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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Over a period of 42 years, 581 patients with presumed hyperparathyroidism underwent an initial cervical exploration. Abnormal parathyroid glands were removed from 495 patients (85.2%). There was a greater probability of operative success in women, patients over 50 years of age, and patients with hypercalcemia, hypertension, or nonspecific abdominal pain. There was no association of operative outcome with some of the "classic" manifestations of hyperparathyroidism--peptic ulcer disease, neuropsychiatric symptoms, pancreatitis, bone disease, or urolithiasis. The probability of surgical success improved with time, increasing from 56 per cent in the 1950s to 97 per cent in the present decade. This improvement appears to be related to greater operative experience, since all four parathyroid glands were more likely to be found with increased experience, and there was a strong correlation between finding four parathyroids and achieving persistent normocalcemia. The most common causes of operative failure were inaccurate calcium assays (the patient was not truly hypercalcemic), an inappropriate diagnosis ("normocalcemic hyperparathyroidism"), and surgical inexperience. These three factors accounted for at least three fourths of all negative explorations. More accurate diagnostic studies, and careful exploration by an experienced surgeon should maximize the probability of a successful operation for primary hyperparathyroidism.
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PMID:Causes of the failed cervical exploration for primary hyperparathyroidism. 341 98

Sixty-eight patients with mild primary hyperparathyroidism were studied for a mean period of 4.5 years (median 3.3). Seven of these patients presented with renal colic while the rest had no symptoms. There was no significant deterioration in mean serum creatinine, total calcium or ionized calcium concentrations during this period. No patient had progressive renal stone or parathyroid bone disease. Hypertension was defined as a systolic or diastolic blood pressure greater than one standard deviation from the age-sex mean, or if hypotensive drugs were required. Thirty-nine per cent were hypertensive at presentation and 42 per cent became hypertensive later. Four patients died from causes unrelated to hypercalcaemia and three required parathyroidectomy when serum calcium concentration rose above 3.0 mmol/l. Patients over 55 with mild asymptomatic primary hyperparathyroidism may be managed conservatively for several years without significant renal impairment, progressive stone disease, parathyroid bone disease or worsening hypercalcaemia. We suggest that observation in these patients could be restricted to six-monthly checks of physical state, blood pressure and serum biochemistry, particularly concentration of calcium creatinine and alkaline phosphatase.
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PMID:The conservative management of primary hyperparathyroidism. 345 52

The factors responsible for the frequent occurrence of hypertension in patients with primary hyperparathyroidism have not been elucidated. Suggested mediators have included hypercalcemia, renal insufficiency, and increased plasma renin activity. However, experimental results have not been reported in any species that test the hypothesis that sustained hypertension in this clinical syndrome is due to consequences of parathyroid hormone (PTH) excess versus unrelated factors (e.g., primary hypersecretion of other hormones, NaCl sensitivity, genetic factors). Moreover, no systematic evaluation of the renin or adrenal cortical responses to chronic PTH excess has been reported in any species. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous b-(1-34) PTH infusion in normal human subjects (n = 4). PTH infusion resulted in persistent hypercalcemia and hypertension, reversible during a 4-8-day recovery period. Transient but significant increases in urinary tetrahydroaldosterone excretion and plasma cortisol concentration were observed as hypercalcemia and hypertension developed. No significant changes in plasma potassium concentration or plasma renin activity were observed, suggesting that hypercalcemia-induced transient hypersecretion of ACTH was responsible for both cortisol and aldosterone responses. The present results suggest that hypertension associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and requires neither the long-term consequences/complications of the clinical disorder (e.g., severe nephrocalcinosis, renal insufficiency) nor primary hypersecretion of additional hormones. These results are consistent with the hypothesis that hypercalcemia alone or in combination with at least permissive levels of PTH can generate short-term, but persistent (12 days) hypertension in human subjects and thus may be the initiating mechanism for hypertension in clinical primary hyperparathyroidism.
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PMID:Chronic continuous PTH infusion results in hypertension in normal subjects. 354 30

This review compares the calcium antagonists with diuretics in the management of mild-to-moderate essential hypertension. The antihypertensive efficacy of calcium antagonists appears comparable to that of oral diuretics such as hydrochlorothiazide when used as monotherapy. Peripheral vascular dilation appears to be the principal mechanism of the long-term blood pressure-lowering effects of both calcium antagonists and diuretics. Peripheral vasoconstrictor responses to cardioreflex-mediated sympathetic nervous system activation is attenuated by calcium antagonists but not by diuretics. Long-term calcium antagonist therapy is generally not associated with reflex activation of the sympathetic nervous system or of the renin-angiotensin-aldosterone axis, whereas diuretic therapy results in considerable activation of the renin-angiotensin-aldosterone system. Calcium antagonists appear to have a greater beneficial effect than diuretics with respect to maintenance of renal blood flow and glomerular filtration rate. Calcium antagonists, because of their effects on coronary blood flow and heart rate-blood pressure product, offer advantages over diuretics in the treatment of hypertensive patients with concomitant ischemic heart disease. Metabolic abnormalities associated with diuretic antihypertensive therapy, such as hypokalemia, hypercalcemia, hyperuricemia, lipid changes, and hyperglycemia, are generally not observed with calcium antagonists. Many of these deleterious metabolic changes observed with diuretic therapy may be minimized by the use of smaller doses of these agents than have generally been employed in the past. Diuretics are less expensive and require less frequent dosing than calcium antagonists. Thus, they continue to be preferable first-line antihypertensive agents in many patients with mild-to-moderate hypertension.
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PMID:Comparison of calcium-entry blockers and diuretics in the treatment of hypertensive patients. 355 13

The metabolic manifestations and operative findings in 10 patients with a diagnosis of parathyroid carcinoma were analyzed to determine whether they differ from those in patients with parathyroid adenomas and similar degrees of hypercalcemia. Two groups of patients with parathyroid adenomas were used for comparison. Group A consisted of eight patients with "atypical" benign adenomas (mean preoperative level of serum calcium: 13.4 mg/dl); group B consisted of 13 patients with benign typical adenomas--all with preoperative serum calcium levels greater than or equal to 13.0 mg/dl (mean: 14.2 mg/dl). The patients with carcinoma (mean preoperative level of serum calcium: 15.3 mg/dl) had a frequency of osteoporosis and osteitis fibrosa cystica (50%) comparable with that of group A (33%) and group B (62%). Seventy percent of the patients with carcinoma had renal disease (nephrolithiasis, nephrocalcinosis, or impaired renal function), whereas only 38% of group A and 15% of group B had similar disorders. The patients with carcinomas had the highest frequency of combined bone and renal disease (50% versus 14% in group A and 15% in group B). Anemia, peptic ulcer disease, and hypertension occurred with similar frequencies in the three groups. Three patients with recurrent parathyroid carcinoma died of profound hypercalcemia, renal failure, or cardiac arrhythmia. In general, although patients with parathyroid carcinomas have more profound metabolic abnormalities than do patients with primary hyperparathyroidism, the metabolic manifestations in patients with parathyroid carcinoma are comparable with those in patients with parathyroid adenomas and profound hypercalcemia. Furthermore atypical adenomas share many anatomic and histopathologic features with parathyroid carcinomas, and distinguishing between the two is sometimes possible only in cases of tumor recurrence.
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PMID:Parathyroid carcinoma versus parathyroid adenoma in patients with profound hypercalcemia. 358 61

A 1-year retrospective study of all serum profiles of patients with hypercalcaemia analysed at the Johannesburg Hospital was carried out to ascertain the causes of hypercalcaemia and physician awareness of primary hyperparathyroidism. Hypercalcaemia was found in 560 subjects (2.9% of 19,200), but in 147 of these (26%) this was not confirmed by repeat estimations. Malignant tumours were the commonest cause (38.4%) and accounted for the most severe hypercalcaemia (mean serum calcium 2.93 mmol/l). Renal disease resulted in significant hypercalcaemia, at times requiring parathyroidectomy. Drug-associated hypercalcaemia was usually mild and reversible on drug withdrawal. Although primary hyperparathyroidism occurred in 21.3% of cases, overall physician awareness of the disease was poor (39%). 'Incidental' profile hypercalcaemia (P less than 0.005) and hypertension (P less than 0.005) were frequent presenting features in this study. Renal disease (P less than 0.001) occurred infrequently.
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PMID:Hypercalcaemia in the Johannesburg Hospital. Differential diagnosis and physician awareness of primary hyperparathyroidism. 361 82

The long-term clinical courses of 212 "cured" (normocalcemic) patients were analyzed for 1 to 25 years (mean, 6.8 +/- 5.4 years). Preoperatively, 181 patients (85%) were classified as having typical symptoms, 22 patients (11%) as having minimal symptoms, and nine patients (4%) as having no symptoms of primary hyperparathyroidism (PHP). Although the formation of urinary calculi was stopped in 91% of patients, deteriorated renal function and hypertension were seen in patients with symptoms (14% and 8%, respectively) and patients with minimal symptoms of PHP (6% and 15%, respectively). Renal function changes and hypertension were unpredictable despite normalization of the hyperactive parathyroid metabolism and had decisive results: 7% of the patients died of uremia or of the consequences of hypertension (stroke). Large, multiple bone lesions healed functionally and were of no prognostic significance. In the majority of patients with symptoms of PHP, gastrointestinal manifestations healed postoperatively, but two patients who had no preoperative gastrointestinal complaints died of acute pancreatitis. Almost all symptoms of the hypercalcemia syndrome disappeared immediately and permanently in patients with symptoms and patients with minimal symptoms of PHP. Neither deterioration of renal function nor elevation of blood pressure were observed postoperatively in "cured" patients who showed no symptoms of PHP preoperatively. Even in these patients, immediate surgical treatment may have avoided the complications of chronic renal failure or hypertension. As soon as organic manifestations, even in mild form, have been established, it seems impossible to predict the course and to prevent an unfavorable clinical outcome.
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PMID:Successful parathyroidectomy in primary hyperparathyroidism: a clinical follow-up study of 212 consecutive patients. 368 53

Hypertension is common in primary hyperparathyroidism, but the mechanisms are not clear. Significant hypercalcemia induces elevation in blood pressure (BP), whereas excessive parathyroid hormone (PTH) lowers BP. However, in chronic renal failure (CRF) and secondary hyperparathyroidism, the hypercalcemia-induced hypertension is more severe. We examined the interaction between PTH and calcium on BP in normal rats and in those with CRF. Calcium caused a dose-related rise in serum calcium and a rise in mean arterial pressure (MAP). For a comparable rise in serum calcium, the increment in MAP in parathyroidectomized (PTX) rats (7 +/- 3 mmHg) was significantly lower (P less than 0.05) than in sham PTX rats (19 +/- 7.3 mmHg). In PTX rats receiving PTH, the MAP response to calcium infusion (17 +/- 2.4 mmHg) was similar to that in the sham PTX rats. The infusion of similar amounts of calcium in CRF rats caused a greater rise in serum calcium. In CRF-PTX rats, the changes in MAP during calcium infusion were significantly lower (P less than 0.05) than in CRF-sham PTX animals, despite similar rise in serum calcium. For a comparable rise in serum calcium, the rise in MAP in CRF rats was greater than in normal rats. These data suggest that the presence of PTH plays an important permissive role for the hypertensive action of the hypercalcemia.
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PMID:Effects of hypercalcemia and parathyroid hormone on blood pressure in normal and renal-failure rats. 370 44

The association of a critical reduction in renal mass with the subsequent destruction of remaining nephrons has been observed in several species. We studied this process in experimental rabbits after 1 2/3 nephrectomy to define the course and its pathogenesis in this species. Control rabbits underwent sham operative procedures. After renal ablation, rabbits became increasingly cachectic and developed polyuria and hypertension. Despite food intake similar to that of controls (grams per kilogram per day), experimental rabbits developed severe hypercalcemia by 5 to 8 weeks after renal ablation, a change that persisted until death. During the study 17 experimental animals died of uremia 9 to 27 weeks after surgery, and the remaining seven experimental and 25 sham-operated rabbits were sacrificed at 5 to 7 months. At death, 19/24 experimental rabbits had severe obstruction of their collecting systems by concretions of gravel (n = 3) or large calcium carbonate stones (n = 16). Renal biopsy at 4 weeks revealed focal interstitial round cell infiltration progressing by 12 weeks to diffuse tubulointerstitial inflammation and fibrosis. Histologic evidence of obstruction was also evident at this time and became extensive on all subsequent examinations. By contrast, the glomeruli remained well preserved without evidence of sclerosis. We speculate that chronic hypercalcemia and, perhaps more significantly, urinary obstruction may have altered intrarenal hemodynamics and prevented the development of progressive sclerosis observed in the rat remnant kidney model. The present study describes an experimental model of chronic hypercalcemia and spontaneous calcium carbonate nephrolithiasis.
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PMID:Subtotal nephrectomy in the rabbit: a model of chronic hypercalcemia, nephrolithiasis, and obstructive nephropathy. 371 20

To assess the consequences of hypercalcemia on systemic and renal hemodynamics, vasoactive hormones, and water and electrolyte excretion in intact, conscious mongrel dogs, measurements in 10 dogs receiving 100 mg/kg calcium gluconate and 10,000 U/kg vitamin D daily for 2 weeks were compared with measurements made in 10 time-control dogs not receiving calcium or vitamin D. Hypercalcemia induced by dietary supplementation with calcium and vitamin D resulted in profoundly reduced glomerular filtration rate (40 vs 78 ml/min in controls; p less than 0.005), estimated renal plasma flow (145 vs 267 ml/min in controls; p less than 0.005), and renal blood flow (254 vs 441 ml/min in controls; p less than 0.005). Renal resistance was significantly increased in the hypercalcemic dogs (0.57 +/- 0.07 vs 0.28 +/- 0.01 mm Hg/ml/min; p less than 0.005). Hypercalcemia also resulted in increased fractional excretion of water (4.8 vs 1.4% in controls; p less than 0.005), sodium (1.4 vs 0.6% in controls; p less than 0.005), calcium (1.7 vs 0.7% in controls; p less than 0.01), and magnesium (10.2 vs 4.1% in controls; p less than 0.005). Systolic blood pressure (160 vs 172 mm Hg in controls; p less than 0.05) and stroke volume were lower (0.024 vs 0.036 L/beat in controls; p less than 0.005) in hypercalcemic dogs, presumably because of the diuresis, while total peripheral resistance was higher (36 vs 31 mm Hg/L/min; p less than 0.05) in controls. Magnesium levels were significantly lower in the experimental group (1.3 vs 1.7 mg/dl in controls; p less than 0.0005). Aldosterone levels, plasma renin activity, and urinary prostaglandin excretion were not significantly affected.(ABSTRACT TRUNCATED AT 250 WORDS)
Hypertension 1986 Nov
PMID:Systemic and renal vascular responses to dietary calcium and vitamin D. 377 Aug 72


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