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Introduction: Chronic heart failure (CHF) has recently been considered as an inflammatory disease. Enhanced production of tumor necrosis factor-α (TNFα) in CHF patients has been proved. To compensate deleterious effects of TNα, the concentration of adenosine is increased in CHF. However, concurrent determination of serum TNFα and enzymatic activities of ADA and its ADA1 and ADA2 isoenzymes, as the main regulators of adenosine concentration, has not yet been carried out.
Materials and Methods: Blood samples were collected from 52 CHF patients and 55 healthy controls. Laboratory routine tests were performed, and after determining the concentration of TNFα, total ADA (tADA) as well as ADA1 and ADA2 isoenzyme activities were measured.
Results: Mean concentration of TNFα increased over 2 fold in CHF patients (12.54 ± 11.69 pg/ml compared with 6.0 ± 6.58 pg/ml in controls). The highest level of TNFα was observed in patients with the final stage of the disease (NHYA IV subgroup), according to the New York Heart Association classification. tADA activity was significantly lower in CHF patients compared with controls (19.29 ± 9.73 and 24.3 ± 6.01 U/L, respectively). ADA2 activity markedly decreased in CHF patients and showed a direct correlation with tADA (r = 0.641, P = 0001). In addition, the lowest levels of tADA and ADA2 activities were observed in patients from the 4th quartile of NYHA classification.
Conclusion: Adenosine deaminase activity is reduced in CHF patients to give rise to the concentration of adenosine, thereby attenuating pathologic consequences of CHF. Therefore, it is concluded that ADA activity is of paramount importance in pathophysiology of heart failure and might be used for diagnostic purposes or treatment targets.
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