Severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection primarily affects the respiratory tract, but gastrointestinal (GI) symptoms may obscure a secondary diagnosis. GI symptoms similar to the ones presented in acute pancreatitis (AP) have been reported. SARS-CoV-2 binds to angiotensin-converting enzyme 2 receptors, which have been identified in the lungs and pancreas. It has been discussed that systemic response to the infection prompts dysregulation in the affected organs. Hyperglycemia is an independent risk factor for increased mortality and thus a detailed assessment must be performed. A 47 year-old man with dyslipidemia arrived at the ER due to a severe constant epigastric pain of 1 day of evolution with back radiation associated with nauseas, emesis, and hyporexia. Upon examination he was tachycardic and in distress due to pain. Laboratories revealed normocytosis, normal hemoglobin, mild thrombocytopenia, hyperglycemia (150 mg/dL), corrected hyponatremia (130 mmol/L), and corrected hypocalcemia (7.4 mg/dL). Amylase (2,332 U/L) and lipase (2,990 U/L) were elevated. Triglycerides were 6,256 mg/dL and glycated hemoglobin was 6.1%. Abdominal CT scan revealed pancreatitis. He was admitted to the ICU due to severe AP due to hypertriglyceridemia with IV hydration and IV insulin infusion. During the first day of admission, he developed respiratory distress requiring intubation, marked abdominal distension, hemodynamic instability, and oliguria. Intra-abdominal pressure yielded 24 mmHg leading to the diagnosis of abdominal compartment syndrome. He underwent emergent abdominal decompressive laparotomy with Bogota Bag placement. COVID-19 PCR test was performed and reported positive. 72 hours later, triglycerides improved and IV insulin was discontinued, but hyperglycemic state prompted subcutaneous basal and correction boluses. Insulin requirement progressively decreased and was discontinued after 14 days. He continued to show clinical improvement and by day 40, the patient was successfully extubated and discharged after physical rehabilitation. SARS-CoV-2 infection has shown a complex multisystem involvement leading to variable presentations which can be fatal if not identified and addressed properly. Albeit, AP is a rare manifestation of COVID-19, clinicians should be aware and pay attention to the related complications. Proposed mechanisms for hyperglycemia and AP include β-cell damage. The pathogenetic role of COVID-19 in hypertriglyceridemia is unclear. Little attention has been paid to the extent of pancreatic injury caused by this virus. To our knowledge this is the second case presenting with hyperglycemia, hypertriglyceridemia, and AP in COVID-19 infection. As the global pandemic is still growing, elucidation of key pathways and mechanisms underlying these associations would aid in the treatment of patients with COVID-19 worldwide.

Hyperglycemic emergencies such as Diabetic Ketoacidosis (DKA) or Hyperosmolar Hyperglycemic State (HHS) are commonly precipitated by infectious processes. Severe Acute Respiratory Syndrome-Coronavirus 2 (SARS-CoV-2) is a novel infectious process prompting hyperglycemic crisis. SARS-CoV-2 at the level of the lungs affects ACE2 functioning which in turns decrease the B cells proliferation at the pancreas and hinders insulin secretion. Advanced age and comorbidities such as hypertension, cardiovascular disease and diabetes mellitus are considered to be a risk factors for severe illness and mortality between patients with SARS-CoV-2. We present the case of a 39-year-old woman with medical history of uterine fibroma, who presented with complains of general malaise, polyuria and polydipsia of one week evolution, associated with sore throat, subjective fever, dry cough, abdominal pain, nausea and vomiting. Physical examination remarkable for dry oral mucosa, decreased skin turgor, and prolonged capillary refills. Vital signs significant for hypertension, tachycardia, and tachypnea. Laboratory work up remarkable for glucose of 1321 mg/dL, HCO3- of 16 mEq/L, serum osmolality of 333 mOsm/kg, serum ketones positive and HbA1C of 15%. ABG’s showed pH of 7.33, PCO2 of 29.8 and a PAO2 of 158.5 mmHg for a high anion gap metabolic acidosis (AG of 15.3 mEq/L), non-anion gap metabolic acidosis with respiratory alkalosis. Chest X-ray revealed bilateral perihilar, peribronchial cuffing. SARS-CoV-2 PCR testing was positive. Clinical and laboratory workup met criteria for diagnosis of HHS and Diabetes Mellitus de Novo most likely secondary to SARS-CoV-2 infection. Patient was treated with aggressive IV hydration and insulin infusion with resolution of hyperglycemia, ketonemia and symptoms. SARS-CoV-2 infection can precipitate acute metabolic complications in patients with diabetes or unknown diagnosis of diabetes. The effect of the virus could be direct effect on β-cell function. To our knowledge, there are only a few cases reported of HHS precipitated by SARS-CoV-2 infection therefore medical awareness is important for early diagnosis of possible triggering factors such as COVID-19 and early management of patients presenting with new onset hyperglycemic emergencies.

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