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Adenosine Deaminase in the Diagnosis of Tuberculous Pleural Effusion

Yash P. Kataria, MD, FCCP; Imtiaz Khurshid, MB, BS
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Affiliations: Greenville, NC 
 ,  Dr. Kataria is Professor of Medicine and Director of the Sarcoidosis Clinic, and Mr. Khurshid is a member of the Section of Pulmonary & Critical Care Medicine, Brody School of Medicine at East Carolina University, Greenville, NC.

Correspondence to: Yash P. Kataria, MD, FCCP, 3E-149 Brody Science Building, Brody School of Medicine at East Carolina University, Greenville, NC 27858; e-mail: katariay@mail.ecu.edu



Chest. 2001;120(2):334-336. doi:10.1378/chest.120.2.334
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In some parts of the United States, pleural tuberculosis accounts for < 5% of all cases of tuberculosis.1 In some countries, the incidence of pleural tuberculosis is much higher. It is generally linked to the local prevalence of tuberculosis. Pleurisy with effusion as a complication of primary pulmonary tuberculosis has been reported to occur in 2 to 38% of children with pulmonary disease, but it is more likely to occur in adolescents and adults.28 However, tuberculous pleural effusion in older patients with classic reactivation of tuberculosis also can occur.1 Tuberculous pleural effusion is thought to result from a delayed hypersensitivity reaction in response to the presence of mycobacterial antigens in the pleural space.9 These mycobacterial antigens may gain access to the pleural space from the rupture of a small subpleural focus.10 A significant number of patients (50 to 59%) with primary tuberculosis who develop pleural effusion may have roentgenographically apparent parenchymal tuberculosis.1,8 Delayed hypersensitivity reaction causes the stimulation and differentiation of lymphocytes that perform a variety of functions, including the release of certain lymphokines that activate macrophages for enhanced mycobactericidal effect.11

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