Why the study?
Conventional diagnostic methods for tuberculous pleurisy have low sensitivity and slow culture turnaround times, creating challenges in differentiating lymphocytic pleural effusions.
Does adenosine deaminase (ADA) testing in pleural fluid improve diagnosis of tuberculous pleurisy in patients with suspected tuberculous pleurisy?
Does adenosine deaminase (ADA) testing in pleural fluid improve diagnosis of tuberculous pleurisy in patients with suspected tuberculous pleurisy?
Adenosine deaminase is a fast, efficient, and economical biomarker for diagnosing tuberculous pleurisy, especially when other diagnostic procedures are negative.
Tuberculous pleurisy (TP) is one of the most common extra-pulmonary tuberculosis forms. Tuberculous pleurisy occurs when Mycobacterium tuberculosis antigen is released from a ruptured caseous focus into the pleural space causing hyperinflammatory response with a rapid influx of lymphocytes. Acid-fast bacilli (AFB) staining, cultures and pathohistological biopsy finding are positive in most patients only in less than 10% of samples. Culture results take about 6-8 weeks which delays the diagnosis. A problem also occurs in the differentiation of effusions with lymphocytic predominance. Adenosine deaminase (ADA) is a biochemical marker with high sensitivity and specificity and is considered a gold standard within biomarkers when it comes to diagnosing TP. Using an algorithm for the values of ADA above or below 40 U/L we can distinguish this type of effusion from other types. ADA in pleural punctate is a fast, efficient, and economical way for clarifying the etiology of a pleural effusion such as tuberculous pleurisy and treatment response during the follow up period.
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Janković et al. (2023) studied this question.
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