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Oxidative status in treatment-naive essential thrombocythemia: a pilot study in a single center

机译:治疗幼稚基本血小板血症的氧化地位:单一中心的试验研究

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Oxidative stress (OS), due to pro-oxidant species [reactive oxygen species (ROS)] excess not counterbalanced by endogenous antioxidant molecules [e.g., reduced glutathione (GSH)], is involved in the pathogenesis of human cancers, but few data are available on essential thrombocythemia (ET). This study aims to investigate OS in ET off-therapy patients. Thirty ET treatment-naive patients were compared with 26 age-matched and gender-matched controls. Serum ROS, urinary 8-hydroxydeoxyguanosine, full blood GSH levels, and reduced/oxidized GSH ratio (GSH/GSSG) were measured. Data were adjusted for gender, age, JAK2 mutational status, smoking, dyslipidemia, or hypercholesterolemia requiring drug therapy, antiplatelet therapy, treatment with acetylsalicylic acid, high-sensitive C-reactive protein levels, and absolute monocyte count. ROS and GSH levels were increased in both patients and controls. Patients showed increased GSSG (p=0.05), reduced GSH/GSSG ratio (p=0.08), and similar 8-hydroxydeoxyguanosine levels when compared with controls. No differences in OS parameters were found between JAK2-positive and JAK2-negative patients. Confounding factors did not modify the results. Our study suggests an OS condition in a cohort of treatment-naive ET patients, not associated with JAK2 mutational status or with chronic inflammation situation. GSH/GSSG ratio, altered in ET patients because of increased GSSG levels, showed the presence of higher GSH levels in ET than controls as a possible compensatory mechanism of an excess of pro-oxidant production. Copyright (c) 2015 John Wiley & Sons, Ltd.
机译:氧化应激(OS)由于促氧化剂物质[反应性氧物质(ROS)过量不抵抗内源性抗氧化分子[例如,还原的谷胱甘肽(GSH)],参与人类癌症的发病机制,但很少的数据是可在基本血小板上(ET)。本研究旨在调查ET off-Therapy患者的OS。将Thirty et治疗 - 幼稚患者与26次匹配和性别匹配的对照进行比较。测量血清ROS,尿8-羟基氧基胍,全血GSH水平和降低/氧化GSH比(GSH / GSSG)。数据进行了调整,适用于性别,年龄,JAK2突变状态,吸烟,血脂血症或高胆固醇血症需要药物治疗,用乙酰胱氨酸,高敏感的C反应蛋白水平处理,以及绝对单核细胞计数。患者和对照组中,ROS和GSH水平增加。患者表现出GSSG的增加(P = 0.05),减少GSH / GSSG比(P = 0.08),与对照相比类似的8-羟基氧基核苷酸水平。在JAK2阳性和JAK2阴性患者之间发现了OS参数的差异。混杂因素没有修改结果。我们的研究表明,治疗幼稚患者队列的OS条件,与JAK2突变状态或慢性炎症情况无关。 GSH / GSSG率因GSSG水平升高而改变等,显示ET中的GSH水平较高,而不是对多余氧化剂产生的可能补偿机制。版权所有(c)2015 John Wiley&Sons,Ltd。

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