从甲状腺到心脏

R. Moncayo, H. Moncayo
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引用次数: 0

摘要

人类疾病的发病机制通常被认为是每个器官或系统独有的。这导致医学实践的专业化,为全球发病机制概念留下了很少的空间。在这篇综述中,我们偏离了辅酶Q10(CoQ10)缺乏的生化概念及其与缺氧反应启动的系统关系。文献中已知继发性辅酶Q10缺乏的几种情况,通过这些情况,相关器官可能受到缺氧的影响并转变为糖酵解代谢。这种情况下最显著的生物标志物是低T3综合征和IL-6的升高。这些参数与辅酶Q10缺乏一起描述了获得性线粒体功能障碍的状况。其他相关的生化缺乏状况会影响镁、硒和铁的水平。糖酵解的可视化可以通过基于使用18F-氟脱氧葡萄糖(18F-FDG)的诊断成像方法清楚地实现。我们介绍了几个18F-FDG诊断成像的例子,以证明我们的获得性线粒体功能障碍和疾病模型。
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From the Thyroid to the Heart
The pathogenesis of human disease is commonly considered to be unique to each organ or system. This has led to specialization in medical practice leaving little space for global pathogenesis concepts. In this review we have departed from a biochemical concept of coenzyme Q10 (CoQ10) deficiency and its relation to the initiation of hypoxia response in a systemic way. Several conditions of secondary CoQ10 deficiency are known in the literature by which the organs involved could be affected by hypoxia and switch to glycolytic metabolism. The most salient biomarkers of this situation are the low T3 syndrome and the elevation of IL-6. These parameters together with CoQ10 deficiency delineate a condition of acquired mitochondrial dysfunction. Additional related biochemical deficiency conditions affect magnesium, selenium, and iron levels. Visualization of glycolysis can be clearly achieved by diagnostic imaging methods based on the use of 18F-fluoro-deoxyglucose (18F-FDG). We present several examples of diagnostic imaging with 18F-FDG to demonstrate our model of acquired mitochondrial dysfunction and disease.
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