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

Two antisera which were raised against bovine parathyroid hormone (bPTH), and which cross-reacted with the human hormone, have been characterized. The antisera which originated from rooster and guinea-pig, were found to contain several populations of antibodies directed against both N-terminal and C-terminal sequences of the hormone. However, at proper dilutions the rooster antiserum did not bind the N-terminal fragment nor could this fragment displace the [125I] bPTH (1--84 amino acid residue) from binding to the antiserum. Furthermore, preincubation experiments with excess N-terminal fragment showed only a negligible reduction in maximal binding of the iodinated intact hormone using the rooster antiserum. In contrast, the guinea-pig antiserum reacted equally well with the N-terminal fragment and the intact hormone, and preincubation with this fragment reduced the binding of the [125I]bPTH (1--84 amino acid residues) by 75%. Gel filtration of hyperparathyroid serum on Bio-Gel P-60 showed immunoreactive material which was measured with both antisera, eluting at a position similar to the intact hormone. However, in the C-terminal specific, but not in the N-terminal specific radioimmunoassay the major component eluted together with or somewhat earlier than the N-terminal bPTH fragment (1--34 amino acid residue), and this peak represented more than 90% of total immunoreactive PTH (iPTH) in serum. This major iPTH component must therefore represent fragment(s) with intact carboxy-terminal sequences. The N-terminal specific radioimmunoassay was unable to measure iPTH in about 80--90% of healthy individuals while the C-terminal specific assay detected iPTH in about 88% of these sera (equal to or above 0.1 micrograms/l). Similarly, the N-terminal specific antiserum measured consistently lower serum iPTH concentrations in patients with primary hyperparathyroidism. In thirty-four out of forty-one patients with surgically verified primary hyperparathyroidism, serum iPTH concentrations equal to or above 0.60 micrograms/l were demonstrated using the C-terminal, specific radioimmunoassay.
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PMID:Development of sequence specific radioimmunoassay of human parathyroid hormone and its use in the diagnosis of hyperparathyroidism. 57 82

The results of radio-immunoassay of parathormone in peripheral venous blood (using an anti-serum preferentially recognising fragments from the carboxyl-terminal pole) were compared with those of blood calcium measured on the same day in 33 cases of primary hyperparathyroidism. In the 28 patients with hypercalcaemia, PTH was invariably high (27 cases) or at the upper limit of normal (1 case). In the 5 patients with normal blood calcium levels, it was normal in 3 cases. It is thus important to take blood calcium levels into account in the interpretation of PTH estimation, that latter being more valid during a hypercalcaemic phase.
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PMID:[The relationship between parathormone and calcium blood levels in primary hyperparathyroidism. Diagnostic value (authors transl)]. 60 36

Preoperative localization of parathyroid adenomas by various methods is today in increasing clinical use. The practical value of the methods is discussed, with particular reference to the PTH radioimmunoassay on selective venous samplings, which is the most reliable. The authors report on their 38 cases with suspected primary hyperparathyroidism during the last six years.
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PMID:[PTH radioimmunoassay on selective venous samplings as a method of localization of parathyroid adenomas in primary hyperparathyroidism (author's transl)]. 62 51

Experiences with 77 patients with primary hyperparathyroidism (HPT) are reported. Among the diagnostic parameters, the serum calcium level is the most significant; a definite diagnosis can be made through PTH-RIA. The problem of HPT diagnosis are discussed. For standardization, our own human PTH preparation, produced from tissue culture of operatively removed human adenoma of the parathyroid gland, has been used. For determination of parathormone, venous blood should be selectively extracted from the neck before every relapse-necessitated operation. The technically expensive and difficult examination methods do not excuse the surgeon from carefully exploring all of the parathyroid glands, though the general procedures to be applied before the first operation are still disputed.
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PMID:[Diagnosis of primary hyperparathyroidism based on determination of parathormone in venous blood of the neck (author's transl)]. 62 52

The influence of hypercalcemia on renal function was studied retrospectively in 13 patients suffering from primary hyperparathyroidism, sarcoidosis, vitamin D intoxication, malignant lymphoma or chronic lymphatic leucemia. Different kinds of treatment, depending upon the primary disease, often induced a rapid fall in the serum calcium concentration. The serum creatinine concentration always fell simultaneously. The serum phosphate concentration fell in all but two patients. Changes in serum calcium and serum creatinine correlated significantly (p less than 0.001), as did changes in serum calcium and serum phosphate concentrations (p less than 0.05). Serum calcium/serum creatinine and serum calcium/serum phosphate ratios were significantly higher in patients with primary hyperparathyroidism than in patients with hypercalcemia of non-hyperparathyroid origin (p less than 0.01, p less than 0.001). This suggests a different effect of calcium on the glomerular filtration rate in hyperparathyroid and non-hyperparathyroid patients, the latter group being more sensitive to the influence of hypercalcemia. Possible explanations for this difference, such as a protective effect of PTH on the glomerular filtration, are discussed.
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PMID:Reversible renal failure caused by hypercalcemia. A retrospective study. 64 44

Various hormones have been implicated in the genesis of hypercalcemia in patients with malignancy. Ectopic secretion of PTH by tumor has been documented in only a few patients; rather, elevated levels of circulating iPTH have been presumed to reflect tumor production of hormone in most patients. Small fragments of PTH, as well as polypeptides larger than native PTH, have been described; their biological roles are unclear. The pattern of immunoreactivity, however, has been used to differentiate patients with ectopic hyperparathyroidism from patients with concomitant primary hyperparathyroidism. Vitamin D-like sterols produced by breast cancer seldom reach plasma levels necessary for physiological effects. Members of the prostaglandin family have been proposed to induce hypercalcemia through osteoclast activation or alteration of the immune system and also to affect the frequency of bone metastases. At present, no direct evidence is available to prove a direct role for these effects and prostaglandins are most useful as possible indicators of disease activity.
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PMID:Mechanisms of hypercalcemia in malignancy. 65 92

In 44 patients, all suffering from a malignant disease with hypercalcaemia, plasma parathormone was measured by a radioimmunoassay measuring the intact PTH molecule. The results as a function of plasma calcium were compared with those in 38 patients suffering from proven primary hyperparathyroidism and with those in 9 cases of hypercalcaemia of other origin. PTH was indetectable in 14 cases of malignant disease and normal in 25 cases. In 5 patients only could PTH and plasma calcium not be separated from primary hyperparathyroidism. 3 patients had an increased PTH level when plasma calcium was lowered by treatment of the underlying disease. In patients with malignant disease hypercalcaemia is rarely caused by increased secretion of PTH. In these cases either primary hyperparathyroidism or ectopic secretion of PTH may be the cause of hypercalcaemia.
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PMID:[Determination of plasma parathyroid hormone in the differential diagnosis of hypercalcemias associated with malignant tumors]. 66 97

After a short presentation of advances in biochemical and clinical analysis of primary hyperparathyroidism, the importance of superselective catheterization of the small jugular veins for PTH radioimmunoassay is shown as an improvement of the preoperative localization technique. Since May 1976, the diagnosis of pHPT could be established in 20 patients. Our own experiences with the method of small vein sampling combined with the radioimmunoassay demonstrate that a reliable localization of overactive parathyroid tumors is possible.
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PMID:[Preoperative location of parathyroid adenomas using supraselective parathyroid hormone determination in the blood of the cervical veins]. 72 Jan 67

In early chronic renal failure, the state of the bones resembles that of type II primary hyperparathyroidism. Cortical bone becomes thinner and more porous, and there is increased extent of surface remodeling. These changes are followed in turn by osteomalacia and osteitis fibrosa, although sometimes these may be alternate rather than successive stages. Bone turnover is less than would be expected for the elevation of PTH level, probably because of 1,25 (OH)2D3 deficiency. The resorption velocity and lamellar bone appositional rates are depressed, but woven bone appositional rate may be increased, possibly because of hyperphosphatemia. Bone mass reflects the summation of three independent processes: loss of lamellar bone due to hyperparathyroidism (depending on the extent of insulation by osteoid); accumulation of partly mineralized osteoid because of osteomalacia; accumulation of woven bone because of osteitis fibrosa. Osteosclerosis may be growth-related metaphyseal, subchondral or diffuse axial, and periosteal neostosis may also occur. Some patients on hemodialysis lose bone because of planing rather than lacunar or dissecting resorption, combined with depression of both lamellar and woven bone formation. Hyperparathyroid bone disease tends to improve slowly after renal transplantation. Persistent hypocalcemia reflects a defect in the calcium homeostatic system and cannot be explained solely by the known stimuli to secondary hyperparathyroidism. The increment in plasma calcium in response to PTH infusion is subnormal, both in early chronic and in acute renal failure, probably because of 1,25(OH)2D3 deficiency. This is also the most likely explanation for the depressed level of blood-bone equilibrium. The activity of all three of the PTH responsive cell systems in bone is depressed in renal failure, probably because all three require 1,25(OH)2D3 in order to function normally. In pseudohypoparathyroidism, as in chronic renal failure, hypocalcemia results from a defect in the regulation of the blood-bone equilibrium. The bone-remodeling system shows all gradations of response, from slight depression of bone turnover to overt osteitis fibrosa, but bone turnover is never as low as in PTH deficiency. These differences may reflect the presence or absence of resistance to PTH of the osteoprogenitor cell as well as of the calcium homeostatic system, or may be due to varying degrees of 1,25(OH)2D3 deficiency, as in chronic renal failure. An increase in plasma calcium in response to PTH can occur either in the untreated state or after treatment with vitamin D because either the error-correcting or remodeling system remains responsive to PTH. Pseudohypoparathyroidism may be subdivided into three types, depending on whether the urinary cyclic-AMP response to PTH remains defective despite treatment with vitamin D, improves with treatment, or is normal before treatment. Only the former is associated with the genetic syndrome of Albright's hereditary osteodystrophy...
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PMID:The actions of parathyroid hormone on bone: relation to bone remodeling and turnover, calcium homeostasis, and metabolic bone disease. Part IV of IV parts: The state of the bones in uremic hyperaparathyroidism--the mechanisms of skeletal resistance to PTH in renal failure and pseudohypoparathyroidism and the role of PTH in osteoporosis, osteopetrosis, and osteofluorosis. 78 23

Using synthetic human parathormone 1-34, a radioimmunological method for measuring this hormone fragment was developed which, as the amino-terminal PTH assay, permits the measurement of the concentration gradient in the neighborhood of OTH-secreting tumors. The use of preoperative location diagnosis in primary hyperparathyroidism is demonstrated with some typical cases, especially in revision operations.
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PMID:[Parathormone determination with synthetic human parathormone 1-34 (PTH) (author's transl)]. 80 27


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