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)

It appears that at present, serum BGP is the one bone protein that has the most promise for assisting in the diagnosis and management of high turnover metabolic bone disease states. If further studies confirm its usefulness in osteoporosis as a predictor of rapid bone loss without the need for bone biopsy, this serum marker will then not only allow early detection but also an appropriate choice of therapy in osteoporosis, i.e. the use of specific inhibitors of high turnover states such as estrogen, calcitonin, or bisphosphonates. In addition, it may also permit more accurate follow-up of patients suffering from diseases such as primary hyperparathyroidism after surgery. In low turnover osteoporosis, it may also serve a useful function to observe whether the osteoblast can be stimulated to enhance bone formation with therapies such as fluoride, anabolic steroids, PTH, etc. As yet, additional measurements, such as bone histomorphometry and other bone mineral markers, are required for definitive diagnosis. Hopefully, the availability of specific well-characterized antibodies against BGP may define its role more accurately. Recently, several other new bone proteins have been identified but at present they have very limited clinical application. Future studies into the structure-function relationship of these bone proteins may identify those markers which will be most relevant to the diagnosis and treatment of metabolic bone disease.
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PMID:Serum and urinary markers of bone remodeling: assessment of bone turnover. 306 73

Hypercalcaemia can be caused by malignant diseases as well as by primary hyperparathyroidism (HPT). The two disorders may occur together and an accurate discrimination between them is sometimes not possible from basal measurements of calcium and parathyroid hormone (PTH) concentrations. In primary HPT the regulation of PTH secretion is maintained, albeit the set-point is shifted to a hypercalcaemic value. Therefore, when serum calcium is lowered by ethylene diamine tetra-acetic acid (EDTA) infusions or calcitonin injections, patients with primary HPT display enhanced secretion of PTH already within the hypercalcaemic range, whereas parathyroid function remains suppressed in malignancy-associated hypercalcaemia. Tests based on this principle enable a specific identification of HPT. The present report describes eight hypercalcaemic patients with disseminated malignancy where HPT could be diagnosed by the use of such stimulatory tests.
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PMID:Dynamic tests of parathyroid function for diagnosis of primary hyperparathyroidism in malignancy. 311 51

A 63-year-old woman was treated medically for primary hyperparathyroidism because of a recent myocardial infarction. She received propranolol alone or combined with either cimetidine, calcitonin or disodium etidronate (EHDP). The treatment did not affect the elevated serum parathormone or urinary cyclic AMP levels, nor did it correct the elevated serum 1,25(OH)2D and the decreased serum 24,25(OH)2D levels in this patient. Propranolol combined with either cimetidine or with EHDP (600 mg/day) caused a mild decrease in the serum calcium level which, however, remained within the hypercalcemic range. Following surgery all parameters returned to normal. We conclude that the above medical regimens were incapable of correcting the hyperparathyroid condition in this patient.
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PMID:Medical treatment of primary hyperparathyroidism: effects on parathormone and vitamin D metabolites. 312 29

Serum calcitonin (CT), parathyroid hormone (PTH), and calcium levels were measured in 23 patients with primary hyperparathyroidism. PTH was determined by a midregion (M-RIA) and a carboxyl-terminal (C-RIA) specific PTH-RIA. Only 2 patients had elevated CT levels. In contrast to the findings in 46 healthy controls, the CT levels did not correlate with calcium levels. Patients who had the highest iPTH values showed a negative correlation between CT and iPTH (M-RIA (n = 7): R = -1.0000, p less than 0.001; C-RIA (n = 13): R = -0.5604, p less than 0.05). The results of the C-RIA were subtracted from those of the M-RIA. In 12 patients with the highest levels of intact PTH (M-RIA - C-RIA), serum PTH concentration was inversely correlated with serum CT concentration (R = -0.7343, p less than 0.01). In the same patients a negative correlation between CT and calcium was found (R = -0.6783, p less than 0.02). These findings suggest that high PTH levels may have a direct suppressive effect on CT concentration and this may be, at least in part, responsible for failure of CT concentrations to rise in many patients with primary hyperparathyroidism.
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PMID:The effect of high parathyroid hormone concentration on calcitonin in patients with primary hyperparathyroidism. 345 May 31

High-resolution real-time sonography was performed in 15 cases of clinically and chemically suspected primary hyperparathyroidism and in 20 patients with different thyroid nodules. The suspected enlarged parathyroid glands and the thyroid nodules were percutaneously punctured under sonographic control. Concentrations of parathyroid hormone, human thyroglobulin, and human calcitonin were measured in the aspirate, and immunocytology was performed. The mean concentration of the aspirated parathyroid hormone in the parathyroid glands was 4,013.6 pmol/l +/- 4,519 (SD) as compared with 14.9 pmol/l +/- 8.7 in the thyroid nodules. Thyroglobulin was present in the aspirated fluid of parathyroid adenomas located behind the thyroid (mean +/- SD, 398.1 ng/ml +/- 317). In comparison, the aspirated thyroglobulin from the thyroid nodules averaged 9,689.7 ng/ml +/- 3,732. Immunocytology for parathyroid hormone was positive in 14 of the 15 biopsied specimens. Of 15 patients who were scanned for suspected hyperparathyroidism, six had concomitant thyroid nodules. It is concluded that the measurement of high concentrations of parathyroid hormone in the aspirate from a cervical mass, with sonographic control of needle position and/or positive immunocytology provides absolute localization of parathyroid tissue.
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PMID:Fine-needle biopsy of parathyroid adenomas. 354 72

Intrathyroidal hyperplastic parathyroid glands were responsible for primary hyperparathyroidism (PHPT) in two of three members in a family. The third had an extrathyroidal parathyroid "adenoma". Both intrathyroidal parathyroid (IThP) hyperplastic glands were the largest ones removed at the time of surgical cure. A review of the literature confirmed our postulate of a higher incidence of familial cases among patients with hyperparathyroidism and IThP with an incidence of 10.34% of IThP in familial cases versus a 4.2% in non-familial cases with PHPT. This contrasts with an incidence of 0.1% of IThP in normal patients. We hypothesize that stimulation of IThP tissue by surrounding calcitonin-producing C-cells might play a role in the seemingly preferential IThP hyperplasia. Recognition of this syndrome of Familial IThP Hyperplasia is important in order to avoid unnecessarily aggressive surgery for hyperparathyroidism.
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PMID:A syndrome of familial intrathyroidal primary parathyroid hyperplasia: case reports and critical review of literature. 354 52

The aim of the present study was to determine the diurnal secretion of melatonin, cortisol, prolactin, and calcitonin during chronic parathyroid hormone-dependent hypercalcemia. Eight women, aged 40-76 years, with primary hyperparathyroidism (PHPT) were studied before and after surgical removal of a parathyroid adenoma. The hormone concentrations in blood were determined at 08, 12, 16, 22, 02, 04, and 06 h. Concomitantly, the excretion of melatonin and cortisol in urine between 07-19 h and 19-07 h, and the clearance of calcium and creatinine were measured. Nyctohemeral serum prolactin and calcitonin were unaffected by moderate parathyroid hormone-dependent hypercalcemia. In contrast, serum cortisol and melatonin were significantly higher during active disease than after surgical cure. Mean 24-h variation of serum cortisol was 349 +/- 34 nmol/liter vs. 223 +/- 17 nmol/liter and mean serum melatonin was 0.13 +/- 0.04 nmol/liter vs. 0.06 +/- 0.02 nmol/liter. Endogenous creatinine clearance was similar before and after surgery, while the clearance of melatonin and cortisol significantly increased after surgery, indicating an increased tubular reabsorption of both hormones during active disease. Fasting morning glucose concentrations were also significantly decreased after successful surgery, 6.1 +/- 0.6 vs. 5.2 +/- 0.5 mmol/liter. It is suggested that the relative hypercortisolism may be the cause of the glucose intolerance in primary hyperparathyroidism. Three to 4 months after surgical cure the serum melatonin levels were significantly lower than those seen in age-matched controls, indicating a melatonin insufficiency in patients successfully treated for PHPT. The meaning of this finding is not yet understood but might be of importance in the development of primary hyperparathyroidism.
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PMID:Melatonin, cortisol, prolactin, and calcitonin secretion in primary hyperparathyroidism before and after surgery. 362 59

A recently developed chemiluminescent immunoassay for 1-84 intact parathyroid hormone (PTH) demonstrated increased specificity by virtue of two-site antibody binding and increased sensitivity by use of a chemiluminescent technique. Basal PTH levels were measured in three groups of subjects: (1) normal (n = 82), (2) hyperparathyroidism (n = 31), and (3) patients with hypercalcemia of malignancy (n = 16). There was good discrimination between normal (1.2 to 9.4 pmol/L) and hyperparathyroid subjects (9.2 to 53.4 pmol/L). In persons with hypercalcemia of malignancy all PTH levels were within the normal range (0.8 to 5.2 pmol/L) or suppressed. PTH release was stimulated by the intramuscular injection of 100 IU salmon calcitonin in 6 normal controls, 10 patients with primary hyperparathyroidism due to adenoma, and 5 with four-gland hyperplasia. There was no significant rise in PTH concentration and out of the normal range in the control subjects, but the adenoma patients demonstrated a mean rise of 24.4%, 26%, and 33%, and hyperplasia patients, a mean rise of 37%, 47%, and 37% over basal levels at 120, 180, and 240 minutes. The mean absolute rise in PTH concentration was 13.4 +/- 7.7 pmol/gm of parathyroid tissue in the adenomas and 27.2 +/- 9.5 pmol/gm of parathyroid tissue in the hyperplastic glands; this difference was significant (p less than 0.05). Serial blood samples from a central vein were taken at surgery for hyperparathyroidism, and the rate of decay of the intact hormone was studied in 9 patients after removal of the parathyroid tissue. This decay was rapid with a half-life of 300 seconds. We conclude that this new specific and sensitive intact PTH assay will provide a valuable means of investigating dynamic aspects of parathyroid physiology.
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PMID:Studies in patients with hyperparathyroidism using a new two-site immunochemiluminometric assay for circulating intact (1-84) parathyroid hormone. 368 55

An acute increase in serum calcium stimulates calcitonin (CT) secretion, but the effects of chronic hypercalcemia are controversial. Histopathological studies have shown C-cell hyperplasia in primary hyperparathyroidism (1 degree HPT), although circulating levels of CT have been variously reported to be normal, elevated, or depressed. We reexamined this relationship using CT RIA in conjunction with a silica extraction technique that conveys improved sensitivity and specificity for monomeric CT. Nine men and seven women with surgically documented 1 degree HPT were studied preoperatively before and after a short calcium infusion (2 mg Ca/kg, for 5 min), as were 72 normal men and 76 normal women. Basal whole plasma immunoreactive CT and silica-extractable CT concentrations in 1 degree HPT were indistinguishable from normal, regardless of sex. In addition, the whole plasma and silica-extractable CT responses to calcium stimulation were normal or blunted in patients with 1 degree HPT. We conclude that hypercalcemia resulting from 1 degree HPT is not associated with augmented CT secretion in response to an iv calcium infusion.
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PMID:Plasma calcitonin in primary hyperparathyroidism: failure of C-cell response to sustained hypercalcemia. 373 44

Treatment with ethinyl estradiol or norethindrone reduces the bone-turnover rate and plasma calcium levels in normal postmenopausal women, without affecting the secretion of calcium-regulating hormones. To assess the effect of these sex steroids in patients with primary hyperparathyroidism, we treated postmenopausal women who had hyperparathyroidism with either ethinyl estradiol (n = 6) or norethindrone (n = 11). After three weeks of treatment, the bone-turnover rate declined and plasma calcium fell from a mean (+/- 1 SE) of 2.77 +/- 0.07 mmol per liter (11.1 +/- 0.3 mg per deciliter) to 2.58 +/- 0.05 mmol per liter (10.3 +/- 0.2 mg per deciliter; P less than 0.01) in the group treated with ethinyl estradiol, and from 2.93 +/- 0.08 mmol per liter (11.7 +/- 0.3 mg per deciliter) to 2.84 +/- 0.08 mmol per liter (11.4 +/- 0.3 per deciliter; P less than 0.05) in the patients who received norethindrone. No significant changes in the plasma levels of parathyroid hormone, calcitonin, or calcitriol were observed after the estrogen-induced increases in vitamin D-binding protein had been taken into account. Since the decline in plasma calcium levels did not stimulate secretion of parathyroid hormone, we conclude that treatment with either sex steroid resets the threshold for secretion of parathyroid hormone. Thus, although the reductions in plasma calcium levels were moderate, sex-hormone therapy may be useful in the treatment of mild hyperparathyroidism in postmenopausal women.
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PMID:Ethinyl estradiol and norethindrone in the treatment of primary hyperparathyroidism in postmenopausal women. 375 18


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