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Query: UMLS:C0020538 (hypertension)
 170,190 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In a retrospective study of 120 patients with surgically proved primary hyperparathyroidism, 71 patients who were normotensive and 49 patients (41 percent) who were either hypertensive at the time of parathyroidectomy or had a history of hypertension were compared. The mean serum calcium levels in the normotensive and hypertensive patients were very similar (11.6 +/- 0.1 [SEM] mg/dl, and 11.8 +/- 0.1), ruling against the hypothesis that hypercalcemia per se is the dominant cause of the hypertension of hyperparathyroidism. The mean serum creatinine levels in the two groups were also very similar (1.02 +/- 0.05 and 1.09 +/- 0.05 mg/dl), indicating that the hypertension of hyperparathyroidism is not the consequence of advanced renal parenchymal damage. The hypertensive patients did not have a significantly higher prevalence of urolithiasis. A review of the data in this and related studies leads to the conclusion that the hypertension of hyperparathyroidism is heterogeneous in origin. The mean serum phosphate level in the hypertensive patients was significantly lower than that in the normotensive patients (2.20 +/- 0.06 mg/dl versus 2.69 +/- 0.09 mg/dl, p less than 0.02), which may be due to a decrease in renal tubular phosphate reabsorption secondary to hypertension.
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PMID:Hypertension and hyperparathyroidism. Inverse relation of serum phosphate level and blood pressure. 685 80

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

Hypertension and hypokalemia were found in a 60-yr-old woman suffering from primary hyperparathyroidism. Laboratory investigations in this patient disclosed 1) elevated levels of plasma aldosterone (PA) which could not be suppressed by a high sodium diet alone or in combination with fludrocortisone (Florinef); 2) a decline of the elevated PA levels after 4 h of ambulation; and 3) low PRA which was unresponsive to stimulation by a low sodium diet coupled with diuretic-induced volume depletion and 4 h of ambulation. These findings were consistent with the diagnosis of primary hyperaldosteronism. Extirpation of a parathyroid adenoma reduced the patient's serum calcium level to normal, and subsequently, a normalization of her blood pressure, serum electrolytes, PA, and PRA were observed. On the basis of these data is is suggested that in this case hyperaldosteronism may have been caused directly or indirectly by primary hyperparathyroidism.
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PMID:Primary hyperparathyroidism: possible cause of primary hyperaldosteronism in a 60-year-old woman. 699 17

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

To elucidate the pathophysiology of elevated blood pressure in hypercalcemic patients, we studied the plasma concentration of catecholamines and their major metabolites (as an index of sympathetic function) and the blood pressure response to norepinephrine infusion (vascular reactivity) in patients with primary hyperparathyroidism, in patients with primary hypertension, and in normal controls. In addition, we evaluated the hemodynamic response to calcium infusion in normotensive and hypertensive subjects. Plasma levels of both norepinephrine and epinephrine and the metabolites normetanephrine and dihydroxyphenyl-glycol were significantly higher in the hypercalcemic group than in the other two groups. Norepinephrine infusion increased blood pressure by 8.5 +/- 1.4 mm Hg in the control group, by 19 +/- 2 mm Hg in the hypercalcemic group and by 29 +/- 3 mm Hg in the primary hypertensive group. Infusion of calcium produced a significant rise in both systolic and diastolic blood pressures and in peripheral resistance in the hypertensives, whereas in the normotensive group only systolic blood pressure increased, associated with a rise in cardiac output. We conclude that the observed increased activity of the sympathetic nervous system in hypercalcemia could account for the elevation in blood pressure and the enhanced vascular reactivity could explain the hypertension in some patients with primary hyperparathyroidism.
Hypertension
PMID:Sympathetic system function and vascular reactivity in hypercalcemic patients. 706 99

The frequency of hypertension in patients with primary hyperparathyroidism has been compared with that found in cases matched for conditions of comparable surgical magnitude, age, race, sex, and days in the hospital. The mean blood pressure of the patients was 143/89 mm Hg, significantly higher than that of controls, which was 130/81 mm Hg (P less than 0.001 for systolic and diastolic pressures). The difference was especially notable in view of the fact that the mean weight of the controls was 169 lb compared to 153.9 lb for the patients. Actual hypertension, defined as a diastolic blood pressure of 90 mm Hg or more and or treatment with hypertensive therapy was much more frequent in the patients (90 of 124; 73%) than in the controls (53 of 124; 43%; P less than 0.001). Serum creatinine was 1.3 mm/dl in patients and 1.1 mm/dl in controls. The blood pressure difference between patients and controls persisted when patients with creatinine levels of 2.0 mm/dl or less were omitted. The blood pressure difference between patients and controls had disappeared by the end of hospitalization. We conclude that primary hyperparathyroidism is associated with modest blood pressure elevation, that renal damage is probably not the mechanism, and that surgical cure perhaps may lower blood pressure. The mean effect of primary hyperparathyroidism is to shift the blood pressure distribution curve to the right by approximately 15/10 mm Hg.
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PMID:A case-comparison study of hypertension and hyperparathyroidism. 708 56

All cases of surgically proven and cured primary hyperparathyroidism, over a five-year period, were reviewed for the presence of hypertension, renal and/or prerenal azotemia, nephrolithiasis, nephrocalcinosis, and patient symptom status. In this group of 23 patients, the prevalence of hypertension was greater than 78% (18 patients), which is statistically significant. Approximately 28% (5 patients) of the 18 hypertensive patients had some degree of azotemia and/or elevated serum creatinine. Most of the 23 patients were symptomatic, over the age of 50, female, and without nephrolithiasis or nephrocalcinosis. The possible etiologic mechanisms of calcium-mediated hypertension are discussed, and the important association of hypertension with primary hyperparathyroidism is emphasized.
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PMID:Hypertension and primary hyperparathyroidism: a five-year case review. 714 70

A patient presented at 5 years of age with polycythemia vera. He subsequently developed splenic infarctions and died at 20 years of age following cerebral hemorrhage and infarctions. Two months before his death, he developed hypertension and had biochemical evidence of primary hyperparathyroidism and possibly pheochromocytoma. Only nine reported childhood cases of polycythemia vera fulfill the criteria of the Polycythemia Vera Study Group. These cases are summarized and the complications discussed. Although none have progressed to myeloid metaplasia or acute leukemia, these patients are at risk of developing thrombo-hemorrhagic complications; available evidence indicates that they should be managed to keep the hematocrit between 40 and 45%.
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PMID:Polycythemia vera in childhood: case report and review of the literature. 721 35

A series of 38 cases of primary hyperparathyroidism seen at a single hospital within a four a half year period is reported. The importance of hypercalcemia in the diagnosis of this syndrome and its screening in cases of arterial hypertension, gout, osteoporosis, and families with type I multiple endocrine neoplasia are underlined. The patients in the present series had a florid clinical history with a mean duration of 14 years. Main symptoms were urolithiasis (52%), arterial hypertension (28.9%), bone involvement and pain (23.7%), and peptic ulcer (18.4%). There were a high proportion of patients with hyperuricemia (26.3%), some with classical symptoms of gout. One patient presented simultaneous pituitary and pancreatic involvement. Surgical therapy was undertaken in 25 patients, of whom 24 (96%) were cured, one of them after reoperation. There were no cases of relapse, hypoparathyroidism, or postoperative death. Surgery is the only rational and definitive form of treatment of hyperparathyroidism; both experienced surgeons and pathologists are necessary to deal with the anatomic and histologic subtleties of this interesting endocrine disorder.
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PMID:[Comments on a series of 38 cases of primary hyperparathyroidism (author's transl)]. 724 69

The clinical spectrum of 100 consecutive cases of surgically proved primary hyperparathyroidism treated from 1974 through 1978 was analyzed. Their laboratory test results were compared with 64 cases of other form of hypercalcemia using multivariate discriminant analysis. The clinical spectrum has dramatically shifted during the past three decades from renal calculi and bone disease to the asymptomatic patient discovered by routine serum chemical analysis. Hypertension was twice as common among hyperparathyroid patients as in the general population but failed to improve in 92% after parathyroidectomy. The most useful discriminant laboratory test in descending order of value were the serum chloride, serum calcium, hematocrit, serum phosphorus, and parathormone. Multivariate discriminant analysis of the serum calcium, phosphorus, chloride, and Hct provided a 98% degree of accuracy in separating hyperparathyroidism from other forms of hypercalcemia.
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PMID:Primary hyperparathyroidism. Changing clinical spectrum, prevalence of hypertension, and discriminant analysis of laboratory tests. 731 24


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