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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A case of 49-year-old Japanese house wife with a functioning parathyroid carcinoma was reported. Because of lack of bone and renal involvements, she was classified as chemical type of primary hyperparathyroidism. Abnormally high levels of serum calcium and a small palpable tumor on the right anterior neck had suspected a functioning parathyroid carcinoma, which was proved histologically after operation. Preoperatively, she had a labile hypertension (116-190/68-126 mmHg) with high plasma renin activity (PRA; 2.3-8.4 ng/ml/h). The marked responses of PRA to furosemide and captopril were accompanied by inappropriate low response of aldosterone. After removal of the tumor, her blood pressure returned to normal with lowered PRA and normal serum calcium. These observations strongly suggested that her elevated PRA might be a main role to yield hypertension.
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PMID:A case of functioning parathyroid carcinoma with hypereninemic hypertension. 634 70

Two patients with both primary hyperparathyroidism and primary hyperaldosteronism are described. Each presented with high blood pressure and a history of renal calculi. Mild hypercalcaemia was associated with raised plasma parathyroid hormone concentrations and a parathyroid adenoma was excised from each. Both patients also had hypokalaemia, hyperaldosteronism and low plasma renin concentrations. Quadric analysis, adrenal vein plasma aldosterone concentrations, adrenal venography and CT scanning all suggested an adrenal adenoma in each patient. This suspicion was confirmed at operation in one patient; the other patient is unfit for adrenal surgery but her blood pressure and plasma potassium concentration have remained within the normal range during prolonged treatment with either spironolactone or amiloride. Because of this unusual association a search was made for parathyroid hormone excess in patients with primary hyperaldosteronism and for aldosterone excess in primary hyperparathyroidism. None was found.
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PMID:Primary hyperparathyroidism associated with primary hyperaldosteronism. 634 7

Patients with primary hyperparathyroidism are frequently hypertensive. Studies were performed to determine whether the hypertension in this disorder could be corrected by saralasin infusion. Five patients with primary hyperparathyroidism and one patient with secondary hyperparathyroidism were salt depleted before saralasin testing by the administration of 1 mg/kg furosemide at 1700 h on the evening before testing. Blood pressure was measured every 2 min by an automatic recording device. Saralasin was given as a continuous iv infusion of 1, 3, 6, and 10 micrograms/kg . min for 30 min. Blood for measurement of PRA was drawn 4 min before, immediately before, and 4, 8, 12, 16, 22, 30, 60, and 90 min after the infusion was begun. Saralasin did not reduce blood pressure in these patients. The mean postsaralasin blood pressure (12--20 min after the start of the infusion) was 155/102 mm Hg compared to the control blood pressure of 156/101 mm Hg (blood pressure at -4 and 0 min). The inability of saralasin to effect a vasodepressor response was unexpected, since the mean PRA before saralasin infusion was elevated at 1895 ng/dl . 3 h (normal range, 409--818 ng/dl . 3 hr; 95% confidence limits). These studies suggest that the hypertension associated with hyperparathyroidism is not renin dependent.
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PMID:Hypertension associated with hyperparathyroidism is not responsive to angiotensin blockade. 698 46

To evaluate the role of the renin-angiotensin-aldosterone system in the hypertension associated with primary hyperparathyroidism, we measured plasma renin activity and aldosterone concentration before and after maneuvers to suppress and stimulate this system in 11 hypertensive patients with primary hyperparathyroidism. We also measured plasma or urinary norepinephrine concentration to examine the role of catecholamines in the hypertension. The results were compared with an age- and race-matched control population. While the mean plasma aldosterone concentrations were normal, the mean plasma renin activity in response to furosemide stimulation was subnormal in subjects with hyperparathyroidism. Plasma or urinary norepinephrine concentrations were within the normal range. Thus a specific abnormality of the renin-angiotensin-aldosterone system or catecholamines could not be identified in these hypertensives with primary hyperparathyroidism.
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PMID:The renin-angiotensin-aldosterone system and hypertension in primary hyperparathyroidism. 704 84

Primary hyperparathyroidism (HPTH) is frequently associated with hypertension. To date, the relationship between these two conditions is still not clear. We have studied 34 consecutive patients with primary HPTH due to a parathyroid adenoma. The diagnosis was later surgically confirmed in 32 cases. Ten of thirty-four HPTH patients were hypertensive. Before adenomectomy (PTHX) and 1-2 months after PTHX, we measured the following parameters in all patients: circulating levels of total and ionized Ca, intact immunoreactive parathormone (iPTH) (1-84), plasma renin activity (PRA), aldosterone, and daily total urinary catecholamine excretion. Moreover, 10 hypertensive HPTH patients, 10 normotensive HPTH patients, compared to 10 to 10 sex- and age-matched healthy normotensive subjects, underwent an acute norepinephrine test to assess vascular reactivity to a pressor agent. Before PTHX, no significant difference was observed between normotensive and hypertensive patients in all the above-mentioned variables, except for PRA and plasma aldosterone levels which were higher in hypertensive patients. Furthermore, the pressor response to the norepinephrine test was significantly greater in hypertensive HPTH patients than in the other 2 groups. After PTXH, serum Ca and intact iPHT (1-84) levels were reduced to normal values in all patients, while blood pressure, PRA and plasma aldosterone levels became normal in 8 of 10 hypertensive patients. The pressor response to the norepinephrine test was similar in the 2 groups. These results are consistent with the hypothesis of a direct effect of PTH on renin secretion which could contribute to the pathogenesis of hypertension and to the vessels sensitization to pressor agents.
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PMID:Hypertension and primary hyperparathyroidism: the role of adrenergic and renin-angiotensin-aldosterone systems. 756 68

To examine the effects of primary hyperparathyroidism separately from those of hypertension per se on blood pressure regulation in patients with primary hyperparathyroidism, we studied the pressor response to infused angiotensin II (AII) and to norepinephrine (NE) in 7 normotensive patients with primary hyperparathyroidism before and after surgical cure, and compared it to that observed in 10 subjects with idiopathic hypertension and 10 normal controls. While the subjects were on an ad libitum diet, we measured urinary and plasma electrolytes, creatinine, and plasma renin activity. Except for calcium, these values were not significantly different among the three groups. The blood pressure was measured basally and in response to graded doses of AII or of NE until a 20-mmHg increase in the diastolic blood pressure was reached ("pressor dose"). The pressor doses of AII and of NE were lower in the normotensive patients with primary hyperparathyroidism than in normal controls [4.6 +/- 2.0 vs. 7.3 +/- 3.5 ng/kg/min (p < 0.05) and 164 +/- 114 vs. 302 +/- 176 ng/kg/min (p < 0.05) respectively] and not significantly different from those found in idiopathic hypertension (3.1 +/- 1.2 and 137 +/- 95 ng/kg/min). When the patients with primary hyperparathyroidism were studied again between 2-6 months after surgical cure, their pressor doses of AII and of NE remained unchanged from their preoperative values (5.4 +/- 2.9 and 137 +/- 80 mg/kg/min). We conclude that the hyperparathyroid condition can disrupt the normal responsiveness to pressor agents even if the blood pressure remains within normal limits, and that this abnormality may persist after surgical cure.
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PMID:Primary hyperparathyroidism and hypertension: persistently abnormal pressor sensitivity in normotensive patients after surgical cure. 807 14

Over the past 40 years primary hyperparathyroidism (PHP) has changed from a rare, severe disease of the bones and kidneys to a common disease with hypertension, peptic ulcer, pancreatitis, easy fatigue and proximal muscle weakness. We have during these 40 years examined one of the greatest group of patients with PHP. PHP had its maximum incidence in women over the age of 40. The disease is four times frequent in women as in man. The incidence of hypertension and peptic ulcer between patients with PHP is higher as compared with the incidence of these diseases in general populations. The severity of bone changes in individual patients with PHP does not result from the direct action of a single hormone only. Parathyroid hormone (PTH) have hypotensive and vasodilator effects on various vascular beds. The resting blood flow in the limbs of our patients with PHP is increased in comparison with control subjects. PTH increases plasma renin activity in normotensive controls. This effect is partly blocked by beta adrenergic blockers.
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PMID:[Primary hyperparathyroidism]. 871 83

Twenty consecutive unselected patients with proven primary hyperparathyroidism (PH), 26 essential hypertensive (EH) patients, and 13 normotensives were studied. Blood pressure (BP) and, under constant salt intake, plasma renin activity (PRA), parathyroid hormone (PTH), urinary and plasma sodium, potassium, aldosterone (ALD), creatinine, total calcium, and phosphate were measured. Patients with PH were also studied 1 and 6 months after successful surgery. In patients with PH, systolic and diastolic BP was significantly lower (P < .001) than in EH patients and higher (P < .005) than in controls. Eight patients with PH (40%) had BP levels greater than 140/90 mm Hg. PTH and plasma and urinary calcium in patients with PH were significantly (P < .01) higher than in controls, while PRA, ALD, phosphate, potassium, and sodium were superimposable in the three groups. PTH in patients with PH was weakly correlated with PRA (positively) and with plasma potassium (negatively) and was not associated with ALD, calcium, sodium, and BP levels. Surgery was followed by a significant reduction (P < .01) in PTH, calcium, and urinary phosphate and an increase (P < .02) in plasma phosphate, potassium, and sodium, whereas PRA, ALD, urinary potassium and sodium, and BP showed no change. In hypertensive patients with PH, PTH, PRA, and plasma and urinary ALD, calcium, and sodium did not differ from the values in normotensive PH patients, and variations in these humoral parameters after surgery were comparable in the two groups. In conclusion, our results show that hypertension is frequently associated with PH. However, the present data raise doubts about the assumption of a renin-mediated causal relationship between hyperparathyroidism and high BP. Indeed, as a unique finding in favor of the hypothesis of a stimulating role of PTH in renin secretion, we observed only a weak relation between PTH and PRA. Thus, unknown and/or unassessed factors related to parathyroid disease cannot be ruled out to explain the hypertension observed in some patients with PH.
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PMID:Renin-angiotensin-aldosterone system in primary hyperparathyroidism before and after surgery. 1009 3

The possible hormonal interactions of parathormone and extracellular calcium level with other endocrine systems were studied. Primary hyperparathyroidism was used first as a clinical model, in which hypercalcemia and normocalcemia occurs before and after surgery, respectively. An increased activity of renin-aldosterone system related to parathormone was found in hyperparathyroidism, and surgery resulted in a small decrease in blood pressure. This change was accompanied by a significant decrease in the activity of the renin-aldosterone system indicating the cessation of the secondary hyperaldosteronism. The role of a relative hyperinsulinism, occurring in hyperparathyroidism, in the pathogenesis of hypertension was not proved. The basal and stimulated secretion of thyreotrophin, the basal growth hormone level, and the stimulated prolactin secretion increased after surgery. Follicle stimulating hormone and luteinizing hormone secretions remained unchanged. The results suggest that extracellular calcium may reversibly modify the secretion of certain anterior pituitary hormones and their stimulus-induced responses. In the second disease, growth hormone deficiency syndrome, studied, long-term growth hormone replacement therapy results in significant but transient changes in bone metabolism: calcium-, alkaline phosphatase-, and phosphate levels increase until 6 to 18 months as compared to the initial values; then these parameters decrease to the baseline level. Parathormone decreases until the first year then returns to the baseline level. Osteocalcin shows similar temporary changes. In spite of the above transient changes, osteodensity increases after 12 months of treatment, and further improvement can be seen after 18 and 24 months, i.e. GH treatment exerts a biphasic effect on bones; resorption increases first followed by an increase in formation. Based on the above results, it can be concluded that both parathormone and extracellular calcium are able to influence the secretion of certain hormones; and--as it is shown in growth hormone replacement therapy--other hormones may cause certain effect on them, too. The better understanding of these interactions may result in a better understanding of the pathomechanism of certain diseases and the improvement of their treatment.
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PMID:[Hormonal interactions of parathormone and calcium metabolism]. 1263 47

Primary hyperparathyroidism (pHPT), caused by solitary parathyroid adenomas in 85% of cases and diffuse hyperplasia in most of the remaining cases, overproduces parathyroid hormone (PTH), which mobilizes calcium to the blood stream. Renal stones, osteoporosis and diffuse symptoms of hypercalcaemia, such as constipation, fatigue and weakness are well-known complications. However, in Western Europe and North America, patients with pHPT are nowadays usually discovered during an early, asymptomatic phase of the disease. It has been reported that patients suffering from symptomatic pHPT have increased mortality, mainly due to an overrepresentation of cardiovascular death. pHPT is reported to be associated with hypertension, disturbances in the renin-angiotensin-aldosterone system, and structural and functional alterations in the vascular wall. Recently, studies have indicated an association between pHPT and heart disease, and studies in vitro have produced a number of theoretical approaches. An increased prevalence of cardiac structural abnormalities such as left ventricular hypertrophy (LVH) and valvular and myocardial calcification has been observed. Associations have been found between PTH and LVH, and between LVH and serum calcium. LV systolic function does not seem to be affected in patients with pHPT, whereas any influence on LV diastolic performance needs further evaluation. The aim of this review is to clarify the connection between pHPT and cardiac disease.
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PMID:Primary hyperparathyroidism and heart disease--a review. 1547 92


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