Case Presentation: A 74 -year-old male with a past medical history of hypertension, hyperlipidemia, benign prostatic hyperplasia, renal cell carcinoma status post right nephrectomy, and peripheral arterial disease, presented to the Emergency Room with 20 days of progressive weakness, shortness of breath, nausea, vomiting, polyuria, polydipsia, and abdominal pain. The patient was vaccinated but not boosted for COVID-19 and had a mild COVID-19 infection one month prior to admission, managed at home. Two years ago, the screening Hba1c was 5.9. The patient was completely unaware of his pre-diabetic state. Medications include metoprolol, statin, and Plavix. Physical exam was significant for dry mucous membranes, decreased skin turgor, and diffuse abdominal tenderness without guarding. Significant labs included elevated WBC to 21.7 K/uL, Blood Glucose (BG) 691mg/dL, Bicarb 6, BUN 36, Cr 1.8, K 5.9, phos 6.2, D-dimer 0.27, lactic acid 2.4, UA with glucose 500, and a persistently positive SARS-CoV2 RT-PCR. Imaging included reassuring CXR, CT abdomen/pelvis with diffuse fatty infiltration of liver, partial right nephrectomy, and bilateral renal cysts. The patient was managed for DKA with IV insulin and IV fluids. Further workup showed a C-peptide 1.03, Hba1c 10.4%, and a negative GAD65 antibody. Once the anion gap was closed and BG was < 200, the patient was transitioned to a basal-bolus regimen. As a newly diagnosed diabetic patient with a lot of distress, diabetic education was provided with appropriate support and close outpatient follow-up.
Discussion: There is a bidirectional relationship between COVID-19 and diabetes [1]. The proposed mechanisms include an association between ACE2 receptor protein, the TMPRSS2 enzyme protein, expressed by beta cells of the pancreas, and SARS-CoV-2 which depends on these markers to enter and infect human cells [2]. COVID-19 might lead to diabetes through a direct attack of pancreatic cells expressing ACE2 receptor, stress hyperglycemia resulting from the cytokine storm, and alterations in glucose metabolism caused by infection [3]. Coronavirus infection changes the function of beta cells of the pancreas by reducing the production and release of insulin from pancreatic islet tissue [4]. Persistent diabetes in COVID-19 patients is related to long COVID syndrome [5]. Close surveillance of these patients is important to maintain good glycemic control and avoid cardiovascular and renal complications [6].
Conclusions: Diabetic ketoacidosis (DKA) is a medical emergency that requires prompt recognition and management. This is a case of a 74-year-old male who presented with Diabetic ketoacidosis (DKA) one month after a mild COVID-19 infection. The interesting association of ACE2 receptors and coronavirus can lead to immune dysregulation, and beta-cell dysfunction causing various effects on glycemic control. Screening high-risk populations and increasing awareness of symptoms will be helpful in the better management of complex metabolic syndromes.