常规血液透析患者甲状旁腺激素过量产生与左心室功能障碍相关

H. Nasri
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引用次数: 0

摘要

甲状旁腺激素(Parathyroid hormone, parathorone)是钙的主要调节剂,也是骨和矿物质稳态的主要调节剂(1)。在慢性肾功能衰竭的进展过程中,心脏和血管疾病开始得早,是这些个体死亡的主要常见原因(1)。甲状旁腺激素是一种由甲状旁腺分泌的含有84个氨基酸的多肽(1,2)。心脏和血管疾病扩展的机制尚不清楚。然而,甲状旁腺激素、维生素D、钙和磷的体内平衡失调是慢性肾衰竭患者心功能障碍的部分原因(2-4)。甲状旁腺激素的分泌被血液中钙浓度的改变所调节。事实上,钙浓度的降低刺激甲状旁腺的钙感应受体分泌甲状旁腺。甲状旁腺激素形成一个严格控制的反馈循环,并对低钙血症作出反应,这种激素有多种目标来增加血清钙浓度(35)。甲状旁腺激素也是肾组织中维生素D生成的关键刺激物,其主要生理调节剂是循环电离钙。甲状旁腺激素对肠细胞、肾组织和骨骼的影响导致血清钙水平维持在一个狭窄的范围内。然而,甲状旁腺激素水平升高与充血性心力衰竭、心血管死亡率、高血压和左心室肥厚的风险增加相关(1-4)。事实上,内皮细胞功能障碍引起的动脉功能紊乱是上述器官功能障碍的原因。因此,心脏组织是甲状旁腺激素的靶器官之一。甲状旁腺激素对心肌细胞有直接的肥厚作用。甲状旁腺激素对心肌细胞有直接作用,激活蛋白激酶C,进一步刺激心脏组织中胎儿型蛋白的肥厚生长和再表达。甲状旁腺激素也是蛋白激酶a的有效激活剂(6-9)。甲状旁腺激素对心脏细胞的肥厚作用也可以通过甲状旁腺激素水平与左心室质量比例的密切联系来检测(5-9)。为了了解甲状旁腺激素与血液透析(HD)患者左心室功能及结构的关系,我们对73例HD患者进行了研究。个体年龄46.5±16岁。个体持续HD的时间为21.5±23.5个月。我们发现血清碱性磷酸酶与左心室射血分数的比例呈显著负相关。我们还发现血清完整甲状旁腺激素与非左心室射血分数比例呈显著负相关,对卫生政策/实践/研究/医学教育的意义甲状旁腺激素分泌不当与血液透析患者心脏疾病的发生和发展密切相关。因此,应注意控制过量的甲状旁激素和慢性肾脏疾病-矿物质骨紊乱的管理。
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Excessive production of parathyroid hormone in association with left ventricular dysfunction in regular hemodialysis patients
Parathyroid hormone (parathormone) is a main regulator of calcium and is a principal regulator of bone and mineral homeostasis (1). Heart and vessel disease starts early during the progression of chronic renal failure and is the mainly common cause of death in these individuals (1). Parathyroid hormone is a polypeptide containing 84 amino acids secreted by parathyroid glands (1,2). Mechanisms of extension of heart and vessel disease are ill-understood. However, dysregulated homeostasis of parathyroid hormone, vitamin D, calcium and phosphorus are responsible partly in cardiac dysfunction in chronic renal failure patients (2-4). Secretion of parathormone is moderated by alterations in concentration of calcium in the blood. In fact, reduced calcium concentration stimulate PTH secretion by the calcium-sensing receptors located in the parathyroid gland. Parathormone forms a tightly controlled feedback cycle and to response to hypocalcemia, this hormone has various targets to increase serum calcium concentration (35). Parathormone is also a key stimulator of vitamin D production in renal tissue and its major physiologic regulator is circulating ionized calcium. The impact of parathormone on intestinal cells, renal tissue, and also bone leads to maintain serum calcium levels within a narrow range. However, elevated levels of parathyroid hormone have been correlated with increased risks of congestive heart failure, cardiovascular mortality hypertension and hypertrophy of left ventricle (1-4). Indeed, disturbed arterial function due to endothelia cell dysfunction is responsible for the above mentioned organ dysfunctions. Thus, cardiac tissue is one of the target organs of parathyroid hormone. Parathormone has a direct hypertrophic property on heart myocytes. Parathyroid hormone has a direct effect on cardiomyocytes, to activate protein kinase C that further stimulates hypertrophic growth and re-expression of fetal type proteins in heart tissue. Parathyroid hormone is also a potent activator of protein kinase A (6-9). The hypertrophic effect of parathyroid hormone on cardiac cells also is detected by a close association between parathormone levels and proportion of left ventricular mass (5-9). To find the relationship of parathyroid hormone with left ventricular function and structure in hemodialysis (HD) patients, we conducted a study on 73 HD patients. The age of individuals was 46.5 ±16 years. The length of time individuals had been on HD was 21.5 ±23.5 months. We found a significant inverse association of serum alkaline phosphatase with proportion of left ventricular ejection fraction. We also detected a significant inverse association between serum intact parathyroid hormone with proportion of left ventricular ejection fraction in nonImplication for health policy/practice/research/medical education Inappropriate parathyroid hormone secretion is intensely associated with establishment and progression of cardiac diseases in hemodialysis patients. Thus attentions should be toward the control of excessive parathormone and management of chronic kidney disease–mineral bone disorder.
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