Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Paget's disease of bone occurs in elderly people and resembles no other disease. The most frequent diagnostic errors are made when it is discovered in young adults, especially after an injury. Forms with osteolysis of the lower limbs are the most misleading, and it is better to avoid biopsies in such cases, as they may be followed by fractures. In geriatric pathology the failure to recognize that cerebral, spinal cord and cardiac manifestations are due to a specific vascular disorder of pagetic origin is a serious error as it deprives the patient of calcitonin which is the only effective therapy. Errors in the interpretation of laboratory results are easily avoided if a low hydroxyproline diet is prescribed during the week that precedes the tests. The biochemical activity should be correlated with the pagetic bone mass. Histology may wrongly suggest primary hyperparathyroidism, but patients with Paget's disease have no hypercalcaemia unless they are bedridden. Treatment relies on calcitonin and/or disodium etidronate (EHDP). Only 50% of the patients require this treatment the indications of which must carefully be weighed. EHDP may have adverse effects on bones, including fractures and pseudosarcomatous osteolysis, notably when it is given in high doses or for limited and/or osteolytic lesions. Pre and post-operative calcitonin therapy is recommended in patients undergoing surgery.
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PMID:[Paget's disease: errors to be avoided]. 249 20

Serum levels of ionized calcium, 25-hydroxyvitamin D (25OHD), and 1,25-dihydroxyvitamin D[1,25-(OH)2D], intact immunoreactive PTH and calcitonin were measured in the laboratory rabbit to evaluate the role of these calciotropic hormones in calcium homeostasis in this species. We confirm the finding of previous researchers that the resting serum ionized and total calcium concentrations are elevated in rabbits compared to those in other species (ionized calcium, 1.70 +/- 0.13 mmol/liter; total calcium, 3.23 +/- 0.25 mmol/liter). The serum calcium concentrations in animals maintained on a breeding farm or in the laboratory did not differ significantly despite nearly 3-fold higher levels of vitamin D in the feed at the farm, which were associated with 3- to 4-fold higher concentrations of 25OHD and 1,25-(OH)2D. Baseline intact PTH levels for the farm and laboratory populations also did not differ significantly and averaged 69.4 +/- 43.6 human pgeq/ml (laboratory animals, 52.1 +/- 28.4; breeding farm animals, 86.0 +/- 49.5 human pgeq/ml). Infusions of calcium gluconate or EDTA for 15 min into anesthetized animals in the laboratory induced dramatic reciprocal changes in the measured circulating levels of PTH. Calcium gluconate infusions (190-300 nmol/g BW) produced 50-85% increases in serum ionized calcium, which were accompanied by 74-91% decreases in PTH levels (from 68.8 +/- 29.2 at time zero to 10.1 +/- 3.1 human pgeq/ml at 15 min) as well as 7-fold increases in calcitonin levels. EDTA infusions (14-120 nmol/g BW) reduced serum ionized calcium by 9-49%, while PTH levels increased by 68-560% (from 61.4 +/- 32.3 at time zero to a maximum of 138 +/- 48.6 human pgeq/ml at 3 min). During the EDTA infusion, the PTH response was variable after 3 min despite further decreases in ionized Ca2+, indicating either exhaustion of PTH reserves or regulation of the secretory response by some parameter other than ionized calcium concentration per se. Thus, the rabbit appears to defend its serum ionized calcium concentration against hypo- and hypercalcemia by rapid changes in PTH secretion and calcitonin. Unlike other mammalian species, however, the changes in PTH occur at relatively high levels of calcium, suggesting that the parathyroid gland of the rabbit is reset to respond to changes in ionized Ca2+ within the physiological range in that species. The relative insensitivity of the rabbit parathyroid to extracellular calcium is analogous to that observed in primary hyperparathyroidism and may be a useful model to study the control of normal and abnormal PTH secretion.
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PMID:Regulation of calciotropic hormones in vivo in the New Zealand white rabbit. 250 95

A 57-year-old female was admitted to our hospital with general lassitude, loss of appetite, nausea, upper abdominal pain, thirst, polydipsia and polyuria. On admission, she had an asymmetrical pear-shaped tumor in the right supraclavicular region and severe hypercalcemia. Plasma C-PTH was elevated to 22.72ng/ml. Plasma calcitonin was also elevated to 336 pg/ml. She died of respiratory and cardiac failure of two weeks after admission without any positive response to the treatment, including hemodialysis. Pathohistologically, the tumor was a parathyroid adenoma. The concentrations of C-PTH, intact PTH and calcitonin in the tumor tissue were markedly high: 4.56 micrograms/g wet, 13.9 ng/g wet and 50.7 ng/g wet, respectively. Immunohistologically, the tumor cells and the fibrous stroma were stained strongly positive to rabbit anti-human calcitonin antibody and rabbit anti-human N-PTH antibody by indirect immunoperoxidase staining. Calcitonin-producing tumors, except for medullary thyroid carcinoma are rarely reported. To our knowledge, this is the first report of such a calcitonin-producing parathyroid adenoma associated with primary hyperparathyroidism.
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PMID:A case of calcitonin-producing parathyroid adenoma with primary hyperparathyroidism. 258 94

Six cases of primary hyperparathyroidism due to hyperfunctioning intrathyroidal parathyroid glands are reported. In five cases, hyperparathyroidism was due to an intrathyroidal parathyroid adenoma; in the sixth case, hyperparathyroidism resulted from an intrathyroidal parathyroid carcinoma. All five patients with adenoma were female with ages ranging from 40 to 70 yr. The patient with carcinoma was a 55-yr-old male. In all five patients with intrathyroidal parathyroid adenoma, thyroidectomy was performed when an abnormal parathyroid gland could not be located in the neck during surgery for hyperparathyroidism. The patient with intrathyroidal parathyroid carcinoma presented with hypercalcemia and a palpable right thyroid mass. The differential diagnosis of intrathyroidal parathyroid adenoma includes thyroid follicular adenoma. In some cases, the possibility of medullary carcinoma of thyroid might also be considered. Immunocytochemical staining for parathormone (PTH), thyroglobulin, and calcitonin is valuable in establishing the correct diagnosis.
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PMID:The intrathyroidal hyperfunctioning parathyroid gland. 258 70

In the submitted review the author pays attention to mechanisms of control of insulin secretion and the mutual interaction of other messengers (cAMP, calcium and inisitol triphosphate) with special attention to the calcium signal which plays a most important role in the stimulation of the excitable B cell. The trigger of the two-stage insulin secretion is cyclic accumulation of calcium in the cytosol of the B cell and the mutual harmony between calcium of the intra- and extracellular compartment. In the early stage of insulin secretion in particular the intracellular compartment is the source of calcium; from there the ion is released due to the action of inositol triphosphate (IP3) activated by phospholipase C. Calcium of the extracellular compartment is mobilized also in the early secretory stage by opening of the depolarization-dependent calcium channels, it plays, however, a more important part during the second stage. Activation of the other messengers, incl. the calcium signal, depends on the type of secretagogue stimulus. During systemic changes of calcium homeostasis in vivo the calcium signal of the B cell is activated or inhibited in different ways. In the course of hypercalcaemia, in particular if acute, the direct influence of calcium ions on insulin secretion is modulated by further factors, e.g. somatostatin, calcitonin, cholecystokinin, glucagon, adrenocortical hormones, opioids and other substances released into the blood stream. In chronic hypercalcaemia which is the result of primary hyperparathyroidism or vitamin D intoxication the action of calcium on the metabolic and hormonal response is enhanced by the ionophoretic action of parathormone or active vitamin D metabolites.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The calcium signal in the regulation of insulin secretion]. 269 62

A case is presented of a woman with primary hyperparathyroidism due to a parathyroid adenoma with deep mediastinal localization successfully treated surgically. The disease was manifested at the beginning with joint pains only, followed by extreme bone, renal and metabolic disorders endangering the life of the patient. The unusually severe sceleton decalcification is linked with the functional exhaustion of the calcitonin C producing cells. The changes in these cells in the resected thyroid tissue were discrepant with the hypercalciemia. A special feature of the case is the combination of parathyroid adenoma with a number of dysmorphic signs, with a persistent thymus and beta-thalassemia (heterozygotic form) with familial predisposition--thalassemia of the mother and malformations of the patient's child. On this basis the authors presume a genetic determination of the basic disease similar to other forms of primary hyperparathyroidism.
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PMID:[A combination of ectopic parathyroid adenoma and thalassemia with manifestations of extreme hyperparathyroidism]. 274 49

Derangements in leukocyte function occur in patients with primary hyperparathyroidism and in those with uremia, which is a state of secondary hyperparathyroidism, suggesting that parathyroid hormone (PTH) may affect leukocyte function. We examined the interaction between PTH and random migration of human polymorphonuclear leukocytes (PMNL) utilizing a modified Boyden chamber. Intact 1-84 PTH but not its amino-terminal (1-34 PTH) or its carboxy-terminal (53-84 PTH) fragments produced marked and significant (p less than 0.01) stimulation of random migration in a dose-dependent manner. Inactivation of 1-84 PTH abolished its effect and other peptide hormones (calcitonin, glucagon, insulin and vasopressin) did not stimulate migration of PMNL. The effect of PTH on migration was not due to action of the hormone on chemotaxis. PTH did not enhance cAMP or cGMP production by PMNL. The stimulation of PMNL motility by PTH was independent of calcium concentration in media, was not mimicked by calcium ionophore and was not blocked by verapamil. Quinidine also produced significant (p less than 0.01) increase in random migration of PMNL and this effect was not additive to that of PTH. Prolonged exposure to PTH (16-20 h) was associated with significant inhibition of random migration of PMNL. The migration of PMNL from patients with advanced renal failure was significantly (p less than 0.01) reduced and there was a significant (p less than 0.01) inverse relationship between random migration of PMNL and serum levels of PTH. Also PTH produced only modest stimulation of random migration of PMNL in most patients with renal failure.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Effect of parathyroid hormone on random migration of human polymorphonuclear leukocytes. 285 73

A rise in the serum calcitonin (CT) following provocative testing has facilitated making the diagnosis of occult medullary carcinoma of the thyroid (MCT) or C cell hyperplasia (CCH) in asymptomatic children of kindred with multiple endocrine neoplasia (MEN) type IIa. Findings were reviewed for seven children varying in age from 3 to 16 years screened at our institution between 1976 and 1986. Three had elevated basal calcitonin (S-CT). Six had significant elevation of calcitonin (delta-CT) after stimulation. Total thyroidectomy was performed in all seven. Five had MCT with bilobar involvement in three. CCH was present in all five. Two patients had no gross, microscopic, or immunohistochemical evidence of MCT or CCH. One of three had an elevated S-CT. The other had a significant delta-CT. All patients have normal postoperative S-CT and delta-CT. Our experience indicates the importance of beginning stimulation tests of affected kindred at less than 3 years of age. It appears, however, that neither elevated S-CT or positive delta-CT are perfect predictors of parafollicular cell pathology. Solitary parathyroid enlargement, second thyroid malignancy, and branchial pouch anomalies may occur with MEN IIa. One patient with MCT had a focus of papillary carcinoma. One patient with primary hyperparathyroidism had a solitary enlarged parathyroid adenoma. Additional findings were the presence of nodules of ectopic thymus in close association with the thyroid gland in three patients.
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PMID:Provocative testing for occult medullary carcinoma of the thyroid: findings in seven children with multiple endocrine neoplasia type IIa. 288 76

Based on the author's experience with more than 20 cases of immobilization hypercalcemia following spinal cord injury, current concepts of this condition are presented. Symptoms may be mild or severe: laboratory findings are essential for differential diagnosis in older individuals, in whom preinjury Paget's disease and mild primary hyperparathyroidism must be ruled out. Most cases of immobilization hypercalcemia are seen in adolescent boys following recent spinal cord injury. Besides sex (male), risk factors include age (less than 21 years), complete neurologic injuries, high cervical levels of spinal cord injury, dehydration, and a prolonged period of immobilization. A preinjury history of large ingestion of milk and/or extreme exposure to sunshine may also be contributory factors. Therapy includes vigorous hydration, saline infusions and diuretics, calcitonin, and steroids. The clinical course, without treatment, may be prolonged to 14 months, but the condition is always self-limiting.
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PMID:Immobilization hypercalcemia following spinal cord injury. 293 20

Calcium ion is one of the factors which modulate erythrocyte deformability. It is known that calciotropic hormones such as calcitonin (CT) and parathyroid hormone (PTH) exert hypocalcemizing and hypercalcemizing effects, respectively. Their action is mediated, at the level of their target cells, through adenylcyclase activation with the production of cyclic 3,5-adenosinmonophosphate (cAMP). Modifications of transmembrane calcium fluxes have been described and were attributed to these hormones. Erythrocyte deformability has been evaluated by Dormandy method of red blood cell filtration in hypocalcemic patients affected by hypoparathyroidism, in patients with hypercalcemia due to malignancy or primary hyperparathyroidism and in normal age- and sex-matched subjects. Erythrocyte filtration values resulted to be significantly increased with respect to normal values in hypercalcemic patients and at the lower limits of normality in hypocalcemic subjects. Subsequently, acute studies were performed in normal volunteers in whom venous infusions of synthetic salmon calcitonin determined a significant reduction of erythrocyte filtration values, whereas venous infusions of the 1-34 synthetic human PTH fragment induced a significant increase in filtration values of red blood cells. An infusion of a cAMP analogue, dibutyryl-cAMP, determined a slight reduction of erythrocyte filtration values. The calciotropic hormones influence erythrocyte deformability through mechanisms that are yet to be clarified.
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PMID:[Calcitonin, parathyroid hormones, calcium ion, cyclic 3,5-adenosine monophosphate (cAMP) and erythrocyte deformability]. 299 4


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