As physicians we are no strangers to viral hepatitis and its penchant for infecting hepatocytes. Even though the virus preferentially targets hepatocytes, it has been shown to infect the biliary epithelium lining the gallbladder and the biliary tree. We present a case of a 32-year-old male with acalculous cholecystitis secondary to Hepatitis B infection. The patient presented to our facility with complaints of right upper quadrant (RUQ) pain, nausea, vomiting and a sense of malaise for 2 days. Upon physical examination, the patient had mild scleral icterus and RUQ tenderness with a negative Murphy's sign. He had an alanine transaminaseof 3569 IU/L, aspartate transaminase of 1868 IU/L, alkaline phosphatase of 117 IU/L, total bilirubin of 6.5 mg/dl and a direct of 4.3 mg/dl. Urine urobilinogen was 0.2 mg/dl (reference range 0.2-1.0 mg/dl). He underwent abdominal imaging on the day of presentation with ultrasound and computed tomography (CT). The CT scan demonstrated prominent enhancement of the gallbladder mucosa with mild gall bladder wall thickening and pericholecystic fat stranding. No biliary stones were seen on either the CT or the ultrasound. The patients abdominal pain persisted leading to a magnetic resonance cholangiopancreatography (MRCP) which showed a distended gallbladder with wall thickening measuring up to 4.6 mm and pericholecystic fluid. An unremarkable biliary tree was seen, confirming a diagnosis of acalculous cholecystitis. He was managed conservatively with antibiotics. Given the disproportionate elevation of liver enzymes, a hepatitis panel was performed which was positive for the Hepatitis B surface antigen and core antibody. Hepatitis e antigen, e antibody and surface antibody was negative. Hepatitis B DNA levels were undetectable. The patient responded to conservative management and was discharged with follow up at the hepatology clinic. Acalculous cholecystitis in viral hepatitis is attributed to infection of the epithelial cells as well as functional changes in biliary flow. In our review of literature, we found sporadic case reports describing this entity however, it may be underreported due to a lack of imaging and self-limited nature. In a series by Karacaer, Z., et al, in 852 patients with viral hepatitis, 0.4% had concomitant cholecystitis, leading us to believe that it may be more common than anticipated. With this case, we aim to reinforce that concomitant viral hepatitis and cholecystitis may not be as rare as thought
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