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Pleural Tuberculosis and the Utility of ADA in Low Prevalence Population

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A6690 - Pleural Tuberculosis and the Utility of ADA in Low Prevalence Population
Author Block: L. L. Seijo1, J. Filopei2; 1Department of Internal Medicine, Mount Sinai Beth Israel, New York, NY, United States, 2Division of Pulmonary Critical Care and Sleep Medicine, Mount Sinai Beth Israel, New York, NY, United States.
INTRODUCTION-Mycobacterium Tuberculosis (MTB) is a deadly disease affecting third of the global population. Tuberculous pleural effusion (TPE) is the second most common manifestation of extra-pulmonary MTB.We describe a case of a Caucasian male presenting to a New York City hospital with TPE. We review the pitfalls of pleural adenosine deaminase (ADA) in a low prevalence region and the subsequent utility of a closed pleural biopsy for making the diagnosis of TPE.
CASE-A 26-year-old male presented to his primary provider with ten days of fever, night sweats, fatigue, and pleurisy. He had a history of latent TB diagnosed by PPD conversion in the setting of direct exposure to active TB, receiving a 9-month course of Isoniazid. Patient received azithromycin without improvement. CT chest was performed revealing a large right pleural effusion and right hilar lymphadenopathy and was sent to our hospital.In the hospital, the patient was well appearing with normal vital signs without laboratory abnormalities. Thoracentesis was performed showing a lymphocytic exudate. Forty-eight hours later, sputum smears, PCR, pleural fluid AFB cultures, ADA (18.2 U/L), and cytology were normal. Serum fungal and viral markers including aspergillus, histoplasma, coccidioides, HIV, CMV, and EBV were negative. We pursued a closed needle pleural biopsy as our suspicion for pleural TB persisted. Pleural biopsy pathology revealed necrotizing granulomas. The patient was given four anti-tuberculous therapy. Pleural fluid culture five weeks later grew MTB. At follow-up, clinical symptoms and pleural effusion resolved.
DISCUSSION-Tuberculous pleural effusions presents as an acute illness in middle-aged males causing fever and pleuritic chest pain. The gold standard for diagnosing TPE includes detection of M. tuberculosis in the sputum, pleural fluid or tissue specimens. Other diagnostic modalities include elevated levels of pleural fluid ADA (>40 U/L) or histological demonstration of necrotizing granulomas.Elevated ADA is an effective and inexpensive way to diagnose TPE. The diagnostic usefulness of ADA depends on the local prevalence of TB with most studies showing benefit in regions of high TB burden.It’s imperative clinicians be aware of scenarios where ADA can be falsely negative, including early stages of disease, the elderly, and active smokers. In cases where the pleural ADA is low but high clinical suspicion remains, a closed pleural biopsy should be pursued as necrotizing granulomas and culture have been shown to be positive in over 90% of TB cases. Pleural biopsy should be performed when the clinical suspicion for TPE remains high even with conflicting biomarkers.
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