A Rare Cause of Diabetes: COVID-19

Abstract

A Rare Cause of Diabetes: COVID-19 Introduction: Environmental factors like viruses have been described in the mechanism of pancreatic beta cell destruction. Various viruses can trigger autoimmunity in individuals genetically predisposed to diabetes. Severe acute respiratory syndrome coronavirus 2 (SARS CoV-2) has been shown to bind to angiotensin-converting enzyme 2 (ACE 2) which is expressed throughout the body, including pancreatic cells, leading to direct injury of the endocrine pancreas. We report a case of coronavirus infection disease 2019 (COVID-19) causing a new onset of diabetes mellitus presentation with hyperglycemia, polyuria, polydipsia and weight loss. Case Presentation: A 53 year-old, previously healthy, male presented with five days of fever, fatigue, dry cough, dyspnea and diarrhea. On admission he was hypoxic, with a body mass index of 25 kg/m2 and no evidence of insulin resistance on physical exam. He was diagnosed with SARS CoV-2 and admitted for high requirements of oxygen without the need of the intensive care unit. He was treated with tocilizumab, atazanavir, hydroxychloroquine, full dose anticoagulation and azithromycin. Dexamethasone 4 mg every 8 hours was given for three days. During this admission, his fasting glucose was 75–108 mg/dL. Once started on steroids his fasting and prandial glucose was 85–96 mg/dL and 140 mg/dL on one occasion. He was eventually discharged with 2 liters of nasal cannula which he required for one week. One and a half months after, he presented to the emergency department due to a 6 kg weight loss, polyuria, polydipsia, malaise and fatigue. On arrival his glucose was 549 mg/dL, without anion gap or ketones. He had no evidence of new infection and SARS CoV-2 test was negative. He was started on insulin glargine at night and insulin Humalog before each meal with corrections. Hemoglobin A1c was 13.4% with a C-peptide 0.36 ng/mL and glucose of 195 mg/dL at the time of C-peptide test. His antibodies, anti-islet cell antibody, zinc transporter 8 and glutamic acid decarboxylase-65, were negative. He was discharged with basal/bolus regimen and followed up outpatient with Endocrinology. During follow-up, his c-peptide normalized and he was tapered off insulin. Discussion: In 2003, atypical pneumonia caused by SARS CoV-2 was reported to be associated with hyperglycemia in patients without prior history of diabetes. At 3 year follow-up, the patients no longer had diabetes. Moreover, patients with mild SARS CoV-2 during the first day of hospitalization had a higher fasting plasma glucose than patients admitted for other causes of pneumonia. It is known that SARS CoV-2 binds to ACE 2 which downregulates the receptor, leading to impairment of insulin secretion and hyperglycemia. SARS CoV-2 also produces a direct injury in beta pancreatic cells. It is imperative to monitor patients post COVID-19 to evaluate for new onset diabetes and likely resolution.