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Chapter 25 : Tuberculosis of the Liver, Biliary Tract, and Pancreas
Category: Clinical Microbiology; Bacterial Pathogenesis
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This chapter reviews the clinical, biochemical, and histopathologic spectrum of tuberculosis (TB) and atypical mycobacteria involving the liver and pancreaticobiliary tract, as well as the hepatotoxicity caused by antituberculosis therapy. Classic Mycobacterium tuberculosis infection in persons not infected with human immunodeficiency virus (HIV) precedes the discussion of the disease in patients with HIV and AIDS and other immunocompromised persons, such as liver transplant recipients. The liver can be involved in all forms of TB (i.e., pulmonary, extrapulmonary, and miliary). In addition, infection confined predominantly to the liver or biliary tract has been recognized with some regularity, especially in areas where TB remains endemic. Pulmonary TB involves the liver less frequently than does miliary TB, with an average of approximately 20% for pulmonary TB and 68% for extrapulmonary or miliary disease. A subset of patients with extrapulmonary TB has the infection confined solely or predominantly to the liver or biliary tract. TB of the pancreas or of the peripancreatic lymph nodes is infrequent compared to the liver. Of greater concern than active TB developing posttransplant is the risk of hepatotoxicity associated with isoniazid (INH) prophylaxis. Antituberculosis agents are among the most common causes of non-acetaminophen-related acute liver failure leading to emergency liver transplantation. Fluoroquinolones are frequently used to replace agents in first-line anti-TB regimens in patients with TB who have drug-induced hepatic dysfunction. With proper clinical and biochemical monitoring, it is thought that the risk of INH and combination chemotherapy- induced hepatic injury can be significantly reduced.
Low-power photomicrograph of the liver of an infant with miliary tuberculosis showing multiple granulomas. Moderate steatosis attributable to severe malnutrition is also present. (Courtesy of K. G. Ishak.)
Section from the liver in Fig. 1 showing two noncaseating hepatic granulomas, one with Langerhans’ giant cells. (Courtesy of K. G. Ishak.)
Higher magnification of a granuloma from Fig. 1 showing central caseous necrosis. (Courtesy of K. G. Ishak.)
Acid-fast organisms (arrows) in a caseating granuloma. (Courtesy of K. G. Ishak.)
Mycobacterium avium in a poorly formed granuloma in a patient with AIDS. (Courtesy of I. K. Ishak.)