Acute Pancreatitis from Triglyceridemia with Concominant Diabetic Ketoacidosis: A Complication of COVID-19 Infection

Introduction: COVID-19 pneumonia is a viral infection that has been shown to affect numerous organ systems causing diagnostic and treatment dilemmas. Previous literature shows that 17% of patients with COVID-19 were found to have acute pancreatitis without any additional risk factors. However, the role of hypertriglyceridemia has not yet been examined. We present a case of acute pancreatitis secondary to triglyceridemia in the setting of COVID-19 infection. Case Report: A 31 year old man with morbid obesity (body mass index of 41.5 kg/m2) and no other past medical history presented with abdominal pain at the periumbilical region radiating to the back associated with nausea and vomiting for five days. He also complained of polyuria and polydipsia for one week. He denied any history of diabetes mellitus (DM), high triglycerides, alcohol use, and gallstones. He also denied any family history of hyperlipidemia. Of note, the patient's wife was sick with COVID-19 3 weeks prior and he tested negative at that time. His vitals were remarkable for sinus tachycardia of 140/minute. Labs were notable for positive PCR for COVID-19 pneumonia, lipase of 520, elevated triglycerides of 7265, and evidence of pancreatitis on computed tomography (CT) scan of abdomen and pelvis. His arterial blood gas was significant for a pH of 7.191 and lactate of 1.9. His chemistry revealed a glucose of 377, anion gap of 26, and a bicarbonate of 8, consistent with a diagnosis of diabetic ketoacidosis (DKA). He was admitted to intensive care unit (ICU) for management of acute pancreatitis and DKA. He was managed with intravenous (IV) insulin drip, Atorvastatin, Niacin, Gemfibrozil and isotonic IV fluids. Following a 10 day ICU course he had complete resolution of DKA and hypertriglyceridemia and was subsequently transferred to the medical floor. Discussion:The proposed mechanism of acute pancreatitis in COVID-19 infection is the entry of the virus via angiotensin II receptor that causes damage to pancreatic cells. This results in decreased insulin production leading to increased peripheral lipolysis and hypertriglyceridemia. The breakdown of triglycerides then often results in DKA. In the case of our patient it is possible that COVID-19 infection is a coincidence but the timing of symptoms, lack of prior history of triglyceridemia, and lack of family history makes COVID 19 the most likely cause. Therefore, in COVID-19 patients with abdominal pain, acute pancreatitis should be considered.