Serum Adenosine Deaminase as Inflammatory Marker in Rheumatoid Arthritis BC08-BC10
Dr. Srinivasarao V.L.N. Pemmaraju,
Professor and Head, Department of Biochemistry, Sri Venkateswara Institute of Medical Sciences, Tirupati, AP-517507, India.
Background: Rheumatoid arthritis (RA) is a prototypical inflammatory joint disease. The degree of inflammation is reflected in the extent of joint damage, which further has influence on the quality of life of patients with RA, including risk of atherosclerosis. Hence, besides clinical indices, estimation of degree of inflammation using biochemical markers helps in effecting optimum treatment strategies. C-reactive protein (CRP) is established as an inflammatory marker in patients with RA. Adenosine deaminase (ADA), an enzyme of purine metabolism is considered as a marker of cell mediated immunity and has also been suggested as a marker of inflammatory process in RA. The present study attempts to study the efficacy of serum ADA activity as an inflammatory marker in RA.
Materials and Methods: Forty six RA patients and forty six age and sex matched healthy controls were included in the study. ADA activity and high sensitivity C-reactive protein (hsCRP) levels in serum were measured in all the subjects. Statistical analyses were done using Medcalc statistical software version 12.2.2.
Results: ADA activity and hsCRP levels were increased in RA patients compared to controls (p<0.0001 and 0.0001 respectively). Significant positive correlation was obtained between hsCRP and ADA in patients (r=0.316, p=0.033). Receiver operating characteristic (ROC) curve analysis revealed statistically significant area under curve (AUC) for ADA that is comparable to that obtained for hsCRP (0.776, p<0.0001 for ADA, 0.726, p<0.0001 for hsCRP). Similar diagnostic utility was obtained with ROC generated cut-off value of 25.3 IU/L (82.6% sensitivity and 65.2% specificity) and with control mean value of 23.48 IU/L (86.96% sensitivity and 54.35% specificity) for ADA.
Conclusion: Findings of the present study indicate the importance of ADA as a marker of inflammation. Considering the higher sensitivity obtained, we propose control mean (23.48 IU/L) as a cut-off for serum ADA activity as an inflammatory marker. Owing to the simplicity and also the cost effectiveness of ADA assay, ADA may be recommended as a marker of inflammation in patients with RA. However, further larger and well controlled studies are needed to establish its role as inflammatory marker.