Tuberculous liver abscess.

Sir, Tuberculous liver abscess is rarely reported. In Hepatic tuberculosis, liver may be involved as part of miliary tuberculosis or as local tuberculosis without obvious extra hepatic disease.1 We recently came across tuberculous liver abscess in an immunocompetent patient with bilateral pulmonary tuberculosis. A 51 years old man presented with history of cough with expectoration, low grade fever, anorexia for eight months, history of upper abdominal swelling for seven months. He was a smoker and alcoholic for twenty years. Patient had underwent Posterior Gastrojejunostomy with truncal vagotomy eight years back for gastric outlet obstruction due to duodenal ulcer. On general examination the patient was afebrile, not jaundiced, and other parameters were normal. On local examination, there was an upper midline scar , liver was palpable 5 cm below the right costal margin. A non tender mass 6X4cm was felt in the left lobe of liver, smooth surface, firm in consistency, moves with respiration. Investigations done were: Hb-12 g%,WBC-16500 (P-87%L-13%), ESR -60 mm at 1 hr. Liver function tests were normal except for raised alkaline phophatase and reversed albumin and globulin ratio. HIV by ELISA, HBsAg were negative. Serum alfa feto protein was within normal range. Sputum microscopic examination showed acid fast bacilli. Chest X-ray PA showed bilateral pulmonary tuberculosis. USG Abdomen showed hepatomegaly with two left liver lobe abscesses each measuring 5 x 4 cm and 3x2 cm . CT Abdomen confirmed the findings. CT guided FNAC caseating granulomatous inflammation with suppurative degeneration suggestive of tuberculous abscess. Pus for culture showed absence of other organisms but acid fast bacilli could not be demonstrated. Patient was started on 4 drug Anti tuberculosis treatment –Isoniazide (300mg), Rifampicin(600mg, Ethambutol (1200 mg), Pyrazinamide (1500 mg ) for four months to be followed by Isoniazide and Rifampicin for two months. Patient showed improvement of symptoms and regression of size of the abscesses on follow –up USG. Although the prevalence of tuberculosis is high in India the occurrence of hepatic TB is rare. Primary involvement of the liver in tuberculosis is rare due to the low tissue oxygen level which makes liver inhospitable for the bacilli. Researchers have described three morphological types of hepatic tuberculosis: a) miliary TB of liver associated with generalized miliary TB, b) primary miliary TB of liver without involvement of other organs and c) a primary nodular lesion termed tuberculoma or frank abscess. Histologically the finding of caseating granuloma is considered to be diagnostic of TB. However, it has also been reported in brucellosis, coccidiodomycosis and Hodgkin’s disease but the clinical presentation is different. The hepatic tuberculoma is usually a large epitheliod tumour composed of conglomerate tubercles with central caseation necrosis. Langerhans-type giant cells may be found in the granuloma and are surrounded by lymphohistiocytic cells, plasma cells and eosinophils.2 It is rare to demonstrate acid fast bacilli in TB hepatic abscess. The frequency ranges from 0% to 45% ; only 10% of cultures yield positive result which is upto 60% in miliary TB cases. We concluded that, the liver abscess is of tuberculous etiology, on the basis of a) evidence of AFB elsewhere b) presence of caseating granuloma and c) good response to ATT. In conclusion, tuberculous etiology should be thought of in any case of liver abscess especially in a country like India where prevalence of tuberculosis and AIDS is high.3 Awareness of this rare clinical entity prevents needless surgical interventions. The prognosis of hepatic tuberculosis is good if diagnosed early and effective treatment is administered. A Kanagaraj*, L RajagopalaMarthandam**, V Sriramakrishnan**, A Rajesh**, P Meenakumari*** *Additional Professor of Medicine; **Assistant Professor in Medicine; ***Post Graduate in Medicine, Department of Medicine, Tirunelveli Medical College, Tirunelveli, Tamil Nadu, India. Received : 5.3.2008; Revised : 2.5.2008; Accepted : 2.6.2008