Case Presentation: A 29-year-old otherwise healthy male presented to the emergency department with a 1-day history of abdominal pain radiating to his back and associated with nausea and nonbilious vomiting. He denied any fever, chills, heartburn, shortness of breath, chest pain, coughing, urinary symptoms, or change in bowel movements. He denied any previous similar pain. He has no prior trauma or abdominal surgeries. In the emergency department, his vital signs were stable and he was alert and cooperative with clear chest auscultation and normal heart sounds. Abdominal exam showed mild tenderness in the epigastric region otherwise soft with no guarding and bowel sounds were positive.His Initial laboratory investigations showed white blood cell count of 15.1 (Ref: 4-10.8 K/UL), hemoglobin of 16.9 (Ref: 13.5-17.5 G/DL), platelet count of 204 (Ref: 130-430 K/UL), lipase of 2157 (Ref: 0-58 U/L), amylase of 750 (Ref: 0-58 U/L), AST 26 (Ref: 0-40 U/L), ALT 20 (Ref: 7-40 U/L), albumin 4.7 (Ref: 3.4-4.8 GM/DL), total bilirubin 0.7 (Ref: 0.3-1.2 MG/DL), gamma glutamyl transferase was 14 (Ref: 1-30 U/L), triglyceride 36 (Ref: <150 MG/DL), and an unremarkable complete chemistry panel. Urine toxicology screen was positive for opioids. His IgG 4 was 18 (Ref: 3-201 MG/DL) and he had negative ethanol level and antinuclear antibodies. Epstein-Barr Virus IgG was positive but IgM was negative. He also has negative human immunodeficiency virus test and acute hepatitis panel. However, his CMV IgM and IgG were positive by enzyme immunoassay. Ultrasound of the abdomen showed no gallstones or evidence of acute cholecystitis. Computer tomography (CT) scan of the abdomen and pelvis showed hepatosplenomegaly and acute pancreatitis. The patient was admitted as a case of CMV-induced acute pancreatitis. He was started on pain medications and intravenous fluids and he was kept nil per mouth. Over the course of hospitalization, his pain improved and the patient was started on a liquid diet, which he tolerated very well. After 48 hours of hospitalization the patient tolerated a general diet and he was discharged home in stable condition.

Discussion: Acute pancreatitis has a significant morbidity and mortality with evidence of increasing incidence annually. The diagnosis of acute pancreatitis requires two of the following: upper abdominal pain (clinical), serum amylase and/or lipase >3x the normal upper limit (laboratory), and/or characteristic abdominal imaging findings. The causes of acute pancreatitis are broad and most cases are attributed to excessive alcohol intake and/or gallstones. Management of acute pancreatitis requires supportive measures, close monitoring, reduced complications and prevention of recurrences. In our case, the patient denied any recent alcohol consumption and he had an ultrasound negative for gallstones along with negative hyperlipidaemia and autoimmune pancreatitis. He was diagnosed with acute CMV-induced pancreatitis given the positive IgM serology.

Conclusions: Acute pancreatitis has a significant morbidity and mortality with evidence of increasing incidence annually. In the absence of common causes of pancreatitis, physicians should be aware of other causes such as infectious agents. Although CMV-pancreatitis is rare in immunocompetent patients, it has been reported in the literature. The role of antiviral in immunocompetent patients should be determined on a larger scale studies.