.13, HIV negative, and significant ketonuria. Chest x-ray revealed bilateral lower lobe patchy infiltrates consistent with COVID-19. He was started on an insulin drip, therapeutic Enoxaparin, and fluid resuscitation. He did not require supplemental oxygen and was not treated with steroids or antivirals. He was transitioned to subcutaneous insulin after one day. He was discharged after an uncomplicated five-day hospital stay. Discussion: There has been an increasing number of reports describing DKA precipitated by COVID-19 in patients with NODM, though our patient presentation is unique because he had a mild COVID-19 course that precipitated severe DKA. This case indicates a more direct role of COVID-19 damaging beta-cells in the pancreas as our patient remained on insulin and no other diabetic medications at discharge and after follow-up, indicating a complete reliance on exogenous insulin and failure of the pancreas to produce insulin seen with type-1 DM. The patient's HbA1c of 13.3 indicates a chronic state of DM, though COVID-19 certainly contributed to establishing NODM and DKA likely by wiping the remaining function of the Beta-cells in the pancreas. This uncommon case presentation demonstrates that even mild COVID-19 can induce DKA, so it is imperative that further research be conducted on its mechanism and prevention in the future.