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 thyroidal content of calcitonin was investigated in patients with euthyroid goitre, patients undergoing laryngectomies or neck operations and finally patients with primary hyperparathyroidism using method of biological titration. Patients with primary hyperparathyroidism had markedly decreased content of calcitonin in the thyroid gland when compared with the content of calcitonin of both groups of patients without calcium metabolism disturbance. Decreased content of calcitonin in patients with primary hyperparathyroidism can be explained by long lasting hypercalcaemia during which the rate of biosynthesis of calcitonin in the C cells does not keep up with the rate of release of calcitonin into the circulation.
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PMID:Calcitonin activity of the thyroid gland in primary hyperparathyroidism. 69 67

Serum calcitonin (Ct) levels, serum calcium, and urine amylast were analyzed in 29 patients with an acute pancreatitis collected at random. In two of the patients the acute pancreatitis complicated a primary hyperparathyroidism. It was found that the calcitonin levels in serum were usually elevated during the acute phase of the pancreatitis. During this phase of the disease 22 of 27 examined patients had Ct-values above the upper normal limit of 1 mug/ml. The patients with normal Ct-values also had moderately elevated amylast values and a less pronounced pancreatitis. Normal Ct-values were usually found in patients more than 10 days after the onset of symptoms. Serum calcium was mostly within normal limits. However, a slight fall in serum calcium or low values was recorded in six patients with a pronounced disese. One patient with hyperparathyroidism normalized a previously elevated serum calcium during the calcitonin release.
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PMID:Serum calcitonin in acute pancreatitis in man. 83 66

In order to investigate the effect of calcitonin (CT) on calcium and phosphorus metabolism in primary hyperparathyroidism (PHP), porcine calcitonin (80 MRC units) was injected intramuscularly at 9:00 a.m. and 5:00 p.m. for 10-14 days in 7 patients with parathyroid adenoma. Fasting blood specimens were drawn at 8:00 a.m. every other day and 24 hour urine samples were collected through out control and test days. To examine the acute effect of CT, blood and urine were checked several times until 8 hours after the first injection. A fall in the fasting serum calcium level observed in 5 patients during the repeated administrations of CT, as well as that observed in 6 patients within 6 hours after the first injection, showed a significant correlation with the initial serum calcium level. Serum phosphorus concentration decreased in all patients 6 hours after the first injection, while fasting levels seemed to remain unchanged. During the repeated administrations, urinary excretion of calcium and phosphrus decreased correspondingly with the fall in serum calcium levels, although no definite tendancy was observed within 8 hours after the first injection. Fasting serum PTH levels during the repeated administrations were measured in 2 patients. In a patient whose serum calcium returned to the initial level on the 7th day of administration, a gradual rise of PTH was observed, while in another patient whose serum calcium was kept lower than the initial level, PTH remained almost unchanged. These results indicate that, under such a condition where there is marked increase of bone resorption as PHP, repeated administrations of CT bring about not only a hypocalcemic effect but also the reduction of calcium and phosphorus excretion through a decreased filtered load. In addition, it was suggested that, in some cases of PHP, the hypocalcemic effect of CT may be abolished by an increase of PTH secretion from the parathyroid glands during long-term administration.
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PMID:[Effect of porcine calcitonin in primary hyperparathyroidism (author's transl)]. 94 35

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

Porcine or salmon calcitonin was given, as emergency treatment for 17 patients with hypercalcaemia, mostly of a severe degree. A lowering of serum calcium was achieved in all of 11 patients with primary hyperparathyroidism and in another 4 with malignancies. In most of the patients, the lowering of serum calcium level was accompanied by a pronounced clinical amelioration. This made possible successful parathyroidectomy without complications in the patients with primary hyperparathyroidism. In all patients except one, a decrease in serum creatinine was observed during treatment. Creatinine clearance was studied during calcitonin treatment in 2 patients and showed an increase. Calcitonin was ineffective in 2 of the patients with hypercalcaemia: one with plasmacell sarcoma of the lungs and another one with sarcoidosis. No serious side-effects were observed. Due to its quick action and lack of toxic effects, calcitonin is recommended when a prompt reduction of serum calcium is of vital importance.
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PMID:Acute treatment with calcitonin in primary hyperparathyroidism and severe hypercalcaemia of other origin. 117 65

The case is reported of a 70-year-old female patient with primary hyperparathyroidism and papillary thyroid carcinoma. At the age of 66, the patient had symptoms of hyperparathyroidism and underwent surgery. The operation revealed no adenoma of the parathyroids; instead, by coincidence, a papillary thyroid carcinoma was discovered. The patient was operated on again 2 years later, and only then was a principal cell adenoma of the parathyroids found and removed. Bone biopsies performed at the same time revealed distinct signs of fibroosteoclasia as well as signs of osteomalacia, probably consequent on a former operation of the stomach. Four years after the first symptoms of hyperparathyroidism the patient died of encephalorrhagia due to a brain metastasis of the papillary thyroid carcinoma. Combinations of hyperparathyroidism with thyroid cancers are relatively frequent. In most of these cases the thyroid carcinoma is a medullary (calcitonin producing) carcinoma, whereas papillary carcinomas are rather unusual. It nevertheless seems to be a typical combination, although its pathogenesis is not yet clear.
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PMID:[Primary hyperparathyroidism and papillary thyroid gland carcinoma]. 122 4

Sixty-nine out of a kindred of 100 members covering five generations were examined and studied, and 34 were hypercalcemic. Sixteen subjects were believed, on the basis of laboratory and clinical observations, to have primary hyperparathyroidism. Eight patients were subjected to exhaustive study to identify polyendocrine involvement before neck exploration. No coexisting endocrine abnormalities were found; operation showed multiparathyroid gland involvement in most instances. Measurement of immunoassayable calcitonin and assessment of renal and gut function were carried out in 37 subjects to search out possible causes of "reactive" parathyroid gland hyperfunction. While no such cause-effect relationship was noted for this kindred, 16 of the subjects so tested had serum calcitonin content below the assay limits of sensitivity. What role this apparent lack of calcitonin played in the development of hyperparathyroidism (or vis versa) needs clarification.
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PMID:Familial hyperparathyroidism. Description of a large kindred with physiologic observations and a review of the literature. 124 90

A patient with acute primary hyperparathyroidism treated with mithramycin preoperatively, underwent neck exploration and two enlarged parathyroid glands were excised: one huge adenoma (6g) and another smaller gland. Mithramycin was administered preoperatively to lower life-threatening hypercalcaemia, and parathyroid slices from the huge adenoma removed at surgery were submitted in vitro to various calcium concentrations in the media to determine the influence of calcium on parathyroid adenoma secretory pattern in acute primary hyperparathyroidism. Mithramycin induced a significant decline in calcium levels and significant elevations of calciotrophic hormones (intact PTH, mid-region specific PTH, calcitonin and calcitriol). Significant suppression in PTH output in vitro was achieved by increasing calcium levels in the media. These results exclude autonomous PTH secretion (non-calcium dependent) as a possible aetiology of acute primary hyperparathyroidism. We suggest that a sudden increase in the set-point of the diseased parathyroid cells in the presence of a huge cell mass accounts, in large part, for both the marked hypercalcaemia and elevated PTH levels in this patient.
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PMID:Non-autonomy of parathyroid hormone secretion in acute primary hyperparathyroidism. 128 27

To improve the sensitivity of thallium-technetium subtraction scintigraphy for preoperative localization procedure of enlarged parathyroid glands in primary hyperparathyroidism, we administered calcitonin intramuscularly 4 hours before the scintigraphy in 14 consecutive patients. Injection of calcitonin reduced plasma levels of ionized calcium from 1.47 +/- 0.10 mmol/l to 1.41 +/- 0.09 mmol/l (p less than 0.01). Concomitantly, serum levels of intact parathyroid hormone increased from 6.4 +/- 2.5 pmol/l to 7.9 +/- 2.6 pmol/l (p less than 0.001). The scintigram after calcitonin injection visualized 11 adenomas (sensitivity 78%) compared to only 9 (sensitivity 64%) in conventional scintigrams. In addition, 5 of the adenomas were more distinctly imaged in the scintigram after calcitonin injection, whereas in only one patient was the conventional scintigram better. Thus, the calcitonin injection improved the scintigram in 7 cases and was inferior in only one case (p = 0.031). We conclude that stimulation of parathyroid hormone secretion with calcitonin results in a better preoperative localization of enlarged parathyroid glands in primary hyperparathyroidism.
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PMID:Thallium-technetium subtraction scintigraphy of enlarged parathyroid glands after calcitonin stimulation of parathyroid hormone secretion. 132 52

Calcitonin is a hypocalcaemia producing hormone and is secreted by C-cells of the thyroid. The current study was undertaken on a hypothesis that C-cell hyperplasia may develop in the secondary hyperparathyroidism of chronic renal failure in response to sustained hypercalcaemia. With an immunoperoxidase staining method for calcitonin, C-cell hyperplasia was noted in four of six cases of autosomal dominant polycystic kidney disease and in three of six cases of acquired renal cystic disease, an overall incidence of 58% compared with an incidence of 36% (five of 14) in cases of primary hyperparathyroidism with parathyroid adenoma. Thus, both primary and secondary hyperparathyroidism may trigger C-cell hyperplasia in an attempt to produce a hypocalcaemic effect.
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PMID:C-cell hyperplasia in secondary hyperparathyroidism. 145 30


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