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

A female patient with acromegaly, hypercalcemia, and Zollinger-Ellison syndrome was found to have a very high plasma concentration (average 2,300 pmol/liter; normal less than 50 pmol/liter) of growth hormone-releasing factor as measured by a radioimmunoassay to human pituitary growth hormone-releasing factor-1-44. The plasma concentration of growth hormone averaged 25 mIU/liter (normal less than 5 mIU/liter) and there was no rise following an intravenous 100 micrograms bolus of human pituitary growth hormone-releasing factor-1-44. Plasma growth hormone and growth hormone-releasing factor levels were unaffected by bromocriptine, insulin-induced hypoglycemia, and sleep. A long-acting somatostatin analogue lowered both the growth hormone-releasing factor and the growth hormone levels. Thyrotropin-releasing hormone stimulation and oral glucose tolerance tests produced significant increases in plasma growth hormone levels whereas the growth hormone-releasing factor level remained unchanged, suggesting that when normal somatotrophs are exposed to maximal growth hormone-releasing factor stimulation, thyrotropin-releasing hormone becomes a secretagogue of growth hormone from the pituitary. It is proposed that in the absence of a radioimmunoassay for growth hormone-releasing factor, a lack of growth hormone response to growth hormone-releasing factor in a patient with acromegaly is compatible with a source of ectopic growth hormone-releasing factor production.
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PMID:Growth hormone secretion dynamics in a patient with ectopic growth hormone-releasing factor production. 392 80

Juvenile-onset hypothyroidism was diagnosed in an adult mixed-breed dog examined because of quadraparesis. Unusual clinical signs attributable to juvenile-onset or congenital hypothyroidism included disproportionate dwarfism; enlarged, protruding tongue; mental dullness; and retention of a "puppy" coat, which was soft and fluffy, without guard hairs. Radiography of the vertebral column and long bones revealed multiple areas of delayed epiphyseal closure and epiphyseal dysgenesis. Myelography demonstrated several intervertebral disk protrusions in the cervical and lumbar regions. Hypothyroidism was confirmed on the basis of a low basal serum thyroxine concentration that failed to increase after the administration of thyroid stimulating hormone. Other laboratory abnormalities included nonregenerative, normocytic, normochromic anemia; mild hypercalcemia; and an impaired growth hormone (GH) secretory response after xylazine administration. At necropsy, the thyroid gland was small and weighed only 0.2g. Microscopic examination of the thyroid gland revealed a loss of glandular tissue, which was replaced by adipose tissue along its periphery. Gross or microscopic abnormalities were not noted in the pituitary gland, and immunohistochemical staining of the pituitary gland revealed a normal number of GH-containing acidophils. This suggests that primary hypothyroidism may result in an impaired secretion of growth hormone, and that pituitary dwarfism or GH deficiency may be difficult to differentiate from hypothyroid dwarfism on the basis of provocative GH testing alone.
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PMID:Juvenile-onset hypothyroidism in a dog. 405 23

A circadian variation in serum calcium, albumin and PTH concentration in normal subjects has been demonstrated. The levels of the three blood constituents were remarkably constant during the day, but striking night and early morning changes occurred. Serum calcium levels were highest at 8:00 p.m. and reached a nadir between 2:00 and 4:00 a.m. Serum albumin levels were parallel to those of serum calcium. PTH levels began to rise after 8:00 p.m., reached the highest levels between 2:00 and 4:00 a.m., and fell to baseline values by 8:00 a.m. The nocturnal fall in serum calcium levels appears to be secondary to dilution of serum proteins by increasing blood volume. The nocturnal rise in PTH levels appears to be independent of serum calcium levels within the normal range but it can be abolished by induced hypercalcemia. Serum phosphate levels were lowest between 8:00 a.m. and 10:00 a.m. and highest between 2:00 a.m. and 4:00 a.m. The data presented suggest that circadian changes in serum phosphate levels are not mediated in toto by parathyroid hormone but they are exaggerated when the secretion of this hormone is inhibited. They are independent of growth hormone levels and activity but they are greatly modified during a prolonged fast.
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PMID:Circadian rhythm in serum parathyroid hormone concentration in human subjects: correlation with serum calcium, phosphate, albumin, and growth hormone levels. 505 63

The effect of mild hypercalcaemia on the growth hormone (GH), C-peptide and glucose responses to arginine infusion in patients with insulin-dependent idiopathic diabetes mellitus (ID) was compared with that observed in patients whose diabetes was secondary to idiopathic haemochromatosis (IH) and chronic pancreatitis (CP). The summated GH responses to arginine infusion alone were similar in all three groups. Mild hypercalcaemia significantly diminished the GH response to arginine in patients with secondary diabetes, but not in those with ID. As the blood glucose and C-peptide responses were similar in the presence of a normal or raised serum calcium, the differences in GH response could not be ascribed to changes in blood glucose levels or to alterations in endogenous insulin release. For reasons as yet unknown, hypercalcaemia appears to have more of a stabilizing effect on the pituitary somatotrophic granules of those with secondary diabetes than in those with ID.
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PMID:The effect of acute hypercalcaemia on arginine induced growth hormone release in diabetic man. 653 33

The authors investigated in 19 healthy women changes in the plasma levels of cortisol and growth hormone during acute hypercalcaemia induced by a load of 8.9 mg Ca2+/kg body weight, administered as intravenous infusion and the effect of hypercalcaemia on the adrenocortical and somatotrophic secretory reserve assessed by the test with insulin hypoglycaemia. Hypercalcaemia causes a rise of the basal cortisol plasma level starting at the 90th minute from the onset of the infusion when the calcium level reaches values of 2.99 mmol/l. The adrenocortical secretory reserve is, however, significantly reduced by hypercalcaemia. Hypercalcaemia does not affect growth levels nor the somatotrophic secretory reserve.
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PMID:Effect of hypercalcaemia on adrenocortical and growth hormone secretion. 668 86

The demands of growth are known to exacerbate the effect of phosphorus deprivation (PD). We examined whether changes associated with PD could be prevented in young rats in which growth and growth hormone (GH) were eliminated by hypophysectomy (HPX) and whether PD in normal intact rats (INT) was associated with increased secretion of GH. INT or thyroxine- and ACTH-replaced HPX rats were fed one of the three diets: 0.31% P (NP); 0.027% P (LP), and 0.31% P, pair-fed with LP-mates (NP-PF). The results indicate that HPX did not qualitatively alter several physiologic responses to PD: (a) serum and urinary phosphorus (P) decreased and urinary calcium (Ca) increased; (b) net intestinal Ca retention fell and duodenal sac uptake of 45Ca rose; and (c) external P balance was restored and duodenal sac uptake of 32P-phosphate increased. Only the hypercalcemia seen in INT, LP rats was prevented by HPX. In INT rats serum immunoassayable GH levels, measured in single samples, were not different between different dietary groups while pituitary bioassayable GH was reduced in both LP and NP-PF rats when compared to the NP rats. Thus, except for hypercalcemia, the physiologic responses associated with PD are not prevented by the elimination of growth and GH, and the development of these responses in INT rats was not associated with a consistent or specific alteration in GH secretion.
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PMID:Role of growth hormone in experimental phosphorus deprivation in the rat. 677 27

Normal calcium regulation depends on the complex interactions of several systems. The specific calcium regulating hormones, parathyroid hormone, calcitriol and calcitonin, affect calcium and phosphorus concentration and supply by acting on bone, kidney and intestine. The changing concentration and supply of ions not only regulate these hormones, but may also influence the function of the target organs, particularly bone, directly. Systemic hormones such as growth hormone and somatomedins, glucocorticoids, sex hormones and thyroid hormone are essential for skeletal growth and development and interact with calcium regulators. Prostaglandins and osteoclast activating factor may be important in local regulation of bone. Disorders of calcium regulation are common, particularly hypercalcemia; however, measurements of parathyroid hormone are not yet ideal and the factors which produce hypercalcemia in malignancy have not been identified. The role of calcium regulating hormones in the pathogenesis and treatment of osteoporosis is controversial. Solution to these problems may be dependent on the identification of additional factors which influence mineral metabolism.
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PMID:Calcium regulation. 703 24

X-linked hypophosphatemia, currently one of the most prevalent varieties of familiar rickets, is attributed to renal phosphate wasting secondary to a gene defect localized to X p22 chromosomal region. The proximal tubular phosphate reabsorption defect is associated with blunted 1,25-dihydroxyvitamin D synthesis to hypophosphatemia or parathyroid hormone administration. It is characterized clinically by hypophosphatemia, growth retardation, and rickets especially in male patients. As the affected patients mature, pseudofractures, skeletal deformities, osteomalacic bone pain, progressive ankylosis, and dental caries occur, which may be alleviated and even prevented with adequate medical therapy. Long term treatment combines phosphate supplementation with calcitriol, augmented occasionally by diuretics. Hypercalcemia, hyperparathyroidism, and nephrocalcinosis are potential complications which require careful monitoring and continued investigations. The use of recombinant human growth hormone to augment renal tubular reabsorption of phosphate and to promote linear growth remains to be examined in well controlled, clinical trials.
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PMID:X-linked hypophosphatemia: molecular biology and treatment controversies. 804

During adolescence, there are marked changes in the metabolism of calcium and phosphorus and a dramatic increase in the rate of bone mineralization under the influence of the sex hormones, growth hormone, and insulin-like growth factor-1. More than 50% of adult bone mass is accumulated during puberty; failure to achieve maximum bone mineralization at this time may lead to osteopenia and its complications in later adulthood. This article discusses the causes, evaluation, and management of adolescents with hypocalcemia, hypercalcemia, and disorders of bone mineralization.
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PMID:Disorders of calcium and phosphorus metabolism in adolescents. 824 48

The changes in normal endocrine physiology which accompany pregnancy result in changes in normal ranges of hormone levels and in specific changes in the course and management of endocrine diseases. This review presents information about the various endocrine diseases and their management in pregnant adolescents. Normal pituitary function during pregnancy is described as is the effect of pregnancy on pituitary tumors such as microadenomas and prolactinomas. The effects of bromocriptine therapy in cases where tumor enlargement occurs during pregnancy are tabulated. Methods of distinguishing placental growth hormone secretion and pituitary growth hormone secretion in patients with acromegaly are presented (with the note that acromegalic patients rarely become pregnant). TSH-secreting, gonadotropin, and nonsecreting tumors are rare in this age group, and there is no evidence that they enlarge during pregnancy. The discussion of the pituitary covers chronic hypopituitarism, Sheehan's Syndrome, lymphocytic hypophysitis, and diabetes insipidus. After reviewing normal changes in thyroid physiology during pregnancy, hyperthyroidism (usually due to Graves' disease), thyroid storm, and hypothyroidism are considered. The adrenal is the next subject, with a brief description of normal changes during pregnancy followed by comments on Cushing's Syndrome, adrenal insufficiency, congenital adrenal hyperplasia, and primary hyperaldosteronism. The symptoms, diagnosis, and treatment of pheochromocytomas, which are uncommon during pregnancy but are associated with high fetal and maternal mortality, are the next topics. After a review of changes in calcium metabolism during pregnancy and hypercalcemia, this report ends with a consideration of diabetes mellitus which includes alterations in maternal carbohydrate metabolism during pregnancy, effects of diabetes on the fetus, and management of insulin-dependent diabetes mellitus during pregnancy (the most likely type to be present in adolescents).
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PMID:Endocrine problems of adolescent pregnancy. 824 53


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