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[Tuberculosis in circulation system]
1Third Department of Internal Medicine, Nagasaki University School of Medicine.
Abstract:
Tuberculous pericarditis develops either via hematogenous or lymphangeal spread, or directly from pulmonary lesions. Tuberculous pericarditis begins with fibrin deposits, granuloma formation, and the presence of live acid-fast bacilli. A pericardial effusion, which is serous but often contains some blood with a high level of protein. Recently, PCR technology has been employed to amplify M. Tuberculosis DNA from pericardial fluid. The elevation of ADA (> 45 U/l) is supportive of the diagnosis. Tuberculous pericarditis is detected clinically either in the effusive stage by nonspecific systemic syndrome or after the development of constrictive pericarditis. The short-course treatment of tuberculous pericarditis should consist of three-drug regimen, such as INH, RFP, PZA, SM, EB. The use of prednisolone is controversial. Tuberculous myocarditis is extremely rare because of low affinity between M. Tuberculosis and myocardium. Most cases of tuberculous pericarditis are clinically silent and diagnosed at autopsy.
Insights
Tuberculous pericarditis, caused by Mycobacterium tuberculosis, presents as fluid accumulation around the heart. Diagnosis aids include PCR and elevated ADA levels, with treatment involving a three-drug regimen.
Area of Science:
- Infectious Diseases
- Cardiology
- Microbiology
Context:
- Tuberculous pericarditis arises from Mycobacterium tuberculosis spread.
- Pathological hallmarks include fibrin deposits, granulomas, and bacilli presence.
- Pericardial effusions are typically serous, hemorrhagic, and protein-rich.
Purpose:
- To outline the pathogenesis, diagnosis, and treatment of tuberculous pericarditis.
- To highlight diagnostic tools such as PCR and Adenosine Deaminase (ADA) levels.
- To discuss treatment strategies and the controversial role of prednisolone.
Summary:
- Tuberculous pericarditis involves Mycobacterium tuberculosis infection of the pericardium.
- Diagnosis is supported by PCR detection of M. Tuberculosis DNA and elevated ADA levels (> 45 U/l).
- Treatment typically involves a three-drug regimen (e.g., INH, RFP, PZA, SM, EB), with prednisolone use debated.
Impact:
- Informs clinical diagnosis and management of tuberculous pericarditis.
- Emphasizes the utility of molecular diagnostics and biochemical markers.
- Contributes to understanding the clinical course and therapeutic options for this serious infection.