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)

The first case of primary hyperparathyroidism associated with renal cell carcinoma, nasopharynx carcinoma and thyroid carcinoma is reported. Selective venous sampling with radioimmunoassays for parathyroid hormone was helpful in the differentiation of primary hyperparathyroidism from hypercalcemia associated with malignancy.
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PMID:Primary hyperparathyroidism with triple cancers consisting of renal cell carcinoma, nasopharynx carcinoma and thyroid carcinoma. 83 5

A theoretical consideration of the relationship between plasma concentrations of calcium and parathyroid hormone suggests that the reported negative correlations between these variables in normal subjects and in patients with secondary hyperparathyroidism, and the positive correlation in patients with primary hyperparathyroidism, may be fortuitous and do not necessarily imply fundamental differences in the negative feedback mechanism.
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PMID:A theoretical analysis of the steady-state relationship between plasma concentrations of calcium and parathyroid hormone. 85 70

Although anemia has not been widely appreciated as a complication of primary hyperparathyroidism, 5.1% of the individuals with this disorder seen at the Massachusetts General Hospital since 1962 had a normochromic, normocytic anemia that could not be related to blood loss,a deficiency state, or uremia. The anemic group had more advanced bone disease and higher levels of serum calcium, alkaline phosphatase, and parathyroid hormone than the nonanemic group. Results of bone marrow biopsies performed in five patients showed variable degrees of myelofibrosis. However, none of the patients had hepatosplenomegaly, a myelophthisic peripheral blood smear, leukopenia, or thrombocytopenia. Removal of the abnormal parathyroid glands led to improvement or correction of the anemia.
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PMID:Anemia in primary hyperparathyroidism. 85 57

A 25-year-old white woman with sporadic hypophosphatemic rickets presented with a 7 year history of chronic mild hypercalcemia, osteitis fibrosa cystic and hypercalcemic nephropathy. Serum immunoreactive parathyroid hormone was elevated by greater than 100-fold and a 3.5 g parathyroid tumor was found at operation. Survey of the literature reveals that of 9 previous cases in which hypercalcemic hyperparathyroidism occurred in association with hypophosphatemic rickets, only two had classical x-linked familial hypophosphatemic rickets. It appears more than likely that this unusual combination of skeletal diseases represents the chance occurrence of primary hyperparathyroidism in patients with underlying x-linked familial hypophosphatemic rickets rather than a complication of phosphate therapy.
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PMID:Hypercalcemic hyperparathyroidism in hypophosphatemic rickets. 87 68

The immunoreactive parathyroid hormone (iPTH) in the plasma of hyperparathyroid man consists largely of carboxyl (COOH)-terminal fragments of the hormone. Although these fragments have been thought to arise principally or solely from peripheral metabolism of intact human PTH {hPTH(1-84)} secreted from the parathyroid gland, there is disagreement about the source of iPTH fragments in vivo. To reexamine this question, we fractionated peripheral and thyroid or parathyroid venous effluent sera from four patients with primary hyperparathyroidism using a high-resolution gel filtration system (Bio-Gel P-150 columns run by reverse flow). The column effluents were analyzed using two PTH radioimmunoassays, one directed toward the amino(NH(2))-terminal region of the molecule, the other toward the COOH-terminal region. In all four thyroid or parathyroid venous effluent sera studied, iPTH was 9-180 times higher than in peripheral serum from the same patient; after fractionation, hPTH(1-84) accounted for only a portion of the total iPTH (35-55% with the assay directed toward the COOH-terminal region of hPTH, >90% with the NH(2)-terminal directed assay.) The remaining iPTH eluted from Bio-Gel P-150 after hPTH(1-84) as NH(2)-or COOH-terminal hPTH fragments. These results suggest that parathyroid tumors secrete large quantities of hPTH fragments. Based on estimates of their molar concentrations in serum, tumor-secreted COOH-terminal hPTH fragments could account for most of these peptides in peripheral serum if their survival times were, as estimated by several other workers, 5-10 times that of hPTH(1-84). We conclude that, in contrast to published information, secretory products of hyperfunctioning parathyroid tissue are probably a major source of serum PTH immunoheterogeneity.
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PMID:Immunoheterogeneity of parathyroid hormone in venous effluent serum from hyperfunctioning parathyroid glands. 91 3

1. Previously published data obtained by magnesium infusion in man were found to conform to a Tm/glomerular filtration rate (GFR) model on the assumption of 80% diffusibility of plasma magnesium. The lower limit of Tm,Mg/GFR was 625 mumol/l. 2. Previously published data concerning the effect of cellulose phosphate on magnesium metabolism in normal subjects, patients with latent hypoparathyroidism and patients with primary hyperparathyroidism were found to conform to the same model, with the same limit for Tm,Mg/GFR for all three levels of parathyroid function. 3. The threshold for magnesium excretion is sharper with less 'splay' than for phosphate, but as for phosophate it is close to the normal blood concentration. 4. Because of the geometrical relationship between different methods of presentation of data, at a constant value for Tm,Mg/GFR changes in magnesium load or in GFR automatically produce changes in fractional magnesium clearance. This is the explanation for the increase in fractional magnesium clearance which occurs which with diminishing renal function. 5. Renal conservation of magnesium is a passive consequence of the fall in plasma magnesium. There was no evidence of augmented tubular reabsorption of magnesium in response to magnesium deprivation in any of the three groups of subjects. 6. The tubular reabsorption of magnesium was not altered detectably by a moderate deficiency or excess of parathyroid hormore. Changes in parathyroid hormone secretion are probably not concerned in normal magnesium homeostasis.
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PMID:The effect of cellulose phosphate on plasma and urinary magnesium at different levels of parathyroid function in man. 95 62

In 82 patients, a preoperative diagnosis of primary hyperparathyroidism has been established by means of transfemoral neck vein catheterization and measurement of serum immunoreactive parathyroid hormone (iPTH). Twenty-five of these patients have had cancer in other parts of the body but with no evidence of recurrence or metastasis. One patient had carcinoma of the colon with metastases, and four were members of families with multiple endocrine adenomatosis (MEA, Types I and II). In six other hypercalcemic patients, high levels of iPTH were found also in the effluent blood from cancer sites other than the parathyroid gland, secondary to ectopic hormone production or pseudohyperparathyroidism. In addition, a high serum level of iPTH was found in the superior vena cava of a seventh patient who had carcinoma of the breast but no clinical or radiological signs of recurrence or metastasis with the exception of an enlarged liver. This iPTH finding was interpreted as being, probably, the result of parathyroid adenoma in either the neck or the mediastinum. At the time of operation, a transcervical mediastinal search was made. Four normal cervical parathyroid glands were found; three were removed. Hypercalcemia persisted after operation, and the patient died. At postmortem examination, microscopic study revealed that the disease had metastasized to lungs and hilar lymph nodes. There was massive metastasis in the liver; the liver contained a large amount of iPTH. The results of these investigations suggest that (1) venous catheterization of the neck veins and the effluent blood from extraparathyroid tumors aid in identifying and localizing iPTH production; (2) primary benign hyperparathyroidism is not uncommon in patients with cancer, and its co-existence must be recognized; (3) high serum iPTH level in the superior vena cava may be found in patients with metastatic or primary cancer of the thoracic cavity; and (4) hyperparathyroidism may be the first hint of a familial multiple endocrine syndrome.
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PMID:Hypercalcemia in patients with known malignent disease. 96 5

Six patients with primary hyperparathyroidism were studied during the first seven days after the operative removal of the parathyroid adenoma with special emphasis on biochemical and hormonal changes during the first 24 h. Serum parathyroid hormone (PTH) levels fell abruptly after the parathyroidectomy and normalized within 3 h. The half-life of the biologically inert c-terminal PTH-fragment (M.W. 7000-7500) was calculated to be about 180 min. No significant changes in serum calcitonin levels were found. The serum phosphorus levels, which were already low pre-operatively, decreased transiently but significantly during the first 90 min after the removal of the parathyroid adenoma. This fall in serum phosphorus preceded a slow decrease of the calcaemia. During the first post-operative week the calcaemia continued to decline, while serum phosphorus levels increased. The pre-operative cholesterol levels were low compared to age-paired normal Belgians. During the first post-operative week the cholesterolaemia decreased even more, whereas at long term follow-up a clearcut increase of the serum cholesterol levels has to be expected.
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PMID:Hormonal and biochemical changes in patients successfully operated for primary hyperparathyroidism. 98 97

Circulating levels of immunoreactive (i) PGE, calcium and parathyroid hormone (iPTH) were examined in 21 patients with neoplasia and 3 patients with primary hyperparathyroidism. Plasma iPGE was elevated in 4 of 11 hypercalcemic cancer patients; all extracts of liver metastases obtained from 3 of these 4 patients had elevated iPGE levels (metastases = 19.43 +/- 3.43, n = 11; normal liver = 2.04 +/- 0.23; ng/g tissue, x +/- SE, P less than .001). In contrast, only one of 10 normocalcemic cancer patients and none of 3 hyperparathyroid patients had elevated plasma iPGE. There were no apparent relationships between the presence of metastases and either hypercalcemia or elevations of plasma iPGE. Serum iPTH levels were undetectable or below the mean of the normal range in 19 of 21 cancer patients; only the three hyperparathyroid patients had elevated levels. Seven hypercalcemic patients were treated with indomethacin; plasma iPGE decreased in 6 (-34 +/- 10% decrement, n = 6, P less than .01). Decreases in serum calcium occurred only in those patients (2 of 6) who had abnormally elevated plasma iPGE prior to the therapy. It is concluded that plasma iPGE elevations are found in some cancer patients, especially those with hypercalcemia, and that this marker may identify those patients who will respond to indomethacin treatment.
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PMID:Plasma prostaglandin E in patients with cancer with and without hypercalcemia. 100 18

A one-year material of 290 patients with clinically verified urolithiasis was screened for primary hyperparthyroidism, by X-ray examination, analysis of calculi, plasma calcium and phosphate, plasma parathyroid hormone and a clinical history examination. Primary hyperparathyroidism was found in 10 patients, 8 with adenomas and 2 with hyperplasia. The results suggest that with the present policy of investigation, there is a considerable underdiagnosis of parathyroid changes in patients with urolithiasis. An interesting finding was the distribution of plasma calcium concentrations in this material, which indicates that patients with urolithiasis have a generally higher lever of plasma calcium than others.
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PMID:Uroliathiasis with primary hyperparathyroidism. A one-year screening. 100 87


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