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环境因素对儿童注意缺陷多动障碍与成人冠心病风险之间关联的影响。

Environmental factors influencing the link between childhood ADHD and risk of adult coronary artery disease.

机构信息

Institute of Health and Environmental Research, Cleveland, OH 44118, USA.

Institute of Health and Environmental Research, Cleveland, OH 44118, USA; New York City Department of Health and Mental Hygiene, New York 11101-4132 USA.

出版信息

Med Hypotheses. 2018 Jan;110:83-85. doi: 10.1016/j.mehy.2017.11.007. Epub 2017 Nov 15.

DOI:10.1016/j.mehy.2017.11.007
PMID:29317076
Abstract

Yorbik et al. reported novel findings regarding a hypothesized relationship between childhood attention-deficit hyperactivity disorder (ADHD) and later risk for coronary heart disease in adulthood. The authors found that mean platelet volume (MPV), a marker of platelet reactivity and a presumable biomarker in patients with cardiovascular disease, was significantly elevated in children with ADHD compared to healthy controls. The mechanistic importance of this novel discovery remains unknown and warrants clarification. We have made the novel proposition that environmental exposure to the agricultural and combustion air pollutant, nitrous oxide (NO), may be an etiological contributor to neurodevelopmental disorders. Clinical studies suggest that NO may enhance platelet hyperaggregation, possibly via its biphasic role as an MAO inhibitor especially at trace levels of exposure or via the generation of oxidative stress. Therefore, this correspondence briefly details the hypothesis that altered biochemical profiles in neurodevelopmental disorders, derived from chronic environmental exposure to the agricultural and combustion air pollutant, NO, may promote coronary artery disease in adulthood.

摘要

约比克等人报告了一项关于儿童注意力缺陷多动障碍(ADHD)与成年后冠心病风险之间假设关系的新发现。作者发现,血小板平均体积(MPV),血小板反应性的标志物,也是心血管疾病患者的潜在生物标志物,在患有 ADHD 的儿童中明显高于健康对照组。这一新颖发现的机制重要性尚不清楚,需要进一步澄清。我们提出了一个新颖的观点,即暴露于农业和燃烧空气污染物一氧化二氮(NO)可能是神经发育障碍的病因之一。临床研究表明,NO 可能通过其作为单胺氧化酶抑制剂的双相作用增强血小板的过度聚集,特别是在暴露于痕量水平或通过产生氧化应激的情况下。因此,本通信简要详细说明了这一假设,即源自慢性暴露于农业和燃烧空气污染物一氧化二氮(NO)的神经发育障碍中的生化特征改变可能会促进成年后的冠状动脉疾病。

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