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Query: UMLS:C0020437 (hypercalcemia)
 10,293 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Treatment with bromocriptine, 30-55 mg daily, in 13 acromegalics for 1-15 months, resulted in a 60% decrease in growth hormone secretion, as judged from the excretion of growth hormone in 24-h urine. Normal excretion was obtained in 10 patients, while 1 patient showed no response. The plasma growth hormone response to O-GTT was improved, but not normalized, in 4 of 7 patients treated for more than 6 months, and marked glucosuria disappeared in two diabetics. While the secretion of TSH, LH and FSH was unchanged, the prolactin secretion was inhibited. The urine excretion of free cortisol showed a 30% decrease, possibly due to a direct effect of bromocriptine on the ACTH-secretion. Hypercalcaemia was never seen, but the initial hypercalcuria showed a modest decrease without measurable changes in the creatinine clearance. The subjective relief during long-term treatment was marked in 10 of 11 patients and the dominating symptoms disappeared in 40-67%, whereas heal-pad thickness, enlarged sellae, and visual fields remained unchanged. No serious side effects were observed. Treatment with bromocriptine seems effective and should be considered as a remedy amongst others, in suitable cases of acromegaly.
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PMID:Long-term treatment of acromegaly with bromocriptine. 41 39

Male rats weighing 220-250 g were injected i.m. daily with 0.1 mg commercial human growth hormone for 3 days or 12 days. The serum concentration of total calcium phosphorus and alkaline phosphatase were significantly elevated for some days and returned to normal values at the end of the test period. The parathyroid glands, as studied by light and electron microscopical morphometry showed signs of reduced activity at the 4th day and also at the 13th day: a lowered nucleo-cytoplasmic ratio and a decrease of rough endoplasmic reticulum, of Golgi apparatus and of plasmalemmal tortuosity. The findings suggest a hypercalcemic effect of growth hormone involving peripheral organs of calcium metabolism, especially kidney and bone, and a secondary suppression of parathyroid glands by hypercalcemia.20
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PMID:Parathyroid function in rats treated with growth hormone. A morphometric study. 82 5

In two adult patients with congenital poikiloderma (Rothmund-Thomson syndrome) the following endocrine abnormalities were found: Patient 1, female, with short stature had primary amenorrhoea and did not develop secondary sexual characteristics. Despite lacking an oestrogen effect on the vaginal smear and the low urinary oestrogen excretion, basal LH and FSH and their response to LH-RH were normal. At age 36 a parathyroid adenoma was diagnosed because of increased immunoreactive plasma parathyroid hormone and persistent hypercalcaemia. After removal of the tumour the patient remained normocalcaemic. The result of growth hormone response to insulin in the intermediate range was suggestive of partial deficiency. In patient 2, male, hypergonadotrophic hypogonadism with small testes and high basal LH and FSH levels as well as increased LH and FSH response to LH-RH were found. Plasma testosterone was normal. Endocrine abnormalities in previously published cases are summarized.
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PMID:Hypogonadism and parathyroid adenoma in congenital poikiloderma (Rothmund-Thomson syndrome). 112 57

The growth hormone response to acute hypercalcemia was studied in 9 normal subjects. Growth hormone, calcium, glucose, phosphate and magnesium levels were determined at 30-min intervals during 4-h infusions. Infusions, performed in random order in the subjects, consisted of either normal saline at 3 ml/min for / h or 15 mg calcium/kg (calcium gluconate at 3 ml/min for 3 h followed by normal saline for the fourth hour. Significant hypercalcemia (P less than 0.05) was achieved within 60 min and maintained throughout the infusion. No change in calcium concentrations occurred during normal saline infusions, and phosphate, glucose and magnesium were unchanges in all studies. Growth hormone levels were significantly higher (P less than 0.05) at 60 min and all subsequent determinations during calcium infusion when compared to normal saline infusions. In 6 of the subjects, standard l-dopa provocative testing with an oral dose of 500 mg was preformed during normal saline and calcium infusions identical to those described above. Peak growth hormone responses did not differ significantly following l-dopa during saline or calcium infusion. These results suggest that an acute increase in circulating calcium promotes greater basal growth hormone secretion without a synergistic increase in hypothalamic mediated growth hormone release by l-dopa.
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PMID:The effect of acute hypercalcemia on growth hormone release in man. 112 88

The effect of excessive growth hormone (GH) on parathyroid function in rats was evaluated in order to determine whether the GH-induced increase in serum calcium (Ca) may be mediated via stimulation of parathyroid hormone (PTH) secretion. Rats receiving injections of bovine GH 2 mg daily for 4 weeks showed a progressive significant increase in both serum Ca and immunoreactive PTH (iPTH) after the second week. Rats receiving daily injections of rat GH, 0.25 mg daily for 3 weeks, followed by 0.5 mg daily for 3 additional weeks, showed a significant increase in serum iPTH during administration of the higher dose, and also a significantly increased parathyroid gland weight and PTH content. The concomitant increase in serum Ca and iPTH suggest that GH stimulates the parathyroid glands to increase PTH secretion, which in turn causes an increase in serum Ca. The parathyroid response increases with the increase in dose and duration of GH stimulus. The data suggest that the hypercalcemia often observed in acromegaly may be due, at least in part, to GH-induced excessive secretory activity of the parathyroid glands.
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PMID:The effect of growth hormone on parathyroid function in rats. 126 22

50 patients with autonomous growth hormone excess (48 with adult acromegaly and 2 with gigantism) were studied between 1966 to 1986 (2.38 pts/year). Characteristic clinical presentation, an increase in growth hormone (GH) uninhibited by glucose, and/or hyperphosphemia and hyperhydroxiprolinuria were present in all patients. No cases of hypercalcemia were recorded. Phosphemia was increased in 55.8%, alkaline phosphatases in 61.7%, calciuria in 26.9% and hydroxyprolinuria in 74.2% of the patients. Basal GH was over 5 ng/ml (89.9 DS +/- 170.9) in 42 pts, and in 37 was not suppressed after glucose administration, 38% had an increased (paradoxical response) and 62% a flat response (less than 50% change of basal values). TRH test was performed in 14 patients, 8 presented an increase in GH titer. Hyperprolactinemia was seen in 4 of 12 patients in whom this hormone was measured. The size of the sella turcica was increased in 93%, and although the larger sellar size correlated to higher levels of GH, correlation was not significant. 20% of the pts had rheumatological disease, 14% goiter, 12% cardiac disease, 26.5% had diastolic hypertension and 4% renal lithiasis (hypercalciuric pts). 38% had hyperglycemia with a diabetic glucose tolerance test and 18% had non-diabetic abnormal glucose tolerance test.
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PMID:[Active acromegaly and gigantism: some clinical characteristics of 50 patients]. 184 71

Calcium-phosphor metabolism was studied in patients with active acromegaly with or without osteoporosis, mean age 45.2 +/- 11.4 years and mean duration of the basic disease 5.52 +/- 3.6 years. No significant deviations and no direct relation with the high serum growth hormone and prolactin levels were found. The normal basic secretion of the calcitrophic hormones--parathyroid hormone and calcitonin and their normal response to the hypercalcemia after intravenous calcium load of the patients with and without osteoporosis reject their direct participation in the pathogenesis of osteopenia. The changed skeletal sensitivity to calcitrophic hormones closely connected with the patients' age and the duration of the basic disease in combination with many other factors probably plays a major role in the pathogenesis of osteopenia.
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PMID:[Calcium-phosphorus metabolism and calcitrophic hormones in patients with active acromegaly with and without osteoporosis]. 223 25

During the 13-year period 1970-1983 only 7 cases of multiple endocrine neoplasia type I (MEN I) were seen at Groote Schuur Hospital, suggesting that the associated gene is rare in this area. Only 1 of these patients was black. Endocrine associations were as follows: hyperparathyroidism--6 cases, pituitary hypersecretion--6 cases (3 each involving growth hormone and prolactin), and pancreatic hypersecretion--3 cases (2 of gastrinoma and 1 of insulinoma). The presenting features were predictably diverse and depended on the component which manifested first. There was little difficulty in reaching a diagnosis on routine investigation. All patients with hyperparathyroidism underwent a 3 1/2-gland parathyroidectomy as the first treatment procedure, normocalcaemia being achieved in 5 cases, but persistent hypercalcaemia in the 6th suggested a supernumerary gland. A pituitary adenoma was removed in 4 cases, but persistent prolactinaemia necessitated bromocriptine therapy in 3. Successful distal pancreatectomy was undertaken in a patient with insulinoma and a patient with gastrinoma, and a further patient with gastrinoma awaits surgery. The overall prognosis in cases of MEN I appears to depend on the most aggressive component, often the pancreatic lesion; our patients have run a surprisingly benign course with only 1 late death, from hypertensive heart disease.
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PMID:Multiple endocrine neoplasia type I. 286 78

Three hundred and eighteen cases of functioning and non-functioning pituitary adenoma were examined by histological, immunocytochemical and electronmicroscopic technique. Fourty-four of them (13.8%) showed evidence of calcospherites in the tumor tissues. A high incidence of calcospherite is found in functioning adenoma, but not in non-functioning adenoma. Calcification was seen most frequently in cases of prolactinoma (23), GH secreting (7), or GH + PRL tumor (2) and less in adrenocorticotropic hormone secreting adenoma (2) and follicle stimulating hormone secreting adenoma (1). Prolactin and growth hormone might be involved in the control of calcium metabolism. This is because, following adenomectomy in patients with prolactinoma or GH-secreting adenoma with hypercalcemia, there is normalization of serum PRL and GH with reduction in serum calcium. Calcospherite is produced in all of metastatic calcification, arterial calcification, dystrophic calcification and calcinosis. In cases of non-functioning adenoma however, the mechanism is believed to by dystrophic calcification.
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PMID:[Pituitary adenoma calcification]. 302 53

The effects of a dietary P deficiency on thyroid function, serum growth hormone, and growth parameters in 10 to 29-day-old broiler cockerels was determined. Chicks fed severely P-deficient diets (.05% or .10% available P) grew more slowly and ate less feed than controls fed .65% P. The deficiency was also accompanied by hypercalcemia, hypophosphatemia, and decreases in percent bone ash, fat-free tibial weight, and tibial length and width. Increases in the relative weights of kidneys, hearts, and pituitary glands (.05% P only) occurred as well. Most of these changes occurred to a lesser extent or not at all in pair-fed controls, showing that they resulted specifically from the P deficiency and were not simply a result of reductions in feed intake. Phosphorus deficiency also was accompanied by peripheral edema and hydropericardium. Relative thyroid weight was unaffected. Serum triiodothyronine was consistently lower in the P-deficient chicks, although effects were significant only in one experiment. Thyroxine levels tended to be low also, but not consistently so. Serum growth hormone in P-deficient chicks in both studies was consistently lower than that in pair-fed controls, but this was significant only when .10% but not .05% available P was fed. The findings suggest that serum levels of both thyroid hormone and growth hormone are altered by P deficiency, but the results were not clearly definitive.
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PMID:Thyroid function, growth hormone, and organ growth in broilers deficient in phosphorus. 345 19


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