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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

A brown tumor is a secondary disorder of bone associated with hyperparathyroidism that arises predominantly in the metacarpals, phalanges, jaw, pelvis, or femur. Rarely does this tumor involve the spine. The authors describe a case of brown tumor in primary hyperparathyroidism, causing spinal cord compression. The first step in diagnosing this lesion in an unusual site is a high index of suspicion. Essentially, this tumor is benign but emergency surgery for tumor removal is recommended in patients showing acute spinal cord compression.
J Neurosurg 1989 Sep
PMID:Paraplegia caused by brown tumor in primary hyperparathyroidism. Case report. 276 96

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.
South Med J 1989 Sep
PMID:Hypomagnesemia and hypertension in primary hyperparathyroidism. 277 81

The "N-tact" immunoradiometric assay (IRMA) from INCSTAR for parathyrin (PTH) in serum involves a 125I-labeled affinity-purified antiserum to PTH 1-34 and an affinity-purified antiserum to PTH 39-84, the latter bound to a polystyrene bead. The mean detection limit, determined in six consecutive assays, was 4 ng/L. The within-batch CV was less than 7% in the range 15 to 2135 ng/L. The between-batch CV was 11.7% and 5.3% at 30 and 371 ng/L, respectively. Serum PTH in 14 proven cases of primary hyperparathyroidism was 49-808 (median 111) ng/L, undetectable (less than 5 ng/L) in 10 cases of primary hypoparathyroidism and in 10 cases of hypercalcemia associated with malignancy, compared with 7-39 ng/L in 45 normal subjects. PTH was 9 to 19 ng/L in four patients with familial benign hypercalcemia. In 39 patients with renal failure, apparent concentrations were 14 to 857 (median 133) ng/L, but sera from these patients pre-diluted with zero standard did not parallel dilutions of the standard, PTH 1-84. PTH concentrations were not significantly decreased in blood or serum kept at 20 degrees C for up to 6 h. After successful removal of a parathyroid adenoma, the mean half-time for disappearance of PTH in vivo in five hyperparathyroid patients was 3.3 min.
Clin Chem 1989 Sep
PMID:Performance and diagnostic application of a two-site immunoradiometric assay for parathyrin in serum. 277 25

Acute primary hyperparathyroidism is a rare disease with a high mortality rate in some series. Between 1960 and 1986, 1000 patients were treated for primary hyperparathyroidism, among them 59 patients with acute hyperparathyroidism. All these patients were successfully operated on; none of them died before surgery. This study reveals the importance of resuscitation and urgent surgery. It is necessary to rehydrate, to correct electrolyte disorders and to lower serum calcium levels, but it is not necessary to obtain normal serum calcium levels before surgery.
Br J Surg 1989 Sep
PMID:Acute primary hyperparathyroidism: experience of 59 cases. 280 4

A family of multiple endocrine neoplasia type I with five confirmed cases in three generations is described. All of them have primary hyperparathyroidism in common. The propositus is 51 year-old male. After a year of symptoms of gastroduodenal ulcer, he was found to have elevated levels of serum gastrin and PTH. The serial imaging studies revealed a tumor in pancreatic head, and Zollinger-Ellison syndrome was diagnosed. The gastrin level was reduced into normal range after extirpation of the tumor, but post surgical elevation of Calcium put the patient under parathyroidectomy, which normalized serum PTH and Calcium levels. His two sisters (I and II), the mother of them, and the daughter of sister I, had neither signs nor symptoms until family study showed hypercalcemia in all. Sister I is a 54 year-old female with enlarged parathyroid. The hyperparathyroidism is of chemical type, but no other endocrinological abnormality is found. The Calcium level decreased after parathyroidectomy. Sister II is a 56 year-old female. The only sign was galactorrhea. Serum PTH and Calcium decreased after parathyroidectomy. The prolactinoma was diagnosed by the increased prolactin levels and enhanced mass lesion in sella turcica. Her serum prolactin levels is now within normal range since she is on bromocryptine. The mother of the above three siblings and the daughter of the sister I are now under further study.
Nihon Naibunpi Gakkai Zasshi 1985 Sep 20
PMID:[A family with multiple endocrine neoplasia type I presenting prolactinoma, Zollinger-Ellison syndrome and hyperparathyroidism]. 286 39

We studied 25-year-old HLA- and blood group-identical male twins who had multiple endocrine neoplasia, type I (MEN I). At the time of initial examination, one twin (case 1) had epigastric pain and diarrhea; he was cushingoid in appearance. Further evaluation revealed primary hyperparathyroidism, Zollinger-Ellison syndrome, Cushing's disease, and hyperprolactinemia. Immunostaining of a resected pituitary specimen demonstrated both prolactin and, to a lesser extent, growth hormone reactivity. The nontumorous adenohypophysis showed corticotropic hyperplasia. In contrast, the other twin (case 2) was asymptomatic. He had only primary hyperparathyroidism and hyperprolactinemia. An invasive pituitary adenoma was resected and showed similar proportions of cells with immunoreactive prolactin and those with growth hormone; no nontumorous gland was available for study. Apparently, factors other than heredity may play a role in the expression of MEN I.
Mayo Clin Proc 1986 Sep
PMID:Nonidentical expressions of multiple endocrine neoplasia, type I, in identical twins. 287 27

Eleven patients who had clinical and biochemical evidence of primary hyperparathyroidism were studied using dual isotope technetium-thallium parathyroid subtraction imaging. The parathyroid scans correctly identified all surgically proven parathyroid adenomas. Three abnormal foci also were identified that were not parathyroid adenomas. These were caused by adenocarcinoma metastatic to a lymph node, primary papillary carcinoma of the thyroid, and parathyroid hyperplasia. This report also demonstrates the importance of surgically examining all abnormal sites of uptake.
Clin Nucl Med 1986 Sep
PMID:Dual isotope parathyroid imaging. 302 75

Ultrasound-guided percutaneous ethanol ablation of a small occult parathyroid adenoma was successfully performed in a patient with persistent primary hyperparathyroidism. This procedure may be an alternative to reoperation for patients in whom surgical treatment is contraindicated or who have an unacceptable risk of postoperative morbidity.
Mayo Clin Proc 1988 Sep
PMID:Persistent primary hyperparathyroidism: successful ultrasound-guided percutaneous ethanol ablation of an occult adenoma. 304 36

The cause of hypertension in primary hyperparathyroidism and its response to corrective surgery remains a matter of controversy. We therefore studied blood pressure, vasoactive hormones and plasma calcium responses to parathyroidectomy in six hypertensive and two normotensive patients with primary hyperparathyroidism. Twenty-four-hour intra-arterial pressure recordings, together with hourly blood sampling for plasma renin activity (PRA), aldosterone, cortisol, catecholamines and calcium levels, were undertaken in each patient before surgery and were repeated under identical conditions 3-6 months after parathyroidectomy. Mean plasma calcium was 3.03 +/- 0.1 before, and 2.35 +/- 0.02 mmol/l after, parathyroidectomy. Changes in arterial pressure were small and variable in individual patients. Group mean arterial pressures before and after surgery were identical. Plasma cortisol and PRA were significantly higher in the hypercalcaemic state (P less than 0.01 and P less than 0.05, respectively) but there was no significant difference in plasma aldosterone or catecholamine levels. No correlations between changes in plasma calcium or parathyroid hormone levels and concomitant changes in plasma concentration of other hormones were observed. Our findings show that correction of primary hyperparathyroidism has no systematic effect on arterial pressure in a heterogeneous group, including some patients with probable background essential hypertension, when evaluated 3-6 months after surgery. Compared with values after corrective surgery, mean levels of PRA and cortisol-but not aldosterone or catecholamines--are elevated in patients with primary hyperparathyroidism. These findings are consistent with an inhibitory effect of raised ionic calcium concentration on the response of the adrenal glomerulosa to angiotensin and adrenocorticotrophic hormone.
J Hypertens 1988 Sep
PMID:Hormone, calcium and blood pressure relationships in primary hyperparathyroidism. 305 96

Hypercalcemia is a relatively common clinical finding; prevalence rates are 1.4 to 3.0 per cent in hospitalized and general clinical populations. Malignancy is the major cause of hypercalcemia in hospital patients, whereas primary hyperparathyroidism (HPT) is the major cause in ambulatory patients. In both hospitalized and ambulatory patients, however, there are many other causes of hypercalcemia, and numerous procedures have been proposed to aid in the differential diagnosis. Unfortunately, no single test is truly diagnostic. The work-up for hypercalcemia requires an integrated knowledge of the strengths and weaknesses of the various procedures as well as an understanding of the various clinical presentations associated with hypercalcemia.
Endocrinol Metab Clin North Am 1988 Sep
PMID:Hypercalcemia. 306 81


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