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Serum adenosine deaminase activity in pleural effusion
  1. VEENA SINGH,
  2. SIMMI KHARB,
  3. P S GHALAUT,
  4. ASHOK JANMEJA
  1. 22/9J Medical Enclave
  2. Pt. B.D. Sharma PGIMS
  3. Rohtak 124001
  4. India

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Pleural effusion is a common complication of many disease processes. Tuberculosis is still one of the most important causes of exudative effusions.1 Over the last decade many workers have emphasised the importance of estimating adenosine deaminase (ADA) in pleural fluid.2 ADA activity in human biological fluid results from the action of two isoenzymes—namely, ADA1 and ADA2—with different affinities on two substrates, 2′ deoxyadenosine and adenosine, respectively. The deaminase ratio (ADA1/ADA2) is of value in the correct differentiation of the aetiology of the disease, whether it is infectious or neoplastic.3

One hundred patients (84 men) with pleural effusions admitted to a chest ward were divided into four groups including 41 patients with tuberculous pleurisy and 15 patients with malignancy. A significant increase in total ADA was observed in those with tuberculous effusion compared with those with benign acellular effusion (98.52 (20.41) vs 16.25 (1.35) IU/l, p<0.001; ADA ratio <0.28 vs 0.30). In addition, patients with metapneumonic pleurisy had high ADA activity (100.35 (25.65) IU/l) with an ADA ratio of 0.55 (0.05), and those with malignant effusion had an ADA ratio of 0.57 (0.040) with total ADA activity of 37.41 (1.64) IU/l. In patients with tuberculous effusion the test had 90% sensitivity and 87% specificity.

We thus observed significantly raised ADA values in patients with tuberculous, metapneumonic and malignant effusions, but the ADA ratio was <0.45 in those with tuberculous effusions and >0.45 in those with malignant or metapneumonic effusions. The ADA1isoenzyme is intracellular in location and is essential for the differentiation of lymphoid cells, particularly T cells.3An increase in ADA1 can be attributed either to extensive cellular necrosis or to increased turnover of lymphoid cells as occurs in metapneumonic pleurisy and malignancy. ADA2 is found only in monocyte macrophages and is released into biological fluids (pleural, peritoneal, CSF and serum) when they harbour a micro-organism.3 High total ADA activity and a deaminase ratio of <0.45 implies an increase in ADA2 and the patient is most likely to be infected with an intracellular organism—for example, tuberculosis. On the other hand, high total ADA activity and a deaminase ratio of >0.45 correlated well with malignancy or empyema in the present study. Our findings suggest that the deaminase ratio may be a useful screening test in the diagnosis of exudative pleural effusions.

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