A 19-year-old Omani female not known to have any significant medical history was referred to our hospital with a history of upper abdominal discomfort more localized to the epigastric region and associated with jaundice and dark urine. There was no history of fever or night sweat nor history of travel. On physical examination, the patient was jaundice; otherwise, the systemic examination was unremarkable.
Complete blood count was within normal limits with a normal white blood count (6.3 10*g/L). Liver function test revealed a picture of obstructive jaundice with a total bilirubin of 52 umil/L, Alkaline phosphatase 302 [iU] /L, and Alanine transaminase 457 [iU]/L. QuantiFERON-Tb gold test was positive.
CT scan of the abdomen and pelvis showed a lobulated and heterogeneous liver hilar mass with a central necrosis, measuring 2.4 x 3.9 cm. The mass was obstructing the proximal common hepatic duct resulting in dilatation of the intrahepatic biliary tree (Figure 1). The mass was associated with multiple enlarged peripancreatic, porta hepatis and hepatoduodenal lymph nodes, measuring up to 1.2 cm. None of the lymph nodes were showing central necrosis. Features were suggestive of a cholangiocarcinoma of the common hepatic duct. Further work-up with a liver MRI redemonstrated the porta hepatis mass. The mass was T2 hyperintense and T1 hypointense and showed moderate enhancement on postcontrast sequence with severe diffuse restriction (Figures 2 and 3). On MRCP, the mass was causing severe narrowing of the proximal 1.8 cm of the common hepatic duct, reaching the confluence and causing moderate dilation of the intrahepatic biliary tree. In addition, the MRI revealed multiple foci of restriction scattered throughout the liver and some of them showed subtle enhancement on postcontrast sequence suggestive of liver microabscess (Figure 3).Constellation of MRI findings was suggestive of localized TB of the porta hepatis; however, neoplastic lesion such as rhabdomyosarcoma and lymphoma could not be excluded and further evaluation with a tissue biopsy was advised. Chest radiograph was normal. Tumor markers were within normal limits including Cancer Ag 19-9 (CA 19-9): 8U/mL (range, 0-37U/mL), Carcinoembryonic antigen (CEA): 1.2 ug/L (range, 0-3ug/L), Alpha fetoprotein: 1.1 ug/L (range 0-15), and Chromogranin A: 47ug/L (range 26-92ug/L)
The patient underwent laparoscopic biopsy and was found to have enlarged porta hepatis lymph nodes. Biopsy was taken from the porta hepatis mass and histopathological examination showed a granulomatous inflammatory process. Although, no definite proof was obtained by culture or polymerase chain reaction (PCR), probable TB diagnosis was made based on the histological and imaging findings, and the patient was treated for 6 months with Rifampicin 150 mg and Isoniazid 75 mg. The patient showed significant response to treatment with dramatic improvement of liver function test. A follow-up liver function test 3 months after starting anti-TB medication showed normalization of Alkaline phosphatase 91 [iU] /L along with improvement of total bilirubin of 24 umil/L and Alanine transaminase 211 [iU]/L. After completion of anti-TB medication, liver function test was back to normal with a total bilirubin of 17 umil/L, Alkaline phosphatase 58 [iU] /L, and Alanine transaminase 16 [iU]/L. A follow-up CT abdomen was performed 10 months later and showed complete resolution of porta hepatis mass and intrahepatic biliary dilatation along with significant regression of previously noted enlarged upper abdomen lymph nodes.