Gene/Protein Disease Symptom Drug Enzyme Compound
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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

A 32-year-old woman developed myalgia, fever, consciousness disturbance, mental disorder, pyramidal tract signs and meningeal irritation signs at about 2 months after a normal labor. Laboratory examination showed hypopituitarism (decreased ACTH, TSH), renal dysfunction and hypercalcemia. A variety of antibiotics, acyclovir and gamma-globulin failed to improve her symptoms. A diagnosis of Chlamydia trachomatis infection was considered from the elevated antibody titers. In this case, minocycline was very effective. Rarely Chlamydia trachomatis infection involved general organs, including the central nervous system. It was interesting that she had endocrine disorders. We must take a look for Chlamydia trachomatis infection because this infection infrequently involves general organs, including the central nervous system and minocycline is very effective for this infection.
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PMID:[Chlamydia trachomatis infection with symptoms and signs of the central nervous system damage--a case report]. 142 47

Congenital hypothyroid dwarfism was diagnosed in a family of Giant Schnauzers. Three female and two male puppies from different litters were evaluated for dwarfism, lethargy, somnolence, gait abnormalities, and constipation. On physical examination, disproportionate dwarfism (n = 5), macroglossia (n = 3), hypothermia (n = 3), delayed dental eruption (n = 3), ataxia (n = 2), and abdominal distension (n = 1) were identified. Results of initial laboratory tests showed anemia (n = 4), hypercholesterolemia (n = 4), hypercalcemia (n = 2), and transudative abdominal effusion (n = 1). Radiographic skeletal surveys disclosed epiphyseal dysgenesis and delayed skeletal maturation (n = 5). A diagnosis of hypothyroidism was established on the basis of low basal serum thyroxine concentrations that failed to increase following the administration of TSH (n = 5) and markedly reduced to absent thyroid image when evaluated with gamma camera imaging of the thyroid gland (n = 4). In the two dogs that were most thoroughly evaluated, the results of thyroid histology, prolonged TSH testing, and repeat thyroid imaging, after three daily injections of TSH, were all consistent with secondary or tertiary, rather than primary, hypothyroidism. When TSH was administered over a period of 3 consecutive days (5 IU/day, subcutaneously), serum thyroid hormone response became normal and resulted in a normal thyroid image in the two dogs re-evaluated with gamma camera imaging. Daily treatment with oral levothyroxine (20 micrograms/kg) resulted in complete remission in puppies (n = 4) treated prior to 4 months of age. The other puppy failed to attain normal breed standards for height.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Congenital hypothyroid dwarfism in a family of giant schnauzers. 174 85

In chronic hypercalcemia, basal TSH has been found to be low, with normal serum circulating concentrations of T3 and T4. This observation suggested a potentiation by hypercalcemia of the thyroid secretory response to TSH. The present study was undertaken to assess the possible influence of hypercalcemia on the T3 secretory response to TSH. Since T3 secretion was studied after stimulation of endogenous TSH by TRH, it was first necessary to find a protocol enabling us to study the effect of calcium on T3 release without affecting TSH secretion. Eighteen subjects underwent two TRH tests, with and without simultaneous calcium infusion, at 2-week interval and in a randomized order. In group A (five subjects) calcium infusion started 1 min after TRH, in group B (five subjects) 10 min after TRH, and in group C (eight subjects) 20 min after TRH. In groups A and B, TSH secretion was markedly blunted by hypercalcemia. In contrast, when calcium infusion was started 20 min after TRH (group C), the TSH secretion profile was no longer different from that in the control study. However, in this situation the increments of T3 and free T3 120 and 180 min after TRH were significantly higher when the subjects were rendered hypercalcemic than in the control study. These findings suggest that calcium might act at two different levels, to enhance the thyroid secretory response to TSH and decrease TSH secretion by acting directly on the pituitary gland. Both effects would produce the association of low serum TSH and normal levels of T3 and T4 observed in chronic hypercalcemia.
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PMID:Effect of acute hypercalcemia on thyrotropin (TSH) and triiodothyronine responses to TSH-releasing hormone in man. 211 41

TSH serum levels and thyroid function in 32 patients with primary hyperparathyroidism and hypercalcemia were compared to those of 30 age and sex-matched normal subjects. Serum T3 and T4 concentrations in hyperparathyroidism were not different from normal. However, basal serum TSH concentrations measured with an ultrasensitive immunoradiometric assay were significantly lower than normal (1.09 +/- 0.49 vs 2.06 +/- 0.85 mU/l, p less than 0.001). In hyperparathyroidism, TSH, but not T4 or T3, was negatively correlated with serum calcium, not with iPTH. The increase in TSH (delta TSH) 30 min after the iv injection of TRH was also significantly blunted in patients with primary hyperparathyroidism; delta TSH was highly correlated with basal TSH in hypercalcemic patients. The basal TSH concentration was higher and no longer different from normal (1.70 +/- 1.2 mU/l) 2 to 12 months after removal of the parathyroid adenoma, when serum calcium was normalized, whereas T3 and T4 did not change. A low basal TSH with normal T4 and low T3 was found in 13 patients with hypercalcemia of malignancy. In these patients, TSH increased after treatment of hypercalcemia with 3-amino-l,hydroxypropylidene-1, 1-bisphosphonate, whereas T4 did not change. The results suggest that the set point of pituitary thyroid feedback control could be decreased in chronic hypercalcemia and that hypercalcemia could render the thyroid more sensitive to TSH.
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PMID:Low basal thyrotropin with normal thyroid function in primary hyperparathyroidism. 251 13

The mammalian thyroid gland is composed of 2 distinct endocrine cell populations concerned with the synthesis of 2 different classes of hormones. Follicular cells secrete the metabolically active iodothyronines whereas the C-(parafollicular) cells are concerned with the production of calcitonin, a hormone that influences blood levels of calcium and phosphorus, and bone cell metabolism. The synthesis of metabolic thyroid hormones is different than in other endocrine glands because the final assembly of hormone occurs within the follicular lumen. This extracellular synthesis of thyroid hormones is made possible by thyroglobulin, a glycoprotein synthesized by follicular cells. The secretion of thyroid hormones under the influence of pituitary thyrotrophin (TSH) from stores in the luminal colloid is initiated by elongation of microvilli and formation of pseudopods. FD&C Red No. 3 is a tetraiodinated derivative of fluorescein which in lifetime studies increases the incidence of thyroid follicular cell adenomas in male Sprague-Dawley rats. The striking changes in circulating levels of thyroid hormones and morphologic evidence of follicular cell stimulation are the result of alterations in the peripheral metabolism of thyroxine. An inhibition by FD&C Red No. 3 of 5'-deiodinase in the liver and kidney would explain the lower serum triiodothyronine (T3) levels. The pituitary, sensing the lowered circulating levels of T3, increased the secretion of thyroid stimulating hormone which resulted in the morphologic evidence of follicular cell stimulation in the long-term studies. Other xenobiotics increase the incidence of thyroid tumors in rodents by a direct effect on the thyroid gland to disrupt 1 of 3 or more possible steps in the biosynthesis of thyroid hormones. Physiologic perturbations alone, such as iodine deficiency or partial thyroidectomy, can disrupt thyroid hormone economy in rodents and, if sustained, increase the development of thyroid tumors. The wide variety of drugs, chemicals, and physiologic perturbations which increase thyroid tumor development appear to act through a secondary (indirect) mechanism to promote tumor development by causing a long-standing hypersecretion of thyroid stimulating hormone. Nodular and/or diffuse hyperplasia of C-cells occurs with advancing age in many strains of laboratory rats and in response to long-term hypercalcemia in certain animal species and human beings. Focal or diffuse hyperplasia often precedes the development of C-cell neoplasms. Radiation and the feeding of diets high in vitamin D resulting in hypercalcemia have been reported to increase the incidence of C-cell tumors in rats.
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PMID:The effects of xenobiotics on the structure and function of thyroid follicular and C-cells. 267 79

Cysteamine depletes pituitary and plasma prolactin in rats. It acts through a nondopaminergic mechanism to alter both immunoactive and bioactive prolactin. The effect of cysteamine on prolactin secretion is reported in normal men. Six normal subjects received a control thyrotropin-releasing hormone (TRH) test at 0900 using 200 micrograms TRH intravenously; serum prolactin and TSH were measured at -10, 0, 10, 20, 30, 60, and 90 min after administration of TRH. Serum calcium and parathyroid hormones levels were measured at -10 min. Seven or more days later, they received cysteamine hydrochloride 15 mg/kg body weight orally every 6 hours for 5 doses. One hour after the last dose, the TRH test was repeated. Peak serum prolactin levels following TRH, prolactin levels at the 10-min time point, and total area from 0 to 30 min under the prolactin secretory curve were significantly decreased by cysteamine administration. TSH levels were unchanged. Serum calcium levels were significantly decreased by cysteamine administration, but parathyroid hormone levels were unchanged. It was concluded that cysteamine reduced TRH-stimulated prolactin secretion. Cysteamine also decreases serum calcium levels and suppresses the anticipated rise in serum parathyroid hormone levels. These effects on serum calcium and parathyroid hormone are similar to those previously shown for WR2721, another sulfhydryl compound. Cysteamine should be further considered as an alternative drug in the treatment of hyperprolactinemia and as a therapeutic agent for hypercalcemia.
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PMID:Cysteamine decreases prolactin responsiveness to thyrotropin-releasing hormone in normal men. 307 53

Calcitonin gene-related peptide (CGRP) in the thyroid has a dual localization to nerve fibers around blood vessels and follicles and to parafollicular (C) cells. CGRP was found to coexist with substance P (SP) in most of the nerve fibers; a few CGRP fibers seemed to lack SP, and a few SP fibers seemed to be devoid of CGRP. In the C cells, CGRP coexisted with calcitonin (CT). Cervical vagotomy (extirpation of the nodose ganglion) eliminated approximately 50% of the CGRP/SP fibers in the thyroid without any overt influence on CGRP/CT in the C cells. Removal of the superior cervical ganglion or chemical sympathectomy (6-hydroxydopamine treatment) affected neither thyroid CGRP/SP nerve fibers nor CGRP/CT-storing C cells. CGRP nerve cell bodies were numerous in the jugular-nodose ganglionic complex (notably in the jugular portion); in many of them, CGRP coexisted with SP. A few scattered CGRP nerve cell bodies also occurred in the laryngeal ganglion, whereas none was found in the thyroid ganglion. Hypercalcemia evoked by vitamin D2 treatment, which is known to degranulate thyroid C cells, reduced the thyroid content of both CGRP and CT. As tested in mice in vivo, CGRP and SP alone or together had no effect on basal or TSH- or isoprenaline-induced thyroid hormone secretion. Vasoactive intestinal peptide-stimulated iodothyronine release, on the other hand, was enhanced by CGRP, but not by SP. SP had no effect on combined vasoactive intestinal peptide-CGRP-stimulated iodothyronine release. These findings suggest that CGRP participates in the control of thyroid hormone secretion and that, like CT, CGRP in the C cells is under control of the serum calcium level.
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PMID:Calcitonin gene-related peptide in thyroid nerve fibers and C cells: effects on thyroid hormone secretion and response to hypercalcemia. 309 6

The effect of 1,25-dihydroxy-vitamin D3 (1,25-(OH)2-D3) on the TRH induced TSH release was investigated. Wistar rats were injected with 1,25-(OH)2-D3 (0.05 microgram/kg/day) for three days, and TRH was injected iv on the third day. Blood was drawn every 10 min during the following 40 min, and TSH was determined. The TSH release was significantly higher in rats treated with 1,25-(OH)2-D3 than in controls. The rats treated with 1,25-(OH)2-D3 were hypercalcaemic and thus, in order to find out if the effect was mediated through hypercalcaemia rats treated as above, were infused with EDTA (30 mg/kg/100 min) starting 60 min before the TRH test. This treatment made the rats normocalcaemic, and the significant increase in the TSH release was still seen in the 1,25-(OH)2-D3 treated rats as compared to controls. The results thus indicate that 1,25-(OH)2-D3 enhances the TRH induced TSH release and that the effect is not mediated through an increase in the serum calcium concentration at the time of the TRH test. In order to find out if the effect could be mediated by changes in intracellular calcium the rats were treated with the calcium antagonist verapamil (25 mg/kg/day) and the adrenergic blocker propranolol (5 mg/kg/day) alone or together with 1,25-(OH)2-D3. In rats treated with verapamil or propranolol alone or 1,25-(OH)2-D3 + propranolol, no effect was observed on the TRH induced TSH release. Verapamil + 1,25-(OH)2-D3 significantly increased the TSH release as compared to both controls and rats treated with 1,25-(OH)2-D3 alone.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The effect of 1,25-dihydroxy-cholecalciferol on the TRH induced TSH release in rats. 310 41

Many studies have shown that in normal man salmon and porcine CT administration in bolus inhibits the release of TSH, LH, GH, and glucose- or arginine-induced insulin secretion. In the present study we investigated the effects of human synthetic calcitonin (hCT) on glucose- or arginine-induced insulin secretion in man. Twenty-two subjects were submitted to i.v. administration of hCT during glucose or arginine test. In our opinion, the most interesting results are those observed with arginine plus hCT at two different dosages (25 micrograms and 12.5 micrograms infused in 30 min). In fact arginine plus hCT (25 micrograms in 30 min) administration induced a significant increase of glycemia at 5, 10 and 20 min (p less than 0.01) and at 30 min (p less than 0.05) and a significant decrease of IRI at 5, 10, 20 and 30 min (p less than 0.001) and at 45 min (p less than 0.005). The highest plasma CT levels were observed at 15 and 30 min (490 and 540 pg X ml-1). Arginine plus hCT (12.5 micrograms in 30 min) infusion induced a similar significant increase in plasma glucose at 10, and 20 min (p less than 0.05) and at 30 min (p less than 0.01) and a significant decrease of plasma IRI at 10 min (p less than 0.05) at 20 min and 30 min (p less than 0.005). The highest plasma CT levels were reached at 20 min and 30 min (250 and 270 pg X ml-1, respectively). Our results clearly demonstrate that physiologic doses of hCT are able to inhibit arginine induced insulin secretion in normal man. Since insulin induces hypercalcemia and food ingestion increases both insulin and CT, one could hypothesize that CT inhibits insulin secretion thus controlling post-prandial hypercalcemia by its osteotrophic effect and by its action upon calcium redistributed within the cells.
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PMID:Effect of human calcitonin (hCT) on glucose- and arginine-stimulated insulin secretion. 352 Nov 78


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