Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Primary hyperparathyroidism was studied in a well-defined geriatric population of 1129 individuals during a three-month interval. Primary hyperparathyroidism was diagnosed in 1.5%. The diagnosis was based on a morphologic and biochemic basis. From clinical material consisting of 400 patients treated surgically for primary hyperparathyroidism during a ten-year period, 158 patients (38%) above the age of 64 were studied. At the preoperative evaluation, neuromuscular symptoms were present in 80%, renal insufficiency and kidney stones in each 16%, constipation and/or anorexia in 38%. Ten per cent were considered asymptomatic. In 80% the primary hyperparathyroidism was caused by a solitary adenoma. Ninety-four per cent became normocalcemic following the operation. Consistent hypocalcemia requiring vitamin-D treatment occurred in 3%, and 2% had a persisting hypercalcemia or later recurrence. The therapeutic effect on the neuromuscular symptoms, constipation, anorexia, and renal stone formation was considered good or fair in most of the cases. Primary hyperparathyroidism in the elderly occurs with a high prevalence. It can be treated successfully by surgical therapy with a low cost of morbidity, mortality, and medical care.
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PMID:Hyperparathyroidism in the elderly. 660 Jun

In a well-defined geriatric population the prevalence of primary hyperparathyroidism was 1.5%. From a clinical material consisting of 400 patients treated surgically for primary hyperparathyroidism during a 10-year period 158 patients (38%) above the age of 64 were studied. Neuromuscular symptoms were present in 80%, renal insufficiency or kidney stones in each 16%, constipation and/or anorexia in 38%. 10% were considered clinically asymptomatic. In 80% the primary hyperparathyroidism was caused by a solitary adenoma. Normocalcaemia was achieved in 94%. Hypocalcaemia requiring vitamin D treatment occurred in 3%, and in 2% hypercalcaemia persisted or recurred. All of these had multiglandular parathyroid disease. The therapeutic effect of the surgical treatment was considered good or fair in most of the cases. No mortality occurred. Primary hyperparathyroidism occurs with a high prevalence in the elderly. It can be treated successfully by surgical therapy with a low cost of morbidity, mortality and medical care.
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PMID:Hyperparathyroidism in the old age. 662 11

In order to elucidate the influence of the parathyroid function on the uric acid metabolism, 24 patients (14 males, 10 females) with primary hyperparathyroidism (PHP) and 17 patients (9 males, 8 females) with idiopathic hypoparathyroidism (IHP) were extensively studied. The mean age was not significantly different between these groups, being 40.3 +/- 2.8 and 39.0 +/- 3.5 respectively. Hyperuricemia was found in 4 patients with PHP, but none of the patients had experienced gout. The serum uric acid levels were significantly higher and uric acid clearances were significantly lower in PHP than in IHP. There was no difference in daily urinary excretion of uric acid and in creatinine clearance between the two groups. In PHP, a positive correlation was observed between the levels of serum uric acid and calcium, both of which negatively correlated to renal uric acid clearance. Although the serum uric acid levels did not correlate to serum PTH levels in PHP, the removal of parathyroid adenoma resulted in a significant fall of serum uric acid levels. In IHP, the administration of PTH induced a small but significant decrease in serum uric acid levels with a coincidental increase in urinary uric acid excretion. Four hours of calcium infusion had no effect on the serum uric acid levels and urinary uric acid excretion. Treatment of IHP with 1 alpha-OH D3 to restore normal serum calcium levels caused significant increase in serum uric acid levels. These data indicate that the parathyroid function influences uric acid metabolism, even in the absence of renal insufficiency, mainly through changes of uric acid clearance. Levels of active vitamin D or chronically abnormal calcium levels in the circulation may be major determinant for uric acid metabolism in parathyroid disorders.
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PMID:[Parathyroid function and uric acid metabolism]. 666 55

Serum total reverse triiodothyronine (rT3) levels are normal in patients with renal diseases with and without renal insufficiency but elevated in nonrenal nonthyroidal illnesses. To evaluate the role of secondary hyperparathyroidism of renal diseases in this difference, serum thyroid hormone levels were studied in 27 patients with primary hyperparathyroidism (PHP) and normal renal function. In PHP, total T3 levels were reduced (118 +/- 6 ng/dL, normal: 147 +/- 3 ng/dL) and correlated with PTH levels. Serum rT3 levels were also decreased (27 +/- 3 ng/dL, normal: 34 +/- 2 ng/dL). Values for serum total thyroxine (T4), T3 uptake ratio, free T4 index, and thyrotrophin were not altered. Serum rT3 levels were increased (63 +/- 13 ng/dL) in patients with hypercalcemia due to malignant neoplasms who had low T3 levels, undetectable PTH and normal renal function. Thus, PTH excess may be the factor responsible for the failure of rT3 levels to increase in PHP and secondary hyperparathyroidism.
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PMID:Serum thyroid hormone indexes in patients with primary hyperparathyroidism. 669 68

Bilateral dense rings in the renal medulla were found on noncontrasted computed tomography in a patient with marked hypercalcemia and suspected primary hyperparathyroidism. The rings were not present on plain radiographs and were obscured on contrasted scans, and may represent occult nephrocalcinosis. Associated findings--renal insufficiency induced by hypercalcemia and interstitial nephritis--may be reversible with early recognition of this CT finding.
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PMID:Renal medullary "rings": possible CT manifestation of hypercalcemia. 670 30

Renal and systemic magnesium metabolism has not been adequately characterized in states of prolonged PTH excess in humans. Whereas acute experimental PTH administration uniformly results in enhanced renal magnesium reabsorption in many species, including humans, numerous clinical reports have documented renal magnesium wasting in human primary hyperparathyroidism. The possibility has been raised, therefore, that secondary consequences of sustained hyperparathyroidism (eg, hypercalcemia, nephrocalcinosis) might override the direct renal effects of PTH. Accordingly, the present studies assessed the effects of chronic (12 days) continuous intravenous (IV) b-(1-34)-PTH infusion in four normal human subjects on plasma, urinary, and intestinal magnesium and calcium homeostasis under metabolic balance conditions. Chronic PTH infusion resulted in a steady-state of hypercalcemia, hypercalciuria, and persistent negative calcium balance, which returned to baseline values in a recovery period. In contrast to plasma calcium concentration, plasma magnesium concentration was not altered by PTH infusion. Significant hypermagnesuria was observed during the period of PTH administration (control, 8.21 +/- 0.43 mEq/24 hours; PTH days 7-12, 10.75 +/- 0.74 mEq/24 hours, P less than 0.05) resulting in an initial, but transient, negative magnesium balance. During days 7-12 of PTH administration, net intestinal magnesium absorption increased sufficiently to result in a return to control magnesium balance. These findings suggest that hypermagnesuria associated with clinical primary hyperparathyroidism results from either direct or indirect effects of PTH excess, per se, and does not require the long-term consequences or complications of the clinical disorder (eg, nephrocalcinosis, renal insufficiency, acidosis).
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PMID:Renal and systemic magnesium metabolism during chronic continuous PTH infusion in normal subjects. 673 67

Four families with familial hypocalciuric hypercalcaemia were studied. The probands presented with abdominal pain, which in three was due to acute pancreatitis; in two the condition was life threatening. Serum concentrations of calcium, magnesium, phosphate, and immunoassayable parathyroid hormone, urinary calcium excretion, and the rate of renal tubular reabsorption of phosphate were measured; the findings were compared with results in 10 patients with primary hyperparathyroidism matched for serum calcium concentration to establish differences between the diseases. Familial hypocalciuric hypercalcaemia should be suspected in patients with hypercalcaemia in whom daily urinary calcium excretion is below 5 mmol (200 mg) provided renal insufficiency, vitamin D deficiency, and ingestion of drugs that reduce calcium excretion have been excluded. Most cases appear to run a benign course, but some may suffer considerable morbidity. Surgical treatment should be reserved for patients with severe complications, when all parathyroid tissue should be removed.
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PMID:Familial hypocalciuric hypercalcaemia and acute pancreatitis. 678 29

Over a period of 6 1/2 years hypercalcemia has been diagnosed in 86 patients. In 55.8% of cases a malignant tumor was the cause of the elevated calcium levels, and in 22.1% of cases primary hyperparathyroidism (p.Hp.) was diagnosed. In the remaining 19 patients hypercalcemia was related to renal insufficiency (5 patients), vitamin-D intoxication (4) and thiazide therapy (3), while other, rarer causes were identified in 7 cases. As expected, bronchial and breast carcinomas were most frequent (52%) in the malignancy group. In patients below age 40 malignancy was never responsible for the hypercalcemia, but in patients over 50 malignancy was present in 65%. Of the patients with solid tumors 54.8% had skeletal metastases, while other organ metastases were found in 33.3% of these. The occurrence of a hypercalcemia in patients with malignancy is associated with a poor prognosis since over 60% of the patients died within as little as one month and over 90% within a year after the occurrence of hypercalcemia. Renal function impairment in hypercalcemia was significantly more marked in the patients with malignancy than in patients with p.Hp. and was closely related to the calcium levels. Pharmacological reduction of the blood calcium level produced a distinct improvement in renal function in 70% of the patients treated. The current hypothesis on the pathogenesis of hypercalcemia among carcinoma patients is briefly discussed.
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PMID:[Hypercalcemia in hospitalized patients. Diagnostic and prognostic aspects]. 731 56

Plasma levels of calcitonin (CT) are highest in patients with medullary thyroid carcinoma (MTC). Plasma CT is also raised in some patients with carcinoma such as that of the breast, the lung or the pancreas, and in pheochromocytoma. It must be kept in mind, however, that plasma CT can be similarly raised in patients with renal failure, non-tumoral pulmonary disease or acute pancreatitis. In hypercalcemia patients with primary hyperparathyroidism the plasma CT is normal or only marginally elevated. It is speculated that the raised levels in pregnant and lactating women and in new-born infants prevent excessive bone destruction at times of greater physiological need for calcium. Larger molecular weight forms than monomeric CT (1--32) are circulating at least in plasma of patients with calcitonin-producing tumors and in renal insufficiency. The biological function of these larger molecular weight forms is not yet known. The discrepancies among the results of different laboratories can in part be explained by the immunoheterogeneity of the hormone and the different antigenic recognition sites of the antisera used. The measurement of plasma CT levels is nevertheless important for the diagnosis of MTC and may prove useful in some patients with malignant tumors unrelated to the C-cells of the thyroid gland. CT-radioimmunoassay may be improved by using antibodies specific to the different forms of circulating calcitonin.
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PMID:[The differential diagnosis of hypercalcitoninism]. 733 Jun 42

The level of parathyroid hormone was measured by heterologue C terminal radio-immunological assay in 69 patients with clinical or radiological manifestations of the type seen in primary articular chondrocalcinosis. They were divided into three groups: P1 with undetermined clinical arthropathies; P2 with sub-chondral and arthosic arthropathies; P3 with radiologically definite chondrocalcinosis. They were compared with 57 control subjects broken up into four groups: T1 with chronic rheumatic arthritis, T2 with low back pain, T3 with primary hyperparathyroidism due to adenoma, and T4 with secondary hyperparathyroidism with renal insufficiency. A form of normocalcemic hyperparathormonaemia was demonstrated in more than one out of two patients in group P1 (15/29). It was seen in three-quarters of the cases in group P2 (12/16). And it was seen in more than a quarter of the cases in group P3 (7/24). This hyperparathormonaemia was statistically significant only in groups P1 and P2 compared to the normals in groups T1 and T2. The results we obtained in this study seem to be in complete concordance with those we obtained earlier in idiopathic hemochromatosis. This hyperparathormonaemia seems to regress with age and is often only discovered when the characteristic articular lesions have appeared. The discovery of normocalcemic hyperparathormonaemia several years before the appearance of the radiological signs of the disease would appear to be an important argument in favour of the diagnosis of early articular chondrocalcinosis. The existence of raised parathyroid hormone in primary articular chondrocalcinosis as well as in idiopathic hemachromatosis is special etiopathogenic interest even if there remain numerous questions concerning its origin and mode of action.
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PMID:[Normocalcemic hyperparathormonemia and articular chondrocalcinosis. Study of 69 patients compared to 57 controls]. 733 2


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