Key result
Adenosine deaminase and sIL-2R levels were significantly elevated in tuberculous pleural effusions compared to non-tuberculous effusions (p < 0.005).
Why the study?
Do levels of sIL-2R, neopterin, and ADA in pleural effusions help differentiate the etiology of pleurisy?
Observational (n=93)
Do levels of sIL-2R, neopterin, and ADA in pleural effusions help differentiate the etiology of pleurisy?
p-value: p=< 0.005
ADA and sIL-2R are useful markers for identifying tuberculous pleural effusions, while neopterin levels can help distinguish malignant and uremic effusions.
May support tuberculous effusion diagnosis; hypothesis-generating and requires prospective validation before practice change.
We evaluated soluble interleukin-2 receptors (sIL-2R), neopterin and adenosine deaminase (ADA) in pleural effusions from 93 patients with tuberculosis, malignancies, uremia, pneumonia and other kinds of pleurisy. There were significantly elevated ADA (102.7 +/- 47 U/l) and sIL-2R (8,238 +/- 4,117 U/ml) values in tuberculous (TB) pleural fluids as compared with other non-TB pleural fluids (p < 0.005). The neopterin levels in pleural fluid were significantly lower in the cancer group (17.3 +/- 7.8 nmol/l; p < 0.005) and most strikingly elevated (309.4 +/- 112.2 nmol/l; p < 0.0001) in patients with uremic pleural effusions. Using cut-off values of 60 U/l in ADA and 5,000 U/l in sIL-2R, 92.0 and 86.9% of pleural effusions were TB in origin. Eighty-four percent of patients with malignant pleural effusions had neopterin levels less than 25 nmol/l.
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Chiang et al. (2009) conducted an observational in Pleural effusions (n=93). Biomarker levels (sIL-2R, neopterin, ADA) vs. Non-tuberculous pleural fluids was evaluated on ADA and sIL-2R levels in tuberculous vs non-tuberculous pleural fluids (p=< 0.005). Adenosine deaminase and sIL-2R levels were significantly elevated in tuberculous pleural effusions compared to non-tuberculous effusions (p < 0.005).
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