A 52-year-old HIV-negative African American man was sent to the hospital for persistent fever and newly elevated liver tests. He noted intermittent fevers over the past 4 years, with minimal outpatient workup pursued but patient was lost to follow-up. He also reported a 100-pound intentional weight loss over the past 2 years, although without significant lifestyle changes to accomplish this and despite increasing abdominal distension over the recent weeks. The patient was born in the United States, works as a bus driver, and had lived in the Bronx, New York, for his entire life. He had no known exposure to TB and neither he nor known family members and friends ever lived or traveled to areas endemic with TB. He also had never lived in a shelter, been incarcerated, and had no history of intravenous (IV) drug use.
Initial laboratory findings were significant for aspartate aminotransferase (AST) 141 U/L, alanine aminotransferase (ALT) 48 U/L, alkaline phosphatase 242 U/L, albumin 2.6 g/dL, total bilirubin 2.2 mg/dL, direct bilirubin 1.4 mg/dK, a platelet count of 79K/microL, and international normalized ratio (INR) of 1.5. Computed tomography of the chest, abdomen, and pelvis with contrast demonstrated left lung upper lobe micronodules, heterogeneous-appearing liver, splenomegaly, and large volume abdominal ascites (Figure 1). Mediastinal, lower thoracic, and abdominopelvic lymphadenopathy was also present. Diagnostic paracentesis yielded white blood cell (WBC) count of 3300 cells/microL, with lymphocytic predominance (82%) and a low serum albumin ascites gradient (SAAG) of 0.8 g/dL. Fluid culture and cytology were negative for bacteria and malignant cells. Ceftriaxone was started for spontaneous bacterial peritonitis given the presence of elevated ascitic neutrophils (363 cells/microL).
Extensive laboratory testing ruled out viral hepatitis and genetic and autoimmune liver disease. Liver biopsy revealed 40% macrovesicular steatosis, mixed portal inflammation, and moderate fibrosis (stage 2/4) consistent with nonalcoholic steatohepatitis. Evaluation for underlying malignancy, including serum protein electrophoresis, urine protein electrophoresis, peripheral flow cytometry, and paracentesis flow cytometry, was normal. A bone marrow biopsy showed normocellular marrow.
Given the presence of lung nodules and marked peritoneal lymphocytosis, a QuantiFERON-TB gold test was sent, which returned positive. Three acid-fast bacillus (AFB) sputum smears were negative, as was the sputum Gene Xpert testing for rifampin resistance. Repeat paracentesis found an elevated adenosine deaminase (114.4 U/L), consistent with TB. Given concern for active TB, the patient was started on empiric rifampin, isoniazid, pyrazinamide, ethambutol (RIPE) therapy for peritoneal TB, after which the patient defervesced and remained afebrile. Although isolated TB peritonitis is very rare, blood and sputum cultures were negative, and no other sources of infection were identified. Three weeks after hospital discharge, the AFB culture from ascitic fluid became positive for growth of Mycobacterium tuberculosis. Based on the susceptibility profile, RIPE therapy was de-escalated to isoniazid and rifampin.