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

Circadian blood pressure variability was recorded in patients with primary hypertension and with different forms of secondary hypertension using ambulatory 24-h blood pressure measurement. A group of 20 patients with different forms of secondary hypertension was compared with a matched group of patients with primary hypertension. Although the mean 24-h blood pressure was not different between the two groups, the patients with secondary hypertension had significantly higher systolic blood pressure during sleep and higher systolic and diastolic blood pressure in the early morning, compared with the primary hypertension group. This nocturnal blood pressure fall was then investigated in various groups of patients with different forms of secondary hypertension and compared with normotensives and patients with primary hypertension. Patients with mild primary hypertension (n = 152) and with severe primary hypertension (n = 30) had the same blood pressure fall (14-16 mm Hg systolic and diastolic) during the night (23:00-05:00 h) as normotensives (n = 20). However, in patients with renoparenchymal hypertension (n = 29), renovascular hypertensions (n = 20), hyperaldosteronism (n = 6), and hyperthyroidism (n = 14), the nocturnal blood pressure fall was significantly (p less than 0.01) reduced. One patient with coarctation of the aorta and nine patients with primary hyperparathyroidism and elevated blood pressure had a normal circadian blood pressure profile with a normal nocturnal blood pressure fall. The heart rate decrease during the night was equal in all patient groups. Ambulatory blood pressure measurement allows blood pressure recording under everyday conditions, including nighttime. In primary hypertension the blood pressure variability exhibits the same circadian variation as in normotension, showing a marked nocturnal fall.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Circadian blood pressure rhythm in primary and secondary hypertension. 179 27

The need for treatment of mild and apparently asymptomatic primary hyperparathyroidism (HPT) is questioned, but a raised incidence of cardiovascular disease has been regarded as evidence in favour of surgery. While it is well known that several risk factors for cardiovascular disease (hypertension, hyperlipidaemia and diabetes mellitus/impaired glucose tolerance) are overrepresented in HPT, it is not known whether surgery provides long-term normalization in these respects and reduces the risk of premature death. In a 15-year follow-up of a cohort of 172 subjects in whom mild hypercalcaemia was initially detected during a health screening, it was found that 56 subjects had died. 17 individuals had been operated on for HPT, 47 individuals were persistently hypercalcaemic, while 45 subjects had serum calcium within the normal range (seven individuals were lost to follow-up). There had been no significant differences in blood pressure between these groups of mildly hypercalcaemic patients and age- and sex-matched controls at the initial screening, but at follow-up blood pressure was significantly higher not only in subjects with persistent hypercalcaemia, but also in those who had been successfully operated on for HPT. Neither of the hypercalcaemic groups showed any significant deviations from the controls with regard to indices of lipid or glucose metabolism. These findings suggest that there is no simple cause-and-effect relationship to account for the propensity toward high blood pressure in primary HPT. Consequently it cannot be assumed that surgery for HPT will eliminate the increased risk of cardiovascular disease in patients with mild HPT.
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PMID:Cardiovascular risk factors in primary hyperparathyroidism: a 15-year follow-up of operated and unoperated cases. 206 9

We describe three cases of women who developed symptoms of primary hyperparathyroidism originated by a parathyroid functional tumor. Ostoporosis, arterial hypertension and nefrolitiasis were the most frequent antecedents. The PTH and calcium levels in bood and urine were elevated. The CT and ultrasound confirmed the diagnosis of parathyroid tumor, which was identified histopathology as oxifilic adenoma. All patients underwent surgical treatment. We consider these cases of clinical interest because this kind of adenoma hardly ever produces hyperparathyroidism.
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PMID:[Oxyphillic adenoma as a cause of primary hyperparathyroidism]. 210 96

1. Blood pressure, left ventricular mass and platelet cytosolic free calcium concentrations were measured in 23 patients with untreated primary hyperparathyroidism, 30 normotensive control subjects and 23 control subjects matched for age, sex and blood pressure. In 12 patients measurements were repeated after parathyroidectomy. 2. Patients with primary hyperparathyroidism had significantly elevated blood pressures (139 +/- 6/86 +/- 3 mmHg, mean +/- SEM) compared with control subjects (125 +/- 2/78 +/- 1 mmHg), but high values persisted after hypercalcaemia was corrected. 3. Despite chronic extracellular hypercalcaemia, intracellular free calcium levels were lower in patients with hyperparathyroidism than in controls matched for age, sex and blood pressure (median concentrations 81.5 nmol/l vs 93 nmol/l, 95% confidence interval 0.1 to 20.1; P less than 0.05) and values tended to increase after parathyroidectomy. 4. Left ventricular mass index was increased in the primary hyperparathyroid group as compared with control subjects matched for age, sex and blood pressure (123 g/m2 vs 100 g/m2, 95% confidence interval -36.1 to -3.1; P = 0.03). Parathyroidectomy resulted in a small reduction of the left ventricular mass index (123.5 g/m2 vs 104 g/m2, 95% confidence interval 46.5 to 2.5; P = 0.1) but no change in blood pressure. 5. Hypertension and left ventricular hypertrophy in primary hyperparathyroidism are associated with relatively low levels of free calcium in platelets.
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PMID:Blood pressure, left ventricular mass and intracellular calcium in primary hyperparathyroidism. 215 37

We retrospectively reviewed 32 patients who underwent parathyroidectomy at our hospital for the last fourteen years. 1) Clinical appearance of primary hyperparathyroidism was in younger age in women. 2) In previous history or at the time of PTX, 9 patients had malignant tumors including 6 thyroid cancers, 36% of the patients with out bone related symptoms had a remarkable decrease in bone mineral content. 3) After PTX, none of patients had recurrent urolithiasis and bone mineral content of all patients was significantly increased in a short time. In addition, upper GI complaints were improved, or hypertension was partially normalized. However, renal insufficiency remained unchanged. 4) In preoperative localization study, Ultrasound sonography (US) demonstrated the best accuracy rate of 88% when only one gland was involved. US was able to detect multiple gland involvement only in 20% of 5 cases. 5) Hypercalciuria was recognized as one of the risk factors of stone formation in patients with primary hyperparathyroidism.
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PMID:[Clinical study on 32 patients who underwent parathyroidectomy at Osaka City University Hospital]. 232 20

11 cases of primary hyperparathyroidism were seen during 1975-1988. Follow up has varied from 1-10 years. Renal disease in the form of renal calculi and nephro-calcinosis was observed in nine cases (81.8%). Two presented in chronic renal failure and required dialysis. Bone disease was found radiologically in six patients (54.5%); two had bone cysts in multiple bones while all six had subperiosteal bone erosion. Hypertension was found in three patients (27.3%). Proximal myopathy was observed in two cases (18.1%). One patient each presented with hypercalcaemic crisis, chondrocalcinosis and acute pancreatitis. The calcification of blood vessels and cornea was seen in two cases.
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PMID:Primary hyperparathyroidism. 238 Jan 35

The authors report a case of primary hyperparathyroidism in a 47 year old woman presenting with cardiac arrhythmias. She had paraoxystic supraventricular tachycardias and rate-dependent ventricular hyperexcitability suggestive of a catecholamine-induced phenomenon which were resistant to antiarrhythmic therapy over a 3 year period; the plasma calcium concentration was 3.30 mmol/l. An ectopic parathyroid adenoma was removed surgically, normalising the biological changes, and no further arrhythmias were detected by Holter monitoring during the 2 year follow-up period. The association of atrial and ventricular arrhythmias seems to be relatively rate in hyperparathyroidism; patients usually present with atrioventricular block and ventricular hyperexcitability. The other cardiovascular abnormalities observed in hyperparathyroidism are hypertension and myocardial hypertrophy. The electrophysiological mechanisms underlying the clinical manifestations remain obscure.
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PMID:[Primary hyperparathyroidism disclosed by heart arrhythmia]. 251 34

The aim of this study was to assess the effect of hypercalcaemia due to primary hyperparathyroidism on the pressor and aldosterone responses to angiotensin II (Ang II) infusion. Five patients with hyperparathyroidism were studied, before and after parathyroidectomy, and were compared with five normal subjects. After 30 min of equilibration, Asp1-Val5 Ang II was infused in all subjects at stepwise increasing dose rates of 2 and 4 ng/kg per min for 30 min each. In the hyperparathyroid patients the baseline levels of plasma parathyroid hormone and calcium were significantly higher than in the controls, and returned to normal after the parathyroidectomy; plasma aldosterone and renin activity were normal both before and after the parathyroidectomy. Two hyperparathyroid patients had high blood pressure levels, which were normalized after surgery. The increase in the aldosterone response from baseline at each time point of the Ang II infusion was greater in the hyperparathyroid patients before than after the operation (P less than 0.05), and greater than in the normals (P less than 0.05). No difference in the increased response of systolic or diastolic blood pressure was observed between the hyperparathyroid patients, either before or after the parathyroidectomy, and the normal subjects. High levels of extracellular calcium or parathyroid hormone, or both, might play a primary role in the aldosterone hyper-responsiveness to Ang II in the hyperparathyroid patients. The similar pressor response to Ang II in hyperparathyroid patients and the normal subjects suggests that hypercalcaemia does not potentiate the vasoconstrictive action of Ang II.
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PMID:Aldosterone and pressor responses to angiotensin II in primary hyperparathyroidism. 263 14

We studied long-term morbidity after parathyroid surgery for primary hyperparathyroidism in 100 patients and compared it with the long-term morbidity of medical follow-up from the literature. The surgical treatment of primary hyperparathyroidism was associated with negative results of neck explorations, persistent hypercalcemia, recurrent hypercalcemia, permanent hypoparathyroidism, or recurrent laryngeal nerve damage in 13 (19%) of 68 patients followed up for five years postoperatively. A review of medical follow-up as reported in the literature showed progression of disease in 8% to 22% of patients followed up for five to ten years. There was no convincing evidence that mild primary hyperparathyroidism resulted in progressive osteoporosis or renal failure. Furthermore, no significant improvement in hypertension, peptic ulcer disease, or renal function followed successful parathyroid surgery. Unless future studies demonstrate progressive osteoporosis or renal damage in untreated, mild primary hyperparathyroidism, medical follow-up is a reasonable alternative to surgery in the compliant patient over 50 years of age.
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PMID:Primary hyperparathyroidism. A review of the long-term surgical and nonsurgical morbidities as a basis for a rational approach to treatment. 270 30

A retrospective study of 89 patients with surgically proven primary hyperparathyroidism was done to gain insight into the pathogenesis of hypertension associated with this condition. The 43 patients (48%) who were hypertensive did not differ significantly from the normotensive patients with regard to age, sex, serum calcium and phosphate levels, and creatinine clearance. However, the mean serum magnesium level was significantly lower in hypertensive hyperparathyroid patients (1.52 +/- 0.24 mEq/L) than in normotensive hyperparathyroid patients (1.76 +/- 0.18 mEq/L; P less than .001), irrespective of use of diuretics in the former group. Although some studies implicate hypomagnesemia in the pathogenesis of essential hypertension, we are unaware of any previous human study reporting a link between hypomagnesemia and hypertension associated with primary hyperparathyroidism. This study suggests that a low level of serum magnesium may play a role in the pathogenesis of hypertension associated with primary hyperparathyroidism, a finding that needs further evaluation.
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PMID:Hypomagnesemia and hypertension in primary hyperparathyroidism. 277 81


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