首页> 外文期刊>EXCLI Journal >Evaluation of adenosine deaminase (ADA) isoenzymes activity and tumor necrosis factor-alpha (TNFalpha) concentration in chronic heart failure
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Evaluation of adenosine deaminase (ADA) isoenzymes activity and tumor necrosis factor-alpha (TNFalpha) concentration in chronic heart failure

机译:慢性心力衰竭中腺苷脱氨酶(ADA)同工酶活性和肿瘤坏死因子-α(TNFalpha)浓度的评估

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Introduction: Chronic heart failure (CHF) has recently been considered as an inflammatory disease. Enhanced production of tumor necrosis factor-? (TNF?) in CHF patients has been proved. To compensate deleterious effects of TNF?, the concentration of adenosine is increased in CHF. However, concurrent determination of serum TNF? 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 TNF?, total ADA (tADA) as well as ADA1 and ADA2 isoenzyme activities were measured. Results: Mean concentration of TNF? 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 TNF? 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.
机译:简介:慢性心力衰竭(CHF)最近被认为是一种炎症性疾病。肿瘤坏死因子-α的产生增加CHF患者中的TNF(TNFα)已被证实。为了补偿TNFα的有害作用,在CHF中增加了腺苷的浓度。但是,同时测定血清TNF?作为腺苷浓度的主要调节剂的ADA及其ADA1和ADA2同工酶的酶活性尚未进行。材料和方法:从52名CHF患者和55名健康对照中采集血液样本。进行了实验室常规测试,并确定了TNFα的浓度后,测量了总ADA(tADA)以及ADA1和ADA2同工酶的活性。结果:TNF的平均浓度?在CHF患者中增加了2倍以上(12.54?11.69 pg / ml,而对照组为6.0?6.58 pg / ml)。 TNF水平最高?根据纽约心脏协会的分类,在患有该疾病最后阶段(NHYA-IV亚组)的患者中观察到了这种现象。与对照组相比,CHF患者的tADA活性显着降低(分别为19.29±9.73和24.3±6.01 U / L)。 CHF患者的ADA2活性显着降低,并与tADA直接相关(r = 0.641,P = 0001)。此外,在NYHA分类的第4个四分位数的患者中,观察到最低水平的tADA和ADA2活性。结论:CHF患者的腺苷脱氨酶活性降低,导致腺苷浓度升高,从而减轻了CHF的病理后果。因此,得出的结论是,ADA活动在心力衰竭的病理生理中至关重要,可用于诊断目的或治疗目标。

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