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)

Primary hyperparathyroidism in the mother during pregnancy is known to result in a high rate of fetal complications; spontaneous abortions, still births, and neonatal tetany occur in excessive incidence. To understand the pathophysiology of neonatal hypocalcemia that accompanies this disorder, transplacental calcium dynamics were studied in female sheep during the last trimester of pregnancy and in their fetal lambs after hysterotomy. Calcium ion was shown to move rapidly across the placenta. However, this organ blocked the passage of both parathyroid hormone and calcitonin from the maternal and to the fetal circulations. Our studies support the hypothesis that in primary hyperparathyroidism maternal hypercalcemia results in fetal hypercalcemia, which leads to suppression of fetal parathyroid gland function. In such a situation, neonatal hypocalcemia would occur after birth when maternal calcium flow is interrupted. Parathyroidectomy performed in the mother, especially during the second trimester of pregnancy when operation is safest, would break this cycle and permit normal serum calcium homeostasis in the fetus.
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PMID:Primary hyperparathyroidism, pregnancy, and neonatal hypocalcemia. 648 12

The mechanism accounting for normal calcemia in certain cases of primary hyperparathyroidism (HPT) remains unclear and more generally the relative importance of each determinant of calcemia has not been systematically studied so far. 52 primary HPT patients with stable calcemias, ranging from 95 to 137 mg/l, were investigated. They all exhibited identical ionized to total plasma calcium ratios. Values of serum iPTH and nephrogenous cyclic AMP were similarly elevated in all patients, and all displayed similar high values for net bone resorption and intestinal absorption of calcium. Tubular reabsorption of calcium was normal or slightly subnormal in the normocalcemic subgroup, and rose in proportion to the increase in serum calcium in the hypercalcemic subgroup. No correlation was found between tubular reabsorption of calcium on the one hand and serum immunoreactive calcitonin, degree of phosphate depletion, sodium urinary excretion or magnesemia on the other. Plasma acid base equilibrium was normal in all patients. Finally, after surgical removal of adenomas, fasting calciuria and intestinal absorption of calcium returned to normal. It is concluded that (1) the main determinant of plasma calcium value in stable calcemia primary HPT is tubular reabsorption of calcium and (2) the absence of correlation between the tubular reabsorption of calcium and the degree of PTH hypersecretion suggests that as yet undetermined factors interfere with the tubular action of PTH.
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PMID:Normocalcemic primary hyperparathyroidism: resistance to PTH effect on tubular reabsorption of calcium. 649 58

Experimental studies have suggested that in primary hyperparathyroidism (HPT) the cells of the hyperfunctioning parathyroid tissue retain some capacity for stimulation and that an increase in secretion of parathyroid hormone (PTH) can occur when the extracellular calcium concentration is lowered within the hypercalcaemic range. We have tested this hypothesis in 23 patients with HPT, 10 patients with hypercalcaemia of other origin (7 of whom had disseminated malignant disease) and 17 normal subjects. In all three groups a single injection of 100 MRC units of salmon calcitonin caused a reduction in serum calcium of approximately 3 to 5%. In the hypercalcaemic patients this reduction was correlated to the basal calcium level (r = -0.57, P less than 0.01). In the patients with HPT, although they all remained hypercalcaemic, the decrease in serum calcium was associated with a mean increase in serum PTH of 10%. Only in 2 patients did such an increase fail to occur despite an adequate decrease in serum calcium. These 2 patients had high basal PTH levels and the lack of response might have been due to a high degree of autonomous parathyroid function. Calcitonin also reduced serum calcium and increased serum PTH in normal subjects. None of the patients with hypercalcaemia of other origin than primary HPT displayed a secretory PTH response to serum calcium reduction. Thus, this test could be of practical clinical value, particularly in patients with borderline PTH values. A calcitonin-induced rise in PTH while serum calcium is lowered within the hypercalcaemic range strongly suggests primary HPT.
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PMID:A stimulation test with calcitonin for differential diagnosis of hypercalcaemia. 649 90

The present study characterizes the immunological and biological activity of circulating forms of parathyroid hormone (PTH) in patients with primary hyperparathyroidism. In addition, the rate of elimination of intravenously injected 125I-labelled bovine parathyroid hormone (125I-bPTH) was studied in patients with this disease before and after operation. The different molecular forms of serum PTH were characterized by gel chromatography followed by radioimmunoassay employing two antisera with specificities directed against the N-terminal and mid-region part of the peptide, respectively. The major part of immunoreactive PTH (iPTH; on the average above 50%) eluted corresponding to fragments with a molecular size about 7,500 daltons in both radioimmunoassays. Specific immunoreactivity coeluting with the intact hormone represented 9-15%. The biological activity of hyperparathyroid serum after gel chromatography was tested in a hormone-sensitive rat kidney adenylyl cyclase assay system. The basal and PTH-stimulated adenylyl cyclase activity (half-maximal) stimulation at 5 micrograms/l or 0.6 nM) was dependent on Mg2+ and ATP. Maximal responses to PTH, calcitonin, and prostaglandin E2 were 50-200% above basal activity and were obtained in the presence of both GTP and Gpp(NH)p (5 X 10(-4) M). Serum from patients with hyperparathyroidism and PTH extracted from parathyroid tissue stimulated the adenylyl cyclase in a dose-dependent manner, as did the chromatographic fraction representing the intact hormone. Elimination of 125I-bPTH from circulation after intravenous injection to patients with this disease suggested that the hormone, but not its degradation products, were removed more rapidly before than after successful surgery. We conclude that the major part of circulating iPTH in patients with primary hyperparathyroidism is unable to stimulate the rat kidney adenylyl cyclase, and that the biological PTH activity is represented by the intact hormone (15% or less of total iPTH). These patients degrade more rapidly the injected 125I-bPTH and this mechanism introduces a new concept to protect target cells against excessive hormone action.
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PMID:Peripheral metabolism of parathyroid hormone in patients with primary hyperparathyroidism as judged by immunological and biological studies. 672 31

Frequently a causal relationship between hyperparathyroidism (HPT) and pancreatitis has been defended. Bess et al. queried the existence of any causality. A series of 686 patients with surgically confirmed primary hyperparathyroidism (PHPT) was analysed with a coincidence of pancreatitis of 1.5% (n = 10). Three patients had an attack immediately after exploration of the neck, which is more than one would expect after a non-related operation. Although these data are not conclusive, a causal relationship cannot be excluded. It is uncertain whether a parathyrotoxic crisis due to surgical manipulation plays a part. In 27 patients a partial or total thyroidectomy was performed at the time of the parathyroidectomy. None of these patients had a postoperative pancreatitis, which means that in this series the recently postulated protective role of calcitonin cannot be confirmed.
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PMID:Primary hyperparathyroidism and pancreatitis. 672 28

Bone Gla protein (BGP) was measured in the plasma by radioimmunoassay (RIA) during treatment of 59 patients with bone diseases including Paget's disease (N = 9), primary hyperparathyroidism (N = 25), chronic renal failure (N = 20), and cancer involving bone (N = 5). Plasma BGP was increased above normal in all patients. BGP decreased in the patients with Paget's disease following the acute and chronic administration of salmon calcitonin. Plasma BGP was higher in women then in men with primary hyperparathyroidism. Following parathyroidectomy, BGP decreased in both sexes but the decrease was significant in women only. Plasma BGP was increased in patients with renal osteodystrophy and did not change after hemodialysis. In the patients with bone cancer, plasma BGP decreased during treatment of the attendant hypercalcemia with salmon calcitonin. Although plasma BGP and serum alkaline phosphatase (AP) levels were generally correlated in these studies, there were examples of dissociation between the two. The measurement of plasma BGP appears to provide a specific index of bone metabolism that may in some circumstances be more sensitive than serum alkaline phosphatase measurement. However, further studies are necessary to establish the clinical value of plasma BGP measurement by RIA in the management of patients with bone diseases.
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PMID:Changes in plasma bone GLA protein during treatment of bone disease. 680 17

Serum calcium, phosphorus, calcitonin, parathyroid hormone, 25-hydroxyvitamin D (25OHD), and 1,25-dihydroxyvitamin D [1,25-(OH)2D] were measured in 6 women and 2 men with medullary carcinoma of the thyroid, 22 normal subjects, 5 patients with chronic renal failure, and 5 patients with primary hyperparathyroidism. Serum 1,25-(OH)2D levels were significantly higher in patients with primary hyperparathyroidism and lower in patients with chronic renal failure than in normal subjects. In patients with medullary carcinoma of the thyroid, the serum calcitonin levels were elevated, but the parathyroid hormone and 1,25-(OH)2D levels were within normal ranges. The serum 25OHD levels were not significantly different in any group. It is concluded that chronic elevation of serum calcitonin has no effect on the serum 1,25-(OH)2D level.
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PMID:Normal serum 1,25-dihydroxyvitamin D in patients with medullary carcinoma of the thyroid. 697 51

Adenolipoma--or parathyroid hamartoma--has been described s a very rare lesion of the parathyroid gland, often unassociated with clinical hyperparathyroidism. A few reported cases in which the diagnosis was discovered pathologically following parathyroid resection for hyperparathyroidism have been called unique. In a 2-year period the diagnosis of parathyroid adenolipoma was made in three instances, with each clinical presentation consistent with primary hyperparathyroidism. In the first patient, a 64-year old man reporting to an emergency department for treatment of migraine headache, a prolonged history of unrecognized hypercalcemia was discovered, and he underwent cervical exploration. At operation, a 105 by 2.0 cm tumor weighing 17.5 gm was encountered. The other two patients were middle-aged women who had hypercalcemia (one requiring preoperative calcitonin treatment). The diagnosis of adenolipoma was made morphologically, although the clinical course was otherwise indistinguishable from other forms of primary hyperparathyroidism. Each of the three patients were cured following adenolipoma resection. This small series of patients in the experience of a single surgeon in a brief period might indicate that this diagnosis is by no means rare, and the functional nature of these tumors was the characteristic that brought them to diagnosis. The hypercalcemia was somewhat more severe in these cases--but the hyperparathyroidism was otherwise unremarkable. The morphologic features of these tumors include unusual size, proliferating fat content, and a fibrillar stroma. Adenolipoma of the parathyroid can cause primary hyperparathyroidism and should be considered in the differential diagnosis of the morphologic lesions of the parathyroid glands that can produce a hypercalcemic syndrome.
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PMID:Parathyroid adenolipoma: clinical and morphologic features. 713 1

Plasma levels of calcitonin (CT) are highest in patients with medullary thyroid carcinoma (MTC). Plasma CT is also raised in some patients with carcinoma such as that of the breast, the lung or the pancreas, and in pheochromocytoma. It must be kept in mind, however, that plasma CT can be similarly raised in patients with renal failure, non-tumoral pulmonary disease or acute pancreatitis. In hypercalcemia patients with primary hyperparathyroidism the plasma CT is normal or only marginally elevated. It is speculated that the raised levels in pregnant and lactating women and in new-born infants prevent excessive bone destruction at times of greater physiological need for calcium. Larger molecular weight forms than monomeric CT (1--32) are circulating at least in plasma of patients with calcitonin-producing tumors and in renal insufficiency. The biological function of these larger molecular weight forms is not yet known. The discrepancies among the results of different laboratories can in part be explained by the immunoheterogeneity of the hormone and the different antigenic recognition sites of the antisera used. The measurement of plasma CT levels is nevertheless important for the diagnosis of MTC and may prove useful in some patients with malignant tumors unrelated to the C-cells of the thyroid gland. CT-radioimmunoassay may be improved by using antibodies specific to the different forms of circulating calcitonin.
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PMID:[The differential diagnosis of hypercalcitoninism]. 733 Jun 42

Primary hyperparathyroidism frequently has a chronic and relatively benign course. Occasionally, however, it may have a stormy presentation requiring prompt adequate diagnosis and urgent surgical treatment. We describe a 71-year-old woman who had severe hypercalcemia, seizures, and coma refractory to treatment with anticonvulsant drugs, intravenous infusion of normal saline, furosemide, glucocorticoids, calcitonin, and hemodialysis. Bone roentgenograms were normal, but a strikingly positive bone scan that also showed marked soft-tissue uptake prompted the diagnosis of primary hyperparathyroidism and the successful surgical removal of a large parathyroid adenoma. This was followed by a remarkable recovery and marked reduction in soft-tissue radioactive uptake on bone scan. The association of hypercalcemia and seizures and the diagnostic value of bone scanning are discussed. An up-to-date review of the literature is presented. We proposed this condition to be named "parathyroid storm" on the basis of the rapid and lethal course unless surgery is performed without delay.
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PMID:Parathyroid storm. 739 15


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