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BILIARY TUBERCULOSIS

 D N Amarapurkar, A D Amarapurkar
*Dept. of Gastroenterology, Bombay Hospital and Medical Research Centre and **Dept. of Pathology TN Medical College, Mumbai.

Tuberculosis involvement of the liver as part of disseminated tuberculosis is well known. However biliary tract obstruction caused by tuberculous lymphadenitis is very rare. We describe 3 cases of biliary tuberculosis presenting with obstructive jaundice over a period of one year.

INTRODUCTION

In recent years tuberculosis has been merged as an important disease in developing as well as developed countries, specially with rising incidence of HIV infection. [1-3] Abdomen is one of the common sites of extra pulmonary tuberculosis. [4-5] Majority of patients do not have associated or antecedent pulmonary tuberculosis. Hepatobiliary involvement is seen in about 80% of pulmonary tuberculosis. [6] Hepatobiliary tuberculosis is a distinct clinical entity. It is different from granulomatous hepatitis or hepatic granuloma associated with advanced pulmonary tuberculosis or miliary tuberculosis. [6] Biliary obstruction from enlarged tuberculous lymph node as a cause of jaundice is very rare. [7], [8] We report three cases of biliary tuberculosis presenting with obstructive jaundice.

CASE 1

A 24-year male presented with history of right hypochondriac pain, fever and jaundice for a period of one month. Physical examination revealed icterus, palpable liver 2 cm below right costal margin. There was no splenomegaly and ascites. Patient gave past history of tuberculous lymphadenitis one and half years back on axillary lymph node biopsy, for which he was treated with antitubercular therapy for one year.

On investigations at admission, haemoglobin was 9.5 gm%, WBC 15,300/cumm, erythrocyte sedimentation rate (ESR) 130 mm at the end of one hour. Total bilirubin was 5.4 mg% (direct 4 mg%), SGOT 141 IU, SGPT 100 IU, alkaline phosphatase 436 IU. Serum albumin was 3.7 gm%, serum globulin 3.8 gm%, serum creatinine 0.6 mg%. HIV was negative. X-ray chest was within normal limits. Ultrasonography (USG) showed lymph node at the head of pancreas with dilated common bile duct (CBD) and intrahepatic biliary radicals. Multiple small abscesses were also seen in the liver ranging from 0.5 to 2 mm, with one large being 5 x 3 cm in right lobe of liver. CT guided aspiration of large abscess showed pus and presence of acid fast bacilli. There was no evidence of malignancy on microscopic examination. Pus culture from the abscess grew no organisms. Endoscopic retrograde cholangiography (ERCP) showed a stricture in CBD with dilatation of intrahepatic biliary radicals, which were not communicating with abscess (Fig. 1). CBD stenting was done and antituberculous treatment was started. After three months of treatment, abscess in the liver and lymph node resolved. CBD stent was removed. Repeat ERCP showed normal CBD and intrahepatic biliary radicals. Repeat laboratory investigations were total bilirubin 0.6 mg% (Direct 0.4 mg%), SGOT 32 IU, SGPT 37 IU, alkaline phosphatase 110 IU.

CASE 2

A 27 year old male came with complaints of anorexia, evening rise in temperature, dull pain in right hypochondriac region for last one month. Night sweats, jaundice for 10 days duration. Patient gave past history of erythema nodosum for last 3 years for which he was investigated extensively. No cause was found and was treated with steroids intermittently. There was no history of tuberculosis of jaundice in past. On physical examination, there was icterus; liver was just palpable with minimal tenderness in right hypochondriac region. Other parameters were within normal limits. Laboratory investigations revealed haemoglobin 14.2 gm%, WBC 6500/cumm, ESR 38 mm at the end of one hour, total bilirubin 7.4 mg% (Direct 4 mg%), SGOT 140 IU, SGPT 400 IU, alkaline phosphatase 190 IU, serum albumin 4.8 gm%, serum globulin 3.8 gm%, serum creatinine 0.89 mg%. HIV was negative. X-ray chest was normal. USG showed lymph node at the porta and head ofpancreas with dilated CBD. CT guided aspiration of porta lymph nodes revealed necrotic material but no AFB could be demonstrated. ERCP showed stricture in mid CBD for which stenting was done and antitubercular therapy was started. Bile was sent for AFB culture and malignant cells which were negative. The stent was removed 4 months later and the biochemical parameters came back to normal with the relief of symptoms.

Fig 1 a
Fig 1 b c
Fig. 1 a b c : Endoscopic retrograde cholangiography showing mid CBD stricture with dilated intrahepatic.

CASE 3

A 34 year male non-alcoholic, non-addict came with complaints of fever with chills, anorexia for 8 days. Loose motions 4 to 5 times per day for 3 days. There was no history of chest pain, cough or dyspnoea. No past history of tuberculosis. On examination patient was febrile. There was icterus, pallor. Lymph nodes were not enlarged. Pulse 90/min, BP 130/80 mm Hg, On respiratory system examination, bilateral crepts were noticed. Per abdominal examination showed just palpable liver. Spleen was not palpable. Cardiovascular and central nervous system disclosed no abnormalities.

Laboratory investigations showed haemoglobin 10 gm%, WBC 9800/cumm, ESR 78 mm at the end of one hour. Smears for malarial parasites were negative, serum bilirubin 4.00 mg% (Direct 2.1 mg%), SGOT 34 IU, SGPT 27 IU, alkaline phosphatase 200 IU. Electrolytes were normal. HIV status was not known. X-ray chest was suggestive of pulmonary tuberculosis. Patient deteriorated very fast and died next day of admission. A complete autopsy was performed. Liver showed multiple tiny abscesses specifically around biliary tree, which were plugged with bile. Five to six other tiny nodules were scattered in parenchyma. CBD was dilated. Gall bladder was normal. A chain of matted lymph nodes was found at the porta measuring into 3x3 cms. Lungs, spleen, kidneys and small intestine showed multiple tubercules on the surface which when stained showed acid fast bacilli. Histopathology of liver showed multiple granulomas consisting of central caseation necrosis surrounded by epitheloid cells, Langhan’s giant cells and lymphocytes. They were mainly destroying bile ducts causing ulceration of its lining with tubercular granulomas within the lumen or in the wall (Fig. 2).

Fig 1d
Fig. 1d : Repeat- Cholangiogram showing normal CBD.

DISCUSSION

The most common causes of biliary tract obstruction are choledocholithiasis and neoplastic disease. When obstruction is due to mass in the region of head of pancreas, the most likely aetiology is malignant disease. However in countrieslike India with high incidence of tuberculosis, we should consider the tuberculous lymphadenitis as a potential aetiology in patients with biliary tract obstruction. Nearly 50 to 80% cases of pulmonary tuberculosis show hepatobiliary involvement but biliary tract obstruction caused by tuberculous adenitis is very rare. [6-8] There are very few case reports in whom obstructive jaundice is described due to tuberculous lymphadenitis causing CBD stricture. Two case reports from our country have described obstructive jaundice as a complication of duodenal tuberculosis. [9], [10] Shah et al [10] have reported a case of duodenal tuberculosis who developed obstructive jaundice due to benign stricture of the terminal CBD. Murphy et al [7] and Kohen et al [8] have reported a case of biliary tract obstruction due to tuberculous adenitis of peripancreatic and porta hepatic lymph nodes respectively; Alvarez et al [6] has studied clinical and other diagnostic modalities in 130 cases of hepatobiliary tuberculosis. The diagnosis of hepatobiliary tuberculosis was established on histological findings of a granuloma with caseation necrosis. Histological samples were obtained from fine needle aspiration, peritoneoscopic liver biopsy, exploratory laparotomy and during post mortem examination. Clinically cases were divided into two groups. Out of 130 cases, 85 (65%) were non jaundiced and 45 (35%) were in jaundiced group which presented with obstructive jaundice resembling CBD stones, periampullary malignancy or liver cell carcinoma clinically. Overall the diagnosis of hepatobiliary tuberculosis was suspected clinically in 106 (82%) cases, prior to histological confirmation. This is in contrast with the report of Vitug et al, [11] where the diagnosis was not even thought clinically. Our two cases appeared to have isolated involvement of peripancreatic and porta lymph nodes giving rise to CBD stricture and obstructive jaundice which is similar to the case reports by Murphy and Kohen et al, [7-8] Out of these two, one case showed multiple liver abscesses. In the case where past history of erythema nodosum was given, presumptive diagnosis of tuberculosis was made. CT guided aspiration of porta lymph node helped us to exclude malignancy. Then patient was given antitubercular therapy for which he responded well. In our third case of disseminated mainly biliary tree was involved.

The pathophysiology of hepatobiliary tuberculosis is similar to extrapulmonary tuberculosis, which results from haematogenous spread from inhalation of tubercular bacilli with healing of primary pulmonary lesion and implantation of organisms in abdominal lymph nodes. Alternatively, peripancreatic or porta node involvement may have been secondary to lymphatic spread from another occult intraabdominal process. [7] Hence; tuberculous lymphadenitis should be regarded as a potential aetiology in patients with biliary tract obstruction.

Fig 2
Fig. 2 : Microphotograph showing ulcerated epithelium of bile duct with tubucular granuloma (HE 100 x ).

REFERENCES

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