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)

Based on the postulate that parathyroid adenoma is practically always a solitary lesion, unilateral parathyroidectomy including the homolateral normal parathyroid was applied as a principle in the treatment of this form of primary hyperparathyroidism. The exploration was confined to the adenoma side if this was the first to be explored. Intraoperative oil-red-O staining of frozen sections was used to exclude the possibility of a multiglandular involvement. This principle was applied in a consecutive series of 102 patients operated for hyperparathyroidism from 1977 to 1981 and diagnosed as parathyroid adenoma. In 43 patients where the abnormal gland was found on the side explored first, unilateral parathyroidectomy was performed on that side, avoiding exploration of the contralateral side. In 45 patients where normal glands were found on the side first explored, unilateral parathyroidectomy was performed on the contralateral side. In 14 patients other types of operations were performed as the above-mentioned principle could not be achieved. At follow-up 1 to 5 years after surgery, no cases of hypocalcemia were recorded. The results of the different operations were compared as to early and late hypocalcemia. Early hypercalcemia was more pronounced after a bilateral exploration. Two of the patients who had an atypical operation had a permanent need for vitamin D in order to maintain an adequate serum calcium level. Surgical principles for various possible exploratory findings are outlined. These are based upon the idea of performing a unilateral parathyroidectomy whenever intraoperative oil-red-O staining excludes multiglandular involvement as a cause for the hyperparathyroidism.
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PMID:Surgical strategy in hyperparathyroidism due to solitary adenoma. 650 9

We describe a study of a boy with neonatal severe primary hyperparathyroidism (NSPHP) and alkaptonuria born to related parents of Turkish origin. The clinical and chemical courses (e.g. of mineral metabolism, of urinary excretion of amino acids and collagen metabolites) in response to various therapeutic approaches including total parathyroidectomy (PTX) are reported. Urinary excretion of calcium was unusually low before and immediately after PTX, and later during an inadvertent vitamin D intoxication. It corresponded to values typical for patients with familial hypocalciuric hypercalcemia (FHH), an autosomal dominant disorder. Both parents and one sibling had episodes of hypercalcemia with inappropriately high parathormone levels; in the father there was also relative hypocalciuria consistent with FHH. On the basis of the genetic and pathophysiologic data reported here, we speculate that homozygosity for the 'FHH-gene' is the cause of the life-threatening manifestation of NSPHP, whereas heterozygosity for the same gene leads to FHH, by comparison a mild disorder. The association of the two very rare recessively transmitted disorders, alkaptonuria and NSPHP, is unique; close linkage of the two genes, one coding for homogentisic acid oxidase, the other for the unknown gene product defective in NSPHP, can be suspected.
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PMID:Neonatal severe primary hyperparathyroidism and alkaptonuria in a boy born to related parents with familial hypocalciuric hypercalcemia. 654 41

Plasma concentrations of 1.25 dihydroxycholecalciferol were measured in 44 patients with malignancy associated hypercalcaemia and related to other hormonal regulators of calcium metabolism. Immunoreactive PTH concentrations were suppressed in all but 2 patients and, as a group, patients with hypercalcaemia of malignancy had lower 1.25 dihydroxycholecalciferol concentrations than normocalcaemic cancer patients. 1.25 dihydroxycholecalciferol concentrations were clearly detectable in a significant proportion (43%) of hypercalcaemia cases however, suggesting that in these patients the active vitamin D metabolite may contribute to the pathogenesis and maintenance of the hypercalcaemia by stimulating bone resorption, and/or by increasing absorption of calcium from the intestine. Measurement of plasma 1.25 dihydroxycholecalciferol concentration does not provide a wholly reliable method for distinguishing the hypercalcaemia of malignancy from primary hyperparathyroidism.
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PMID:Circulating vitamin D metabolites and hypercalcaemia of malignancy. 654 74

The records of 400 patients operated on for primary hyperparathyroidism during 10 years were reviewed. Seventy-three per cent of the patients were women. The mean age at operation was 58 years. Renal stones was the main indication for surgery in 52 per cent of the men, but only in 17 per cent of the women. Forty-four per cent of the women and 22 per cent of the men had neuromuscular symptoms. Fifteen per cent of the patients were asymptomatic. Hypercalcemia was moderate in most cases with mean S-Ca less than 3.0 mmol/l in 80 per cent. A conservative surgical approach with microscopical identification of one or two glands only was used in 2/3 of the cases. Subtotal parathyroidectomy was performed in less than 10 per cent. Single adenoma was found in 70 per cent, double adenomas in 4 per cent, hyperplasia in 17 per cent and cancer in 1 per cent. The outcome of the operation was normocalcemia in 86 per cent. Seven per cent had persistent hypercalcemia. Seven per cent were hypoparathyroid and had to take calcium or vitamin D to be normocalcemic. The frequency of hypoparathyroidism was highest in the group of patients where all four parathyroid glands had been biopsied during the operation. The results support a conservative surgical strategy with careful bilateral exploration without biopsy of all four glands.
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PMID:Surgery for primary hyperparathyroidism. Experience with 400 patients during 10 years (1972-1981). 659 66

A 48-year-old woman underwent jejunoileal bypass surgery for obesity while hypercalcemic. Three years later, she developed symptomatic osteomalacia impairing her daily activities. Bone biopsy confirmed the clinical diagnosis of osteomalacia, and treatment with 8000 U daily of vitamin D and milk resulted in striking improvement of clinical symptoms and resolution of her osteomalacia both chemically and histologically. The patient, however, again became hypercalcemic and a parathyroid adenoma was subsequently removed with restoration of serum calcium values to normal. Neither the occurrence and successful treatment of gross symptomatic osteomalacia consequent to jejunoileal bypass surgery, nor the obscuration of primary hyperparathyroidism by osteomalacia has been hitherto well documented in the United States.
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PMID:Symptomatic osteomalacia after jejunoileal bypass surgery in a patient with primary hyperparathyroidism. A study of the change in bone morphology and vitamin D metabolites before and during treatment. 660 88

The effects of 1,25-dihydroxycholecalciferol (1,25-(OH)2D3) and 24,25-dihydroxycholecalciferol (24,25-(OH)2D3) on parathyroid hormone (PTH) release from human parathyroid cells were investigated using an in vitro system of dispersed cells. The cells were obtained from 7 patients with primary hyperparathyroidism (HPT) and adenoma, 4 patients with primary HPT due to hyperplasia and 2 patients with parathyroid hyperplasia secondary to chronic renal failure. The dispersed cells were incubated in tissue culture medium at low, normal and high external calcium concentrations for 2-16 h. There was a gradual suppression of PTH release (5-55%) when the calcium concentration in the medium was increased from 0.5 to 3.0 mM, thus indicating retained regulation of hormone release. The addition of 1,25-(OH)2D3 in concentrations of 0.1 and 1 ng/ml and of 24,25-(OH)2D3 in concentrations of 1.0 and 10 ng/ml during the incubations did not further affect the amount of PTH released by the cells. The concentrations of the different vitamin D metabolites tested closely correspond to levels observed under normal physiological conditions and during treatment with high doses of vitamin D in vivo. Thus, the findings contradict the idea of any direct short-term regulatory effect of either 1,25-(OH)2D3 or 24,25-(OH)2D3 on the secretion of PTH from hyperfunctioning human parathyroid tissue.
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PMID:Effects of 1,25- and 24,25-dihydroxycholecalciferol on parathyroid hormone release from human parathyroid cells in vitro. 660 1

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

We compared serum concentrations of immunoreactive PTH and plasma levels of vitamin D metabolites in 11 patients with adenomatous primary hyperparathyroidism and 32 individuals with the syndrome of familial benign hypercalcemia or familial hypocalciuric hypercalcemia (FHH). Serum immunoreactive PTH was elevated in the hyperparathyroid group but indistinguishable from control in FHH, despite comparable degrees of hypercalcemia. Plasma 25-hydroxyvitamin D concentrations were normal in both groups, but plasma 1,25-dihydroxyvitamin D levels in FHH were significantly lower than control (P less than 0.0025) or hyperparathyroid (P less than 0.01) values. FHH is pathogenetically distinct from primary hyperparathyroidism and should not be thought of simply as a variant of that condition.
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PMID:Vitamin D metabolism in familial benign hypercalcemia (hypocalciuric hypercalcemia) differs from that in primary hyperparathyroidism. 669 36

The autotransplantation of normal as well as adenomatous parathyroid tissue is currently being used with increasing frequency. In the present report, we describe our experiences with the successful transplantation of adenomatous or hyperplastic parathyroid tissue in seven patients. Prior to transplant surgery, six of these patients had recurrent or persistent primary hyperparathyroidism. The last patient was on hemodialysis for chronic renal failure and was presumed to have tertiary hyperparathyroidism. A large superior mediastinal parathyroid adenoma was found at a second neck exploration. In all patients, the only remaining parathyroid tissue was either adenomatous or hyperplastic. A total of 30 to 75 mg of this parathyroid tissue was diced and transplanted into single subfascial pockets of the forearm muscles (6) or sternocleidomastoid muscle (1). Following transplantation, all patients required transient calcium and vitamin D supplements for six to 12 weeks. In follow-up studies of ten months to 12 years, all patients have remained eucalcemic with normal parathyroid hormone levels. The use of a single subfascial pocket (versus the popular method of multiple implants) may explain the lack of recurrent hyperparathyroidism in our small population.
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PMID:Successful autotransplantation of parathyroid adenomas in seven patients. 685 73


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