Obstructive jaundice secondary to hepatic hilar tuberculosis without pulmonary involvement
Mohammad N. Kloub1, Khaled Elfert2, Ahmed Elnajjar3, Ahmad Alnasarat4, Ghaith Alhadidi5, Atheer Anwar5, Raed Atiyat6
1 Department of Internal Medicine, Saint Michael’s Medical Center, Newark, USA
2 Department of Internal Medicine, SBH Health System, New York, USA
3 Department of Internal Medicine, Gastroenterology and Hepatology, Hamad Medical Corporation, Doha, Qatar
4 Department of Internal Medicine, Wayne State University/Detroit Medical Center Sinai Grace, Detroit, USA
5 General physician
6 Department of Internal Medicine, Division of Gastroenterology and Hepatology, Saint Michael’s Med-ical Center, Newark, USA
Doi: 10.12890/2024_004277 - European Journal of Case Reports in Internal Medicine - © EFIM 2024
Received: 28/12/2023
Accepted: 11/01/2024
Published: 19/01/2024

How to cite this article: Kloub MN, Elfert K, Elnajjar A, Alnasarat A, Alhadidi G, Anwar A, Atiyat R. Obstructive jaundice sec-ondary to hepatic hilar tuberculosis without pulmonary involvement. EJCRIM 2024;11:doi:10.12890/2024_004277.

Conflicts of Interests: The authors declare there are no competing interests.
Patient Consent: Written informed consent was obtained from the patient for publication of the details of their medical case and any accompanying images.
Acknowledgement: The authors would like to acknowledge the internal medicine department at Saint Michael’s Medical Center and Hamad Medical Corporation for supporting this publication.
This article is licensed under a Commons Attribution Non-Commercial 4.0 License


Tuberculosis (TB) is primarily a respiratory infection with huge mortality and morbidity worldwide. Extrapulmonary TB infection is common, affecting lymph nodes, pleura, and abdomen, but the prima-ry biliary presentation without lung involvement is exceedingly rare. We report on a 38-year-old male patient presented with isolated obstructive jaundice secondary to TB infection. This case highlights the importance of considering TB infection in the differential diagnosis of obstructive jaundice, especially in the endemic area. We also provide a literature review on TB infection, mainly in the biliary tract.



Tuberculosis, biliary TB, obstructive jaundice


Tuberculosis (TB) is a mycobacterium infection caused by Mycobacterium tuberculosis and is consid-ered a main infectious cause of serious morbidity and mortality, which is reported to have claimed around 1.7 million lives in 2016[1]. However, with the efforts and policies implemented to control the transmission of TB, transmission has been reduced and is expected to decrease annually by 10%[2]. Although TB is primarily a respiratory infection, extrapulmonary manifestation is quite common (30%)[3]. Gastrointestinal manifestations were observed among 11% of patients, with the ilium being the most commonly GI-involved organ[4]. Moreover, it has been reported in the literature that TB could affect the hepatobiliary system, but the primary biliary presentation is a rare entity, and in this case re-port, we shed light on this important aspect.


A 38-year-old man born and raised in India presented experiencing right upper quadrant pain for ten days, associated with itching and dark urine. He had no history of fever, weight loss or respiratory symptoms. On examination he was icteric, but his abdomen was soft with no tenderness.
The results of the basic workup (Table 1) showed elevated direct bilirubin, alanine transaminase (ALT), aspartate transaminase (AST) and alkaline phosphatase (ALP). HIV antibodies, hepatitis anti-bodies, carcinoembryonic antigen (CEA), CA 19-9, sputum acid-fast bacilli, sputum TB PCR and QuantiFERON TB tests were all negative. A chest X-ray was unremarkable; a Mantoux tuberculin skin test was not done as the patient had received BCG vaccine earlier.

(click to enlarge)

Table 1. Blood test results

Ultrasound of the abdomen revealed echogenic sludge within the gallbladder lumen, mild prominent central intrahepatic biliary duct, and prominent upper common bile duct (CBD) measuring 9 mm. Mag-netic resonance cholangiopancreatography (MRCP) showed a partially obstructing subacute narrowing in the mid-CBD with wall enhancement. Also, it showed a cluster of necrotic conglomerate peripancre-atic lymph nodes. Endoscopic ultrasound (EUS) (Fig. 1 and 2) was performed afterwards and showed a mass lesion adjacent to the pancreatic head and neck at the liver hilum compressing the proximal CBD, measuring 24 × 19 mm.

(click to enlarge)

Figure 1. Endoscopic ultrasound images demonstrate the mass/enlarged lymph nodes at the liver hilum com-pressing the common bile duct. CBD: common bile duct, PV: portal vein, HA: hepatic artery, LN: lymph node, IVC: inferior vena cava, AO: aorta.

(click to enlarge)

Figure 2. Endoscopic ultrasound images demonstrate the mass/enlarged lymph nodes at the liver hilum com-pressing the common bile duct. CBD: common bile duct.

A fine needle biopsy was obtained from the mass lesion at the liver hilum, and the histopathological examination revealed necrotising granulomatous inflammation. Moreover, TB PCR and culture tests from the same lesion were positive. The patient was started on anti-TB medication (isoniazid, rifampic-in, pyrazinamide, and ethambutol) for a total duration of six months and followed in the Gastrointesti-nal clinic, where he reported total resolution of his symptoms, and repeated blood tests during his vis-its revealed improvement of bilirubin, liver enzymes and ALP until they reached normal levels after three months of treatment.


Although TB infection is a common respiratory infection, it can affect any organ, and abdominal organ involvement is one of the most prevalent forms of extrapulmonary manifestations. This happens even in the absence of lung involvement, as only 20–25% of patients with gastrointestinal TB have concur-rent pulmonary TB, which can be explained by direct swallowing of the infected sputum from primary pulmonary TB[4,5]. While the small bowel is the most commonly affected gastrointestinal organ, TB in-fection can occur in any part of the gastrointestinal system, including the hepatobiliary system. Biliary TB (BTB) is rare, and the first case of isolated BTB was only recognised and reported in 1989. BTB can occur due to primary biliary involvement or due to compression of the biliary tree by affected ad-jacent organs, such as affected lymph nodes or hepatic granuloma. BTB pathogenesis includes spread-ing from the portal tract to the bile duct (which is the most common way of infection), inflammation-related periportal adenitis and ascending through the ampulla of Vater and along the CBD[5,6].
Patients with BTB usually present with weight loss, abdominal pain, jaundice, and anorexia mimicking choledocholithiasis, cholangiocarcinoma and other causes of obstructive jaundice. Moreover, biliary involvement tends to be associated with biliary strictures, making it difficult to differentiate from chol-angiocarcinomas[5,6].
Different imaging modalities can be used to assess the biliary tree including ultrasound, magnetic reso-nance cholangiopancreatography (MRCP), endoscopic retrograde cholangiopancreatography (ERCP) and EUS. Imaging usually reveals a mass lesion and ductal dilatation that resemble cholangiocarcino-ma, which is a more likely diagnosis in such cases. Nevertheless, TB should be considered in the dif-ferential diagnosis, particularly in patients who immigrated from endemic areas. While ERCP has the advantage over other imaging modalities by allowing the placement of biliary stents to decompress the biliary systems, EUS is considered an important diagnostic tool. The definitive diagnosis of a primary hepatobiliary TB is made by acid-fast bacilli smear, culture of a specimen and histopathological evi-dence of caseating granuloma, which can be obtained by fine needle aspiration/biopsy guided by EUS[5-8].
Using standard anti-tuberculous medications has shown high efficiency in treating and eradicating my-cobacterial infection in situations such as in our case. Notably, the strictures left behind may require surgical or endoscopic interventions on an individual basis[9].


BTB is an exceptionally rare but potentially life-threatening infection with huge mortality and morbidi-ty. This report highlights the importance of considering extrapulmonary tuberculosis as a cause of ob-structive jaundice and recognising it as a part of the differential in patients with hepatic hilar mass le-sions. This is relevant even with negative TB workup from the sputum, especially in places where TB infection is still common such as South-east Asia. Early recognition and treatment are crucial to pre-vent complications.

  1. Koch A, Mizrahi V. Mycobacterium tuberculosis. Trends micriobiol 2018;26:555–556.
  2. Churchyard G, Kim P, Shah NS, Rustomjee R, Gandhi N, Mathema B, et al. What we know about tuberculosis transmission: an overview. J Infect Dis 2017;216:S629–S635.
  3. Mbuh TP, Ane-Anyangwe I, Adeline W, Thumamo Pokam BD, Meriki HD, Mbacham WF. Bacteri-ologically confirmed extra pulmonary tuberculosis and treatment outcome of patients consulted and treated under program conditions in the littoral region of Cameroon. BMC Pulm Med 2019;19:17.
  4. Cantres-Fonseca OJ, Rodriguez-Cintrón W, Del Olmo-Arroyo F, Baez-Corujo S.) Extra pulmonary tuberculosis: an overview. In: Chauhan NS, editor. Role of microbes in human health and diseases, London: IntechOpen; 2018, p. 5560.
  5. Chong VH, Lim KS. Hepatobiliary tuberculosis. Singapore Med J 2010;51: 744–751.
  6. Lee SY, Kang CY, Low SC, Chow KH. Tuberculous biliary stricture. Clin Jf Gastroenterol 2012;5: 53–58.
  7. Colovic R, Grubor N, Jesic R, Micev M, Jovanovic T, Colovic N, et al. Tuberculous lymphadenitis as a cause of obstructive jaundice: a case report and literature review. World J Gastroenterol 2008;14:3098–3100.
  8. Sivaraj SM, Sivacharan P, Mallikarjuna GR, Vamsikrishna PR, Ramakrishna BA, Thirunavukkarasu S. Primary biliary tuberculosis: a case report and review of literature. Arch Intl Surg 2013;3:150–153.
  9. Amarapurkar DN, Patel ND, Amarapurkar AD. Hepatobiliary tuberculosis in western India. Indian J Pathol Microbiol 2008;51:175–181.