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)

Two patients with hypercalcemia and hyperthyroidism had elevated levels of parathyroid hormone (PTH). When the patients were made euthyroid with appropriate medical therapy, both the levels of PTH and calcium returned to normal. Since thyroid hormone can increase tissue responsiveness to catecholamines, and since catecholamines can stimulate PTH secretion, we postulate that the elevated levels of PTH were secondary to thyrotoxicosis. In patients with coexisting hyperthyroidism and hyperparathyroidism, primary hyperparathyroidism should only be diagnosed when the patient is eumetabolic.
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PMID:Thyrotoxicosis, hypercalcemia, and secondary hyperparathyroidism. 44 69

Malignant disease and primary hyperparathyroidism are the most common causes of hypercalcemia, but there are many minor causes. Mechanical or humoral factors, or both, may underlie the increase in bone resorption. Parathyroid hormone (PTH) is a major mediator of bone resorption, but many other humoral agents have the same effect, eg, prostaglandin, osteoclast-activating factor, and thyroid hormone. Serial determination of total calcium concentration is the most important laboratory test in hypercalcemia. Other useful tests include the determination of serum and urinary phosphorus concentration, chloride/phosphate ratio, urinary cyclic adenosine 3',5'-monophosphate (cAMP) level; carboxyl-terminal PTH assay; corticosteroid challenge; and appropriate radiologic studies. Nephrogenous cAMP and urinary prostaglandin determinations are research tools that hold great promise in the future. Differentiation between PTH- and non-PTH-mediated hypercalcemia determines subsequent steps in diagnosis and treatment.
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PMID:Differential diagnosis of hypercalcemia: a mechanistic approach. 48 78

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

A patient with thyrotoxicosis presented with weight loss and hypercalcaemia, leading to an erroneous diagnosis of occult malignant disease. Intercurrent illness and drug treatment of hypercalcaemia in this patient caused a depression of circulating thyroid hormone levels, leading to a delay in diagnosis. Radionuclide studies of thyroid function, in contrast, consistently suggested a thyrotoxic state. It is suggested that in this situation, radionuclide studies may give a more accurate assessment of thyroid status than biochemical tests, which may be difficult to interpret in the presence of non-thyroidal illness.
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PMID:'Apathetic' thyrotoxicosis presenting with hypercalcaemia and spurious normalization of serum thyroid hormone levels. 244 2

It has been generally believed that reverse triiodothyronine (reverse T3, rT3) is biologically inactive. Nevertheless the serum rT3 level is very high in fetal life, when the serum calcium level is higher than in the maternal. For this hypercalcemia in fetal life, there is no convincing evidence that any major calcium regulating hormone is responsible. And the assumption that rT3 may be concerned in active transport of calcium at placenta could be suggested. In this study nuclear protein was isolated from human placenta by extraction with 0.4M KCl buffer and binding studies utilizing radioactive rT3 were carried out. Scatchard analysis presented a curvilinear pattern, suggesting two classes of receptors: One with a association constant (Ka) of 1.14 X 10(8) M-1 and a limited capacity (Bmax) of 32.0 X 10(-15) mol/100 micrograms DNA and the other with Ka = 4.34 X 10(6) and Bmax = 454 X 10(-15). Its relative affinities for several thyroid hormone analogues were calculated. If the affinity for rT3 was assigned l, that for triiodothyronine would be 1/40, thyroxine: 1/63, Triiodothyroacetic acid: 1/18. Sulfhydryl agents affecting these binding characteristics were also studied. The Ka was not substantially changed but the Bmax was notably decreased by dithiothreitol (43%) and 2-mercaptoethanol (26%). In liver nuclei, the binding characteristics of rT3 receptor were analyzed for comparison. In this case only a single class of low affinity-high capacity rT3 binding site with a Ka of 6.69 X 10(6) was detected, a finding which was apparently different from those in placenta.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Nuclear binding sites for reverse triiodothyronine in human placenta. 262 41

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

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 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

Mineral metabolism and bone histomorphometric status were evaluated in 31 hyperthyroid patients (HT) without clinical or radiological bone disease, both before and after treatment of hyperthyroidism. Blood and urine biochemical data were compared with those obtained in sex and age-matched controls. Iliac bone biopsies were available from 12 untreated HT and from 6 of them after treatment for analysis of trabecular bone. Mean plasma calcium was increased in HT but true hypercalcemia was seen in only one case and mean plasma immunoreactive parathormone (iPTH) was normal. Urine calcium excretion was markedly increased, especially in the fasting state. Biochemical parameters decreased after treatment, except for serum alkaline phosphatase and iPTH that, respectively, remained high and increased. Untreated state was characterized by an hyperremodelling state with enhanced activities of bone formation and bone resorption. Bone mineralization was normal. The mineral and bone changes were related to serum thyroid hormone levels. After treatment, the extent of formation surfaces still increased. The fact that, even though calcium metabolism abnormalities were corrected, active resorption surfaces did not change, suggests that trabecular osteoclastic resorption is not an important cause of mobilization of bone calcium to extracellular fluids in HT.
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PMID:Effect of thyrotoxicosis and its treatment on mineral and bone metabolism. 357 53

Although patients with primary hyperparathyroidism (1 degree HPT) were euthyroid, we measured serum thyroid hormone levels in 16 patients with 1 degree HPT together with 17 patients with hypercalcemia due to malignant diseases (HCM). In patients with 1 degree HPT, serum levels of T3, T4 and T3U were within normal range, but serum rT3 (reverse T3) levels (205 +/- 37 pg/ml, mean +/- SD) were significantly decreased as compared with those in normal controls (276 +/- 44 pg/ml, P less than 0.01). A significant inverse correlation was observed between the serum levels of rT3 and parathyroid hormone (PTH) (r = 0.54, P less than 0.05). After parathyroidectomy, serum rT3 levels were significantly elevated (240 +/- 56 pg/ml) compared to preoperative levels (P less than 0.01). Low levels of serum rT3 seemed to be attributed to the high levels of serum PTH. On the other hand, serum levels of T3 and T4 were low and serum rT3 levels were high in patients with HCM. Low serum rT3 allows for the differentiation of patients with 1 degree HPT from those with HCM.
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PMID:Low serum reverse T3 levels in patients with primary hyperparathyroidism. 362 22


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