Portal hypertension due to cirrhosis is the most common cause of ascites. However, in patients with multiple risk factors for ascites, determining the etiology can sometimes present a diagnostic challenge. We present a case of new onset ascites in a 59 year old African American man with concomitant HIV (CD4 54) and chronic active hepatitis C infection, and suspected tuberculosis corroborated by elevated Adenosine Deaminase (ADA). In this unusual case, despite suggestive symptoms and signs, we found the cause of his ascites was neither infection nor liver disease, but rather metastatic gastric malignancy. Ultrasound with Doppler did not show cirrhotic features or vascular thrombus in the liver, while diagnostic and therapeutic paracentesis revealed a low Serum Albumin- Ascites Albumin Gradient (SAAG) and high ascitic fluid WBC count with monocytic predominance. Repeat ascitic fluid testing confirmed low SAAG, and ADA was elevated at 26.3 IU/mL. Laparoscopy revealed innumerable peritoneal lesions resembling tuberculous seeding of the peritoneum. However, peritoneal histopathology returned as metastatic signet cell adenocarcinoma. Esophagogastroduodenoscopy (EGD) revealed a large, firm, ulcerated gastric body tumor, and pathology was consistent with diffuse signet ring cell carcinoma. In this case, cirrhosis and tuberculous infection were highly suspected, however there was no evidence of cirrhosis, and although acid-fast smear and Quantiferon testing were negative, tuberculous peritonitis was strongly considered due to history of HIV and high monocyte predominance of ascitic fluid with elevated ADA. Both findings are suggestive of tuberculous peritonitis, however, ADA can also be elevated in the setting of malignancy and the pre-test probability of tuberculosis should be considered when sending ADA levels. Confirmation of the diagnosis with peritoneal biopsy is paramount.
Gadani A, Yfantis H, Xie G and Quezada S