{"title":"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","authors":"H. Nasri","doi":"10.15171/JPD.2018.02","DOIUrl":null,"url":null,"abstract":"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.","PeriodicalId":16657,"journal":{"name":"Journal of Parathyroid Disease","volume":"3 1","pages":"3-4"},"PeriodicalIF":0.0000,"publicationDate":"2017-06-10","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Excessive production of parathyroid hormone in association with left ventricular dysfunction in regular hemodialysis patients\",\"authors\":\"H. Nasri\",\"doi\":\"10.15171/JPD.2018.02\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"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. 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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.