McCarty Mark F, Barroso-Aranda Jorge, Contreras Francisco
Oasis of Hope Hospital, Tijuana, Mexico.
Med Hypotheses. 2009 May;72(5):581-3. doi: 10.1016/j.mehy.2008.12.023. Epub 2009 Feb 1.
There is suggestive evidence that chronic elevations of parathyroid hormone (PTH), associated with poor vitamin D status or low calcium intake, can increase risk for insulin resistance, weight gain, hypertension, and left ventricular hypertrophy, while stimulating production of acute phase reactants. New evidence that elevated PTH is prognostic for increased vascular mortality in very elderly subjects, prompts an examination of the possible impact of PTH on risk for arrhythmias. The cardiac effects of PTH are mediated by G protein-coupled receptors that activate phospholipase C (PLC). Catecholamines, angiotensin II, and endothelin have been shown to be arrhythmogenic for ischemic myocardium in animal studies; the receptors mediating this effect are all likewise linked to activation of PLC. Thus, it is reasonable to presume that a sufficient concentration of PTH can be arrhythmogenic in the ischemic heart. The extent to which this effect can be evoked by the high-normal PTH levels prevalent in many elderly subjects, can be assessed in epidemiological studies.
有提示性证据表明，与维生素D状态不佳或钙摄入量低相关的甲状旁腺激素（PTH）长期升高，会增加胰岛素抵抗、体重增加、高血压和左心室肥厚的风险，同时刺激急性期反应物的产生。新证据表明，PTH升高对非常老年受试者的血管死亡率增加具有预后意义，这促使人们研究PTH对心律失常风险的可能影响。PTH的心脏效应由激活磷脂酶C（PLC）的G蛋白偶联受体介导。在动物研究中，儿茶酚胺、血管紧张素II和内皮素已被证明对缺血心肌有致心律失常作用；介导这种效应的受体同样都与PLC的激活有关。因此，有理由推测，足够浓度的PTH在缺血性心脏中可能有致心律失常作用。在许多老年受试者中普遍存在的高正常PTH水平能在多大程度上引发这种效应，可以在流行病学研究中进行评估。
