Hepatic Tuberculosis

Hepatic tuberculosis is relatively uncommon. Because it lacks specific symptoms and signs, the clinical rate of misdiagnosis and mistreatment is relatively high. Most hepatic tuberculosis is a part of miliary tuberculosis of the whole body, known as secondary hepatic tuberculosis; patients mainly present with clinical manifestations caused by extrahepatic tuberculosis of the lungs, intestines and other organs, generally without clinical symptoms of liver disease. After anti-tuberculosis treatment, the intrahepatic tuberculosis can be cured accordingly, making clinical diagnosis of hepatic tuberculosis very difficult.

Common Symptoms

Fever of unknown origin; cachectic facies; ascites; night sweats; abdominal pain; low-grade fever; hepatomegaly; intrahepatic calcification; liver enlargement

Etiology

Mycobacterium tuberculosis belongs to the order Actinomycetales, family Mycobacteriaceae, genus Mycobacterium; it is a pathogenic acid-fast bacillus, mainly divided into human, bovine, avian and murine types. The strains pathogenic to humans are mainly the human type; the bovine type rarely causes infection. M. tuberculosis is slender and curved in shape with blunt rounded ends, no spores or capsules, and no flagella, approximately 1 to 5 μm in length and 0.2 to 0.5 μm in width. In specimens it appears dispersed, in clumps or arranged in chains. M. tuberculosis is an obligate aerobe; it does not multiply under anaerobic conditions but can survive for a relatively long time. Under favorable conditions, it multiplies once every approximately 18 to 24 hours. Lipid components account for approximately one quarter of the bacterial weight, and it is acid-fast on staining. M. tuberculosis has strong resistance to dryness, strong acids and strong alkalis, and can survive in the external environment for a long time; it can survive 20 to 30 hours in sputum and 6 to 8 months in dark, damp places. However, its resistance to moist heat is very low: boiling for 5 minutes or direct exposure to sunlight for 2 hours kills it, and ultraviolet disinfection is highly effective. Human and bovine strains are obligate parasites, with humans and cattle respectively as their natural reservoir hosts; both have equal pathogenicity for humans, monkeys and guinea pigs. Drug resistance of M. tuberculosis can develop from naturally resistant bacilli in the bacterial population, or can be rapidly produced by using a single anti-tuberculosis drug in the human body, i.e., acquired drug-resistant bacilli. Drug-resistant bacilli can cause therapeutic difficulties and affect efficacy. Prolonged contact of M. tuberculosis with streptomycin can also produce dependence, the so-called drug dependence, but dependent bacilli are rarely seen clinically. Hepatic tuberculosis is caused by dissemination of various extrahepatic tubercle bacilli to the liver; sometimes because the extrahepatic primary focus is small or has healed, the primary lesion cannot be identified; statistics show that the primary focus can be identified in only 35% of cases. The liver has abundant blood supply and lymphatics; generally, tubercle bacilli entering the human body can reach the liver, but the liver has strong regenerative and repair capacity and an abundant mononuclear phagocyte system, and bile also has an inhibitory effect on the growth of tubercle bacilli. Therefore, not all tubercle bacilli invading the liver can form lesions. Hepatic tuberculosis occurs more readily only when the body's immune function is low, or large numbers of tubercle bacilli invade the liver, or the liver itself has certain lesions such as fatty liver, liver fibrosis, cirrhosis or drug-induced injury. In recent years, it has been found that the incidence of hepatic tuberculosis is significantly increased in people infected with the human immunodeficiency virus (HIV) or in such patients, suggesting that cellular immunity plays an important role in the development and progression of hepatic tuberculosis. The routes by which tubercle bacilli invade the liver include: 1. Hepatic artery: the main route of hepatic tuberculosis; in systemic hematogenous disseminated tuberculosis or active tuberculous lesions anywhere in the body, due to reduced immunity or certain local factors, the tuberculous focus ruptures, tubercle bacilli enter the blood circulation and reach the liver through the hepatic artery. 2. Portal vein: a small number of hepatic tuberculosis cases can be infected through the portal vein route; tubercle bacilli in tuberculous lesions of organs or tissues at the origin of the portal venous system, such as intestinal tuberculosis or mesenteric lymph node tuberculosis, invade the liver through the portal vein. 3. Umbilical vein: tubercle bacilli in placental tuberculous foci during the fetal period enter the fetal body through the umbilical vein, causing congenital hepatic tuberculosis. 4. Lymphatic system: intrahepatic lymphatics directly communicate with the celiac lymphatic plexus and retroperitoneal lymph nodes, so intra-abdominal tuberculosis can enter the liver through lymphatics to form infectious foci. 5. Direct extension: tuberculous foci in organs and tissues adjacent to the liver can directly invade the liver. The basic pathological change of hepatic tuberculosis is granuloma, which can develop into different pathological types depending on the number of invading tubercle bacilli, the site and the state of the body's immune function. They are generally classified as: 1. Miliary type: the most common, a part of systemic hematogenous disseminated miliary tuberculosis; the lesions are miliary-sized up to 2 cm, hard, white or grayish-white multiple small nodules widely scattered throughout the liver. This type is serious in condition and difficult to diagnose clinically, mostly discovered at autopsy or exploratory laparotomy. 2. Nodular type: less common; the lesions are relatively localized, forming single or multiple hard grayish-white nodules of more than 2 to 3 cm, which may even fuse into masses, resembling tumors, also known as tuberculomas. 3. Abscess type: necrosis at the center of the tuberculous focus forms white or yellowish-white caseous pus, which may be single or multiple; the abscess cavity is mostly unilocular, with multilocular being rare. 4. Biliary type: hepatic tuberculosis involves the bile ducts or abscesses rupture into the bile ducts, forming biliary tuberculosis lesions, manifested as thickening, ulceration or stricture of the bile duct wall; this type is very rare. 5. Hepatic serosal type: manifested as miliary tuberculous foci on the liver capsule or capsular proliferation and thickening forming the so-called "frosted liver," which is relatively rare.

Treatment

Pharmacotherapy, traditional Chinese medicine treatment, supportive treatment

Preventive Measures

1. Control the source of infection: discovering and managing the source of infection is an important link in tuberculosis prevention and control; early detection and early treatment should be achieved. For this purpose, regular collective lung health examinations should be conducted and a registration management system implemented. 2. Cut off transmission routes: manage and dispose of patients' sputum; the main methods include carrying out mass hygiene campaigns, widely publicizing tuberculosis prevention knowledge, developing good hygiene habits, not spitting on the ground, having tuberculosis patients spit into paper and burn it, or cough into a sputum cup containing 2% cresol soap solution or 1% formaldehyde solution (which sterilizes in approximately 2 hours), and exposing contaminated articles directly to sunlight (sterilizing in several hours). 3. BCG vaccination: BCG vaccination can enhance the body's resistance to tubercle bacilli and is conducive to preventing the occurrence of tuberculosis. Currently, China stipulates that BCG is given immediately after birth, with an additional dose for those who test negative. Ethnic minorities, border residents entering inland cities, or new recruits must undergo tuberculin testing; those who test negative receive BCG vaccination.

Department of Visit

It is recommended to visit the hepatology department. Before visiting, you can book an appointment and connect with specialists through this platform.

Reminder: The above information is for health education reference only and cannot replace professional medical diagnosis. If you have related symptoms, please seek timely medical attention at a regular hospital.