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Query: UMLS:C0221002 (primary hyperparathyroidism)
 4,921 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The overproduction of parathyroid hormone as caused by a simple hyperplasia or an adenoma leads to pathological changes in various organs which are termed primary hyperparathyroidism. The blood phosphates increase in case of long-standing disturbances of the metabolism, e.g. chronic renal insufficiency. In this way and due to other causes, the production of parathyroid hormone is increased. The resultant clinical picture is termed secondary hyperparathyroidism. Both forms are associated with osseous changes also in the maxillofacial skeleton. Tertiary hyperparathyroidism may develop from secondary hyperparathyroidism if the metabolic disorder in the renal form cannot be eliminated by kidney transplantation and if the process in the parathyroid becomes independent (autonomous hyperparathyroidism). Besides these three forms, there are two others, quaternary hyperparathyroidism and quinary hyperparathyroidism, which are described.
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PMID:[Hyperparathyroidism]. 36 8

1. The distribution of intact parathyroid hormone-(1-84) [PTH-(1-84)] and of its COOH-terminal fragments was determined in human serum by column chromatography. In addition to PTH-(1-84) (peak I), COOH-terminal fragments having molecular weights of approximately 4000-7000 (peak II) and immunoreactive components co-eluting with human PTH-(1-12) (peak III) were observed. 2. Mean concentrations of intact PTH-(-84) and of its COOH-terminal fragments were significantly raised in chronic renal failure as compared with those of normal subjects. Mean amounts of peak II were higher in patients with chronic renal insufficiency than in nutritional vitamin D deficiency, in pseudohypoparathyroidism and in primary hyperparathyroidism, despite comparable amounts of PTH-(1-84). 3. In chronic renal failure as well as in a group of patients with vitamin D deficiency, pseudohypoparathyroidism and primary hyperparathyroidism and in controls, significant linear relations were found between the serum concentrations of calcium and log (peak II/peak I). Our findings suggest that the conversion of intact PTH-(1-84) into COOH-terminal fragments by the parathyroid glands (resulting in a raised secretion of fragments) and/or in peripheral organs may be directly related to the serum concentration of calcium. However, the degradation of the fragments may also be suppressed in a calcium-dependent manner.
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PMID:Distribution of circulating immunoreactive components of parathyroid hormone in normal subjects and in patients with primary and secondary hyperparathyroidism: the role of the kidney and of the serum calcium concentration. 51 52

The basis for the radioimmunoassay of parathormone (PTH) as a routine method is a new sheep antiserum and a labelled PTH stabilised by a modification of the purification technique. The antiserum is obtained by immunisation with pig and cattle parathormone, it is C-terminal specific and is used in the assay in a final dilution of 1:35000. The affinity to human PTH is markedly greater than of the antisera used up to now. Two purification steps of 125J labelled bovine PTH lead to a tracer with a nonspecific binding of approximately 5% which increases to approximately 10% within 6 weeks. All normal sera investigated so far were measurable quantitatively (normal range 0.7 to 2.5 mul/equiv.). The lower sensitivity range was at 0.3 mul/equiv. All patients with chronic renal insufficiency and dialysis patients have an increased PTH concentration (3.9 to greater than 20 mul/equiv.). This also applies to patients with primary hyperparathyroidism (2.9 to greater than 20 mul/equiv.).
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PMID:[A highly sensitive C-terminal specific radioimmunoassay for human parathormone as a routine method (author's transl)]. 99 60

The effect of lithium on PTH release from human parathyroid tissue was studied using a perifusion system and an immunoradiometric assay for intact human PTH. Tissue was obtained from three patients undergoing surgery for thyroid disease, three patients with secondary hyperparathyroidism due to chronic renal insufficiency, and four patients with primary hyperparathyroidism due to a parathyroid adenoma. Addition of lithium in concentrations equivalent to the therapeutic serum levels normally attained in man (1.3 mmol/L) resulted in a significant (P less than 0.05) increase in PTH release under normocalcemic (1.15 mmol/L) conditions from normal and hyperplastic tissues. The magnitude of the lithium-induced response of PTH release ranged from a 1.4- to 5.3-fold increase above basal levels (perifusion with 1.15 mmol/L calcium alone) and was comparable to the response during a low calcium (0.42 mmol/L) perifusion. Although the response to lithium was delayed compared to that of hypocalcemia, PTH returned to basal levels immediately after removal of either stimulator. In contrast, parathyroid adenomas did not respond to either lithium or hypocalcemia in a characteristic manner, but, rather, functioned in an autonomous fashion with repeated pulsatile bursts of PTH release that were not suppressible even under hypercalcemic (1.70 mmol/L) conditions. These in vitro studies suggest that lithium therapy may elevate serum PTH levels in some patients and could, thus, be responsible for hypercalcemia in them.
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PMID:Lithium stimulates the release of human parathyroid hormone in vitro. 337 82

1252 patients were examined by 125I-photonabsorptiometry, a non-invasive method for direct determination of bone mineral content. These patients were divided into 21 groups with different diagnoses including primary skeletal disorders and diseases of internal medicine (endocrine, gastrointestinal, renal) with possible secondary skeletal involvement. The findings are analyzed on the basis of well established own normal ranges, which were obtained from determinations on 1058 healthy people. The well reproducible and quantitative results allow to cover the frequency and severity of deficits in bone mineral mass occurring with the diseases mentioned above. As examples the findings in primary hyperparathyroidism and in chronic renal insufficiency before and during hemodialysis are shown in more detail. While the radiation exposure is practically negligible, control measurements can be performed regularly, which supply a good judgement of the course of disease with and without treatment.
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PMID:[Clinical significance of direct measurement of bone mineral content. 125I photon absorption measurement in 1252 cases]. 683 81

1. Plasma membranes were prepared from parathyroid adenomas in patients with primary hyperparathyroidism and from hyperplastic glands obtained from patients with chronic renal insufficiency. The basal and isoproterenol- or sodium fluoride-stimulated adenylate cyclase activities were measured in membranes in the presence of several vitamin D3 metabolites. 2. 24,25-Dihydroxycholecalciferol (10 and 1000 pmol/l) decreased isoproterenol- and sodium fluoride-stimulated adenylate cyclase activities in membranes prepared from parathyroid glands. 1,25-Dihydroxycholecalciferol (1000 pmol/l) inhibited the isoproterenol-stimulated adenylate cyclase activity. 25-Hydroxycholecalciferol and vitamin D3 had no effect on adenylate cyclase activities. Basal adenylate cyclase activity was not affected by any of th vitamin D3 metabolites tested. 3. These results indicate that 24,25-dihydroxycholecalciferol inhibits the isoproterenol- and sodium fluoride-stimulated adenylate cyclase activities in parathyroid tissues. Such an inhibition could explain the very rapid decrease in parathyroid hormone secretion after 24,25-dihydroxycholecalciferol administration that has been previously reported.
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PMID:Human parathyroid gland adenylate cyclase activity: inhibition by 24,25-dihydroxycholecalciferol in vitro. 697 85

Medullary nephrocalcinosis occurs in various diseases as a non-specific renal manifestation. We present 5 patients (hypophosphataemic rickets, type 1 renal tubular acidosis, primary hyperparathyroidism, hypercalcaemia of unclear origin, chronic renal insufficiency requiring dialysis) in whom a medullary nephrocalcinosis was demonstrated by means of sonographically detectable changes in the renal medulla region. The sonographic appearance of medullary nephrocalcinosis is characterized by detection of echo-enhanced structures in the region of the renal pyramids. The presence of a medullary nephrocalcinosis can generally be confirmed with adequate reliability on the basis of sonographic findings and characteristic clinical pictures. In individual cases it is difficult to distinguish between medullary nephrocalcinosis and renal calyx calculi.
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PMID:Medullary nephrocalcinosis: sonographic findings in adult patients. 775 19

The Ca2+ receptor is the primary mechanism regulating the secretion of parathyroid hormone (PTH). Ligands that activate this receptor (calcimimetics) represent a novel means of lowering plasma levels of PTH. Two mechanistically distinct classes of calcimimetics that inhibit PTH secretion have been identified: type I calcimimetics are full agonists of the Ca2+ receptor and include Ca2+ and other polyvalent inorganic and organic cations; whereas type II calcimimetics, typified by phenylalkylamine compounds, behave like positive allosteric activators and increase, in a stereoselective manner, the sensitivity of the Ca2+ receptor to activation by extracellular Ca2+. The phenylalkylamine calcimimetics are orally active and decrease the plasma levels of PTH and Ca2+ in patients with primary hyperparathyroidism (HPT), a disease that so far has resisted pharmacological intervention. Such compounds are similarly safe and effective in reducing PTH levels and preventing parathyroid cell hyperplasia in rats with HPT secondary to chronic renal insufficiency and they lower plasma levels of PTH in dialysis patients with secondary HPT. Calcimimetic compounds may provide a novel therapy for treating both primary and secondary HPT.
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PMID:Calcimimetic Compounds: a Direct Approach to Controlling Plasma Levels of Parathyroid Hormone in Hyperparathyroidism. 1032 97

Parathyroid cells can sense small changes in plasma Ca2+ levels by virtue of a cell surface Ca2+ receptor. Calcimimetics are newly synthesized compounds that act as agonists or positive allosteric modulators at the Ca2+ receptor and can suppress parathyroid hormone secretion. The first-generation calcimimetic, NPS R-568, has undergone clinical trials in primary hyperparathyroidism and in hyperparathyroidism secondary to chronic renal insufficiency. The data accumulated so far demonstrate that calcimimetics have potential as therapeutic agents for hyperparathyroidism and related bone diseases such as osteitis fibrosa.
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PMID:The calcium receptor and calcimimetics. 1049 33

Treatment of excessive secretion of parathyroid hormone (PTH) in primary hyperparathyroidism (I degree HPT) as well as in secondary hyperparathyroidism (II degree HPT) in chronic renal insufficiency is symptomatic, short-term acting and far from expectations. Recognition of properties of calcium receptor (CaR) expressed on parathyroid principal cell membranes created possibilities to explore new compounds that could alter directly PTH secretion and provide a novel therapy for direct correction of increased secretion of the hormone in these disorders. Ligands that activate this receptor and inhibit PTH secretion are called calcimimetics. Recently clinical trials with NPS R-568, a calcimimetic of the Ist generation, and AMG 073, a representative of calcimimetics of IInd generation, were completed. Calcimimetics, taken orally, effectively lower increased secretion of PTH and hypercalcemia in I degree HPT, by "pharmacologic parathyroidectomy". Such compounds are also safe and effective in dialysed patients with II degree HPT in chronic renal insufficiency: they decrease PTH plasma level and prevent parathyroid cell hyperplasia. The other compounds, called calcilytics and represented by NPS 2143, inhibit CaR resulting therefore in increase of PTH secretion. Administration of calcilytics would provide a valuable alternative to inhibit progression of osteoporosis. Subcutaneous, pulsative low doses of recombinant PTH (ALX1-11) administration induces increase of bone formation. Such an effect to some extent was obtained by transient increase of endogenous PTH secretion induced by oral administration of calcilytic NPS 2143 to osteopenic ovariectomized rats, especially if it was accompanied by supplementation of estrogens.
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PMID:[Calcimimmetic and calcilytics: new perspectives of correction of abnormal parathormone (PTH) secretion]. 1497 81


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