Diagnosis of tuberculous pleurisy using the biologicL parameter adenosine deaminase

E A Dosumu, K Osagie, A Shuaib, Department of Medicine, National Hospital, Abuja, Nigeria; and J A Momoh, Department of Chemical Pathology, National Hospital, Abuja. Corresponding author: Professor E A Dosumu, P O Box 8683, Wuse Post Office, Abuja, Nigeria. Email: [email protected] Introduction The necessity to improve diagnosis and the need to identify tuberculosis (TB) as a global crisis have been discussed by Iseman.1 Adenosine deaminase (ADA) activity is greatest in the lymphoid tissues,2 most especially in T-lymphocytes.3 ADA can help in the differentiation of lymphoid cells3,4 and the maturation of macrophages.5 Cellular immune response, and in particular the activation of T-lymphocytes,6 is reflected by the presence of ADA in pleural fluid. ADA activity has been implicated in TB, malignancies, collagen vascular disease, e.g. systemic lupus erythematosus (SLE), and empyemas.6,7 ADA1 and ADA2, having two different molecular forms Abstract Adenosine Deaminase (ADA) isoenzyme levels in the pleural fluid have not been used before in Nigeria to make a diagnosis of tuberculous (TB) pleural effusions. Our objective was to identify the ADA isoenzymes as a diagnostic tool for tuberculosis (TB) in pleural effusions. One hundred and twenty patients (120) with exudative effusions and ADA activities >20 U/l, due to causes that satisfied certain diagnostic criteria, participated in this study. Of the effusions studied, 85 were tuberculous effusions, 20 were infective effusions, 10 were malignant effusions, and 5 were other exudative effusions (pancreatitis and lung embolus). The ADA isoenzymes in the pleural fluid were identified in each case using polyacrylamide gel electrophoresis. Microbiology and cytology (including differential cell counts) were also carried out on each specimen. The study was carried out between 1 January and 31 2005. The differential white cell counts of the effusions were: tuberculous, 90% lymphocytes and 5% neutrophils; empyematous, 15% lymphocytes and 73% neutrophils; and non-empyematous, 22% lymphocytes and 72% neutrophils. ADA1c and ADA2 were the predominant isoenzymes observed in tuberculous effusions while ADA1c and ADA1m were predominant in infective effusions (non-empyematous). It was concluded that ADA2 activity is a more efficient diagnostic marker of tuberculosis effusions than total ADA activity. and with unique properties, have been identified in humans.8 A different gene locus code for each isoform,8 ADA1 may exist in two forms: a monomer, ADA1, and a dimer, combined by a protein, ADA1+CP. These ADA subtypes have been referred to as ADA1m and ADA1c, respectively.9 ADA1 has been shown to have the highest activity in lymphocytes and monocytes, whereas ADA2 originates from monocytes.10 Serum from both normal subjects and patients with increased ADA activity contains ADA1c and ADA2 and is the predominant isoenzyme in patients with increased ADA activity, except in acute lymphoblastic leukaemia where ADAIC is found in excess.10 However, ADA1m has been reported in the serum of one patient with acute lymphoblastic leukaemia.10 Ungerer and Grobler,11 and Kurata and colleagues,12 have identified ADA2 and ADA1 in pleural fluid, with ADA2 being predominant in TB. These finding were later revalidated by Ugerer and colleagues9 and showed that para-infective effusions were associated with both ADA1m and ADA1c, while tuberculous effusions were associated with the ADA2 isoenzyme. This present work was performed in order to establish whether the different ADA isoenzymes could enhance the diagnosis of tuberculosis pleural effusions.