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

The vicinity of several hormone-producing glands as part of the anatomy of the intestinal tract and the resulting interaction has been confirmed by the discovery of hormonal factors of a specifically gastro-intestinal origin. Today we are mainly interested in the interaction between intermediary metabolism and incretory intestinal function; this is characterized by the joint action of conventional glandular hormones such as insulin and pancreatic glucagon as well as by the incretion of diffuse intestinal organs, hormones such as secretin, pancreozymin, motilin, VIP and GIP. The latter are at present subject of active research with the object of discovering their physiological significance be it as tissue hormones or as humoral agents with a "long distance" impact; their role within pathophysiology is also of interest. GIP ("gastric inhibitory peptide"), apart form acting upon the intestinal tract, also causes a marked rise in insulin production; this GIP possibly is the factor responsible for the difference in glucose tolerance following i. v. or oral administration of glucose, something that scientists have been trying to discover for a long time. We have also endeavored to investigate somatostatin. This substance was originally discovered as a hypothalamic factor with inhibitory action on growth hormone secretion; in the meantime, however, cells containing and possibly also producing somatostatin have also been detected in the intestine and particularly in the islets of Langerhans (D-cells). Since somatostatin inhibits insulin secretion and especially glucagon release as well as the exretory functions of the stomach and of the pancreas, the significance of this hormone possibly is that of a tissue hormone with inhibitory action on adjacent cells. As factor inhibiting both endocrine and exocrine secretory processes it would combine these two complexes. The possible therapeutic significance of somatostatin administration to diabetics would lie in the saving of insulin. A third sector of present-day research deals with the interaction between the calcium metabolism and the hormones involved as well as the intestine. We know that patients suffering from primary hyperparathyroidism are prone to contract stomach ulcers and pancreatitis; patients with a gastrinoma and a hyperfunction of the epithelial bodies suffer from a Zollinger-Ellison-sindrome and this again suggests association with endocrine polyadenomatosis (Wermer syndrome). The inhibitory action of the parathormone antagonist calcitonin on the exocrine functions of the intestinal tract, such as the acid secretion of the stomach and the enzyme secretion of the pancreas, have already given rise to some considerations and experiments relative to treatment. It is to be hoped that because of all the joint observations cited above there will be better intergration of research both from the aspect of gastro-enterology and endocrinology. This might hopefully elucidate some of the unresolved problems ranging from basic research to practical application.
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PMID:[Interaction between gastrointestinal hormones and endocrine regulation]. 0 83

Of 53 patients who had hyperparathyroidism assocated with multiple parathyroid gland enlargement, 39 (74%) had primary hyperparathyroidism without clinical or laboratory evidence of associated endocrine gland dysfunction, 2 had documented familial primary hyperparathyroidism, and 12 had hyperparathyroidism as part of the multiple endocrine neoplasia syndrome. When last studied, 31 of the 39 patients with nonfamilial hyperparathyroidism had normal serum calcium levels, 3 had permanent hypoparathyroidism, 2 had recurrent hyperparathyroidism, and 3 were lost to follow-up. The two patients with familial hyperparathyroidism were treated by removal only of enlarged parathyroid glands, and in each, hyperparathyroidism recurred. Five patients with multiple endocrine neoplasia, type 1, were treated by removal only of enlarged parathyroid glands, and hyperparathyroidism recurred in four. Four patients with multiple endocrine neoplasia, type 1, were treated by removal of three or more parathyroid glands, and there were no instances of recurrent hyperparathyroidism. In one patient, permanent hypoparathyroidism developed. Three patients with multiple endocrine neoplasia syndrome, type 2, had total parathyroidectomies as a part of thyroidectomy for medullary thyroid carcinoma. In each patient, permanent hypoparathyroidism developed. When primary hyperparathyroidism occurs in the absence of a definite history of polyendocrine or familial disease, only the glands that are definitely enlarged should be removed, and normal-appearing glands should be tagged rather than risk the possibility of permanent hypoparathyroidism that may attend routine subtotal parathyroid gland excision.
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PMID:Primary hyperparathyroidism with multiple parathyroid gland enlargement: review of 53 cases. 3 39

Hypercalcaemia is often associated with malignant disease. Causes of elevated serum-calcium levels in the absence of bony metastases include parathyroid-hormone production by the tumour, osteolytic factors made by the tumour, and coexistent primary hyperparathyroidism. By measuring nephrogenous cyclic-A.M.P. excretion to assess parathyroid-hormone function, we have determined the mechanism of such hypercalcaemia in 15 patients. Nephrogenous cyclic A.M.P. ranges from 0.05 to 2.40 mumol/g of creatinine in normal subjects, from 2.27 to 8.45 mumol/g in patients with primary hyperparathyroidism, and from 0.50 to 1.30 mumol/g in patients with proven non-hyperparathyroid hypercalcaemia without malignancy. 9 patients (60%) with hypercalcaemia and malignancy had normal levels of nephrogenous cyclic A.M.P. (range 0.35-2.07 mumol/g creatinine). The other 6 (40%) had elevated nephrogenous cyclic A.M.P. (range 2.70-5.55 mumol/g) consistent with increased parathyroid-hormone secretion. Surgical exploration of the neck in these patients showed that the increased parathyroid-hormone secretion was secondary to primary hyperparathyroidism, not ectopic hyperparathyroidism. Thus, the data indicate that coexistent hyperparathyroidism may be common in patients with hypercalcaemia and malignancy and that the measurement of nephrogenous cyclic A.M.P. is very useful in identifying patients at risk for hyperparathyroidism.
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PMID:Primary hyperparathyroidism in paraneoplastic hypercalcaemia. 7 31

Early effects of parathyroid hormone (PTH) deficiency were studied in 12 patients with primary hyperparathyroidism due to single parathyroid adenoma by following the precise time course of changes in plasma calcium (Ca) and immunoreactive parathyroid hormone (IPTH) after parathyroid surgery and by prelabeling 2 patients with radiocalcium (Ca*). Surgical removal of the adenoma was immediately followed by a sudden increase in plasma Ca which preceded the usual fall. The increase in plasma Ca commenced simultaneously with the fall in iPTH and was accompanied by a parallel increase in specific activity (sp. act.) of plasma Ca*. Specific activity continued to rise for 2 h in both prelabeled patients, whereas blood calcium was already falling thereafter reaching a markedly low removal rate constant as long as plasma Ca decreased. When plasma Ca began to rise, sp. act. resumed a descending course. Our findings indicate that the initial hypercalemia depends on PTH withdrawal and results from a rapid flux into general extracellular fluid (ECF) of calcium coming from a compartment with higher sp. act., contained within the miscible pool, immediately followed by a reduction in calcium transfer from bone. These results suggest that acute PTH deficiency determines an outflow of calcium from bone cells and support the theory that PTH initiates its action by modifying their intracellular calcium content.
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PMID:Significance of early increase in stable and radioactive plasma calcium after parathyroidectomy in primary hyperparathyroidism. 11 82

A patient with metastatic islet cell carcinoma of the pancreas, recurrent peptic ulcer disease, and hypergastrinemia (Zollinger-Ellison syndrome) developed symptomatic hypercalcemia and renal insufficiency; she was treated with streptozotocin after parathyroidectomy failed to control her hypercalcemia. Shortly after somewhat less than the usual recommended dose of streptozotocin was administered, the serum calcium concentration fell to near normal with complete resolution of symptoms. Seven months after therapy, mild hypocalcemia, consistent with her degree of renal impairment was noted. However, mild hypercalcemia recurred 13 months after therapy. Shortly after streptozotocin therapy, the mean serum gastrin concentration fell to near normal with radiographic disappearance of the anastomotic ulcer. At 7 and 13 months after therapy, serum gastrin levels were normal. Streptozotocin therapy was accomplished without major complications; specifically, without a detrimental effect on the creatinine clearance. Thus, although hypercalcemia in patients with pancreatic islet cell tumors is often due to associated primary hyperparathyroidism, in some patients it may be due to secretion of a hypercalcemic substance from the tumor and may respond to streptozotocin. Similarly, hypergastrinemia in patients with islet cell tumors may also respond to streptozotocin.
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PMID:Pancreatic islet cell carcinoma with hypercalcemia and hypergastrinemia: response to streptozotocin. 13 70

Twelve parathyroid chief cell adenomas from patients with primary hyperparathyroidism were incubated in a tissue culture system in the presence of different calcium concentrations and for various time periods. The endocrine response of the tissue was examined electron microscopically and radioimmunologically. After incubation in a medium of low calcium concentration the parathyroid adenomas showed ultrastructural signs of stimulation with proliferation of the hormone-synthesizing organelles. The development of the ultrastructural response could first be observed after four hours and increased up to several days. Radioimmunologically, an increase of the hormone secretion could be demonstrated. Converse results were obtained after incubation of the tumor tissue under suppressive culture conditions. To check for de-novo synthesis of the hormone released the tissue was incubated in a 75Se-methionine-containing medium. This resulted in radioactivity of the secreted parathyroid hormone, indicating de novo synthesis in our culture system. The biological potency of the released hormone was demonstrated by comparison of the PTH out of the medium with the international human MRC standard using two different radioassays.
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PMID:Correlation of electron microscopic and secretory response of human parathyroid adenomas with different calcium concentrations in organ culture. 15 Jan 11

Hypercalcemia calls first for supportive measures, eg, adequate hydration, movement or mobilization of the patient to the greatest amount tolerated, and reevaluation of drugs being taken. When immediate lowering of the serum calcium level is not clinically mandatory, oral administration of furosemide, corticosteroid, or phosphorus should be considered. In acute emergencies, saline loading and parenteral furosemide therapy should be tried first, except in a patient with renal failure and congestive heart failure, in whom peritoneal dialysis or hemodialysis should be used instead. Calcitonin can be given for the first 12 to 24 hours to lower serum calcium concentration until a definitive management plan is formulated. Corticosteroid, if not contraindicated, should be started as soon as possible. In severe primary hyperparathyroidism with hypophosphatemia, phosphorus can be given intravenously until oral phosphate therapy can be established. Surgery, of course, should be performed as soon as possible. In most cases of neoplasia, mithramycin given according to a recommended schedule is safe and frequently effective. In desperate cases, additional use of prostaglandin synthesis inhibitors probably now is justified by empirical observations. All of these therapeutic measures are used only to stabilize electrolyte balance so that the primary cause of the hypercalcemia can be treated.
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PMID:Management of hypercalcemia. 15 84

A test was developed to diagnose various forms of hypercalciuria. A two-hour urine sample after an overnight fast and a four-hour urine sample after 1 g of calcium by mouth were tested for calcium, cyclic AMP and creatinine. The 24 patients with absorptive hypercalciuria had normocalcemia and normal fasting urinary calcium (less than 0.11 mg per milligram of urinary creatnine). Urinary calcium was high (greater than or equal to 0.2 mg per milligram of creatinine) after a calcium load. Of the 28 patients with primary hyperparathyroidism (resorptive hypercalciuria), 25 had hypercalcemia and 21 had high fasting urinary calcium. Urinary cyclic AMP, elevated in 30 per cent of fasting patients, was high (greater than 4.60 mu moles per gram of creatinine) in 82 per cent of cases after calcium load. Six patients with renal hypercalciuria had normocalcemia, high fasting urinary calcium, and high (greater than 6.86 mu moles per gram of creatinine) or high-normal fasting urinary cyclic AMP was normal. This simple test should facilitate the differentiation of various causes of hypercalciuria.
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PMID:A simple test for the diagnosis of absorptive, resorptive and renal hypercalciurias. 16 60

1. The metabolism of an intravenous pulse dose of double-isotope-labelled cholecalciferol has been studied in control subjects with widely differing states of vitamin D nutrition and in patients with primary disorders of parathyroid function. 2. The formation of labelled 1,25-dihydroxy-cholecalciferol [1,25-(OH)2D3] and labelled 24,25-dihydroxycholecalciferol [24,25-(OH)2D3] has been related to the prevailing concentrations in serum of 25-hydroxycholecalciferol [25-(OH)D3], immunoreactive parathyroid hormonel, calcium and orthophosphate (Pi). 3. In control subjects with relative vitamin D deficiency [serum 25-(OH)2D3 was related inversely to the serum 25-(OH)D3 and serum calcium, and directly to serum immunoreactive parathyroid hormone. No formation of 1,25-(OH)2D3 was detectable to form labelled 24,25(OH)2D3 preferentially. 4. No control subject produced significant amounts of both labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously. 5. All subjects with primary hyperparathyroidism produced significant amounts of labelled 1,25-(OH)2D3 and labelled 24,25-(OH)2D3 simultaneously; the renal turnover of 25-(OH)D3 was apparently greater than in nutritionally matched controls. Serum labelled 1,25-(OH)2D3 in this disease was not correlated with serum 25-(OH)D3, immunoreactive parathyroid hormone, calcium or Pi. Production of labelled 24,25-(OH)2D3 was inappropriately high for the prevailing nutritional state. 6. The indirectly estimated their concentration of 1,25-(OH)2D3 showed only a fourfold variation in control subjects (45-180 pmol/l), compatible with its having a regulated hormonal function. 7. The data suggest that the production of 1,25-(OH)2D3 from a pulse dose of cholecalciferol is normally regulated, directly or indirectly, by the parathyroid hormone.
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PMID:Vitamin D metabolism and parathyroid function in man. 16 31

Effects of parathyroidectomy on parathyroid function and calcium (Ca) metabolism were carefully evaluated in 6 patients with primary hyperparathyroidism without symptoms normally attributed to the disease and in 7 with bone disease or nephrolithiasis. Before parathyroidectomy, both groups of patients demonstrated evidence of the sequelae of parathyroid hormone (PTH) excess, since they presented one or more of the following features: low bone density by 125I-photon absorption, hypercalciuria (urinary Ca greater than 200 mg/day on an intake of 400 mg/day), negative Ca balance (absorbed Ca less than urinary Ca), elevated fasting urinary Ca greater than 0.2 mg/mg creatinine for a night-time sample after a 6-hour fast), and decreased renal function (creatinine clearance of less than 65 ml/min). Following parathyroidectomy, most of these deleterious effects were reversed commensurate with the return of immunoreactive serum PTH, serum Ca, and urinary cyclic AMP toward normal. These quantitative non-invasive techniques may be useful for the initial evaluation and follow-up of patients with asymptomatic primary hyperparathyroidism.
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PMID:Metabolic effects of parathyroidectomy in asymptomatic primary hyperparathyroidism. 17 69


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