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 is commonly associated with Hashimoto's thyroiditis. The raised TSH levels might induce hyperparathyroidism, as suggested by some experimental data. It might also explain the development of hyperparathyroidism after neck irradiation and lithium therapy.
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PMID:[Hyperparathyroidism and Hashimoto's thyroiditis: coincidence or consequence?]. 237

TSH serum levels and thyroid function in 32 patients with primary hyperparathyroidism and hypercalcemia were compared to those of 30 age and sex-matched normal subjects. Serum T3 and T4 concentrations in hyperparathyroidism were not different from normal. However, basal serum TSH concentrations measured with an ultrasensitive immunoradiometric assay were significantly lower than normal (1.09 +/- 0.49 vs 2.06 +/- 0.85 mU/l, p less than 0.001). In hyperparathyroidism, TSH, but not T4 or T3, was negatively correlated with serum calcium, not with iPTH. The increase in TSH (delta TSH) 30 min after the iv injection of TRH was also significantly blunted in patients with primary hyperparathyroidism; delta TSH was highly correlated with basal TSH in hypercalcemic patients. The basal TSH concentration was higher and no longer different from normal (1.70 +/- 1.2 mU/l) 2 to 12 months after removal of the parathyroid adenoma, when serum calcium was normalized, whereas T3 and T4 did not change. A low basal TSH with normal T4 and low T3 was found in 13 patients with hypercalcemia of malignancy. In these patients, TSH increased after treatment of hypercalcemia with 3-amino-l,hydroxypropylidene-1, 1-bisphosphonate, whereas T4 did not change. The results suggest that the set point of pituitary thyroid feedback control could be decreased in chronic hypercalcemia and that hypercalcemia could render the thyroid more sensitive to TSH.
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PMID:Low basal thyrotropin with normal thyroid function in primary hyperparathyroidism. 251 13

The prevalence of thyroid, parathyroid, and salivary abnormalities was determined in 91 women who received an average of 112 fluoroscopic chest examinations during pneumothorax treatment for tuberculosis more than 40 yr previously and in 72 women treated for tuberculosis by other modalities. Thyroid abnormalities were determined by physical examination, scintiscans, and measurements of serum free T4 index, TSH, and thyroid microsomal antibodies. Thyroid nodules were diagnosed in 7.7% of the exposed and 4.2% of the comparison group (prevalence ratio, 1.8; 90% confidence interval 0.6-5.7). Autoimmune thyroid disease was diagnosed in 15.2% of the exposed and 6.9% of the comparison group (prevalence ratio, 2.2; 95% confidence interval, 0.8-6.2). No salivary tumors were detected. Two exposed women and 1 comparison woman had primary hyperparathyroidism. Although absorbed dose to the thyroid could not be precisely determined, approximately 60 rads would be expected to yield the observed excess of thyroid nodules. While the prevalence ratios were not significantly increased in the exposed group, the results suggest that susceptibility of the thyroid to nodules from cumulative radiation doses of this magnitude could be increased even when the doses are accumulated over years and that such x-ray exposure of the thyroid gland may predispose the patient to the development of autoimmune disease.
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PMID:Thyroid, parathyroid, and salivary gland evaluations in patients exposed to multiple fluoroscopic examinations during tuberculosis therapy: a pilot study. 333 10

The influence of changes in the serum calcium concentration on TSH secretion was evaluated in patients with primary hyperparathyroidism and idiopathic hypoparathyroidism and in normal subjects. Serum calcium concentrations were 12.7 +/- 0.8, 9.0 +/- 0.4, and 5.7 +/- 0.5 mg/100 ml in hyperparathyroid, normal, and hypoparathyroid subjects, respectively, and were significantly different from each other. Serum T3 and T4 concentrations were comparable among the three groups. The basal serum TSH concentration was highest in hypoparathyroid, lowest in hyperparathyroid, and intermediate in normal subjects. However, all values were within normal limits and were not significantly different from each other. TRH-stimulated TSH secretion was significantly greater in hypoparathyroid patients and significantly less in hyperparathyroid patients than in normal subjects, respectively. The TSH response to TRH was normalized when the serum calcium concentration was normalized by parathyroidectomy in a hyperparathyroid patient or by 1 alpha-hydroxyvitamin D3 administration in a hypoparathyroid patient. To further clarify the mechanism responsible for the modified TSH response to TRH in the hypercalcemic state, rats were made chronically hypercalcemic by the administration of 1 alpha-hydroxyvitamin D3 (0.2 micrograms/100 g BW, ip, for 10 days) and 3% calcium chloride in drinking water. The pituitary TSH content of hypercalcemic rats was significantly greater than that of control rats. The results suggest that decreased TSH secretion produced by chronic hypercalcemia is due to diminished TSH release, rather than to decreased pituitary TSH reserve.
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PMID:Thyrotropin secretion in patients with hyperparathyroidism or hypoparathyroidism: effect of serum calcium on thyrotropin release. 640 63

The responses of TSH and PRL to intravenous doses of 500 micrograms of TRH were investigated in 26 patients with primary hyperparathyroidism. Fourteen patients (54%) showed low responses of TSH with peak values of less than 5 microU/ml (Group A). Twelve patients showed normal responses of TSH to TRH (Group B). Among the 26, 12 cases belonging to Group A and eight in Group B were reexamined after the correction of serum calcium level by parathyroidectomy. After successful treatment, the responses of TSH to TRH in six of the 12 patients in Group A returned to normal, whereas those in the remaining six were unchanged. The responses in the eight patients in Group B after surgery were not changed when compared to those before treatment. The basal values of PRL and the responses of PRL to TRH were normal in all patients and did not change after treatment. We showed that patients with primary hyperparathyroidism have a high incidence (54%) of suppressed TSH response to TRH. Hypercalcemia was obviously one of the causative factors in inducing this abnormality in six patients. However, persistently suppressed responses of TSH to TRH were observed in the other six patients in Group A even after the correction of the serum calcium level by surgery. This finding suggests a primary failure of the TSH-regulatory mechanism in some cases of primary hyperparathyroidism.
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PMID:The suppression of TSH in the presence of the normal PRL responses to TRH out of 26 patients with primary hyperparathyroidism. 641 19

To investigate whether chronic endogenous hypercalcemia influences TSH and/or PRL release from pituitary thyrotrophs and lactotrophs in man, 10 patients with endogenous hypercalcemia, due either to cancer or to primary hyperparathyroidism, were injected with 25 micrograms TRH iv. The TSH and PRL responses were compared with those obtained in an age-, sex-, and weight-matched group of patients comprised of 10 normocalcemic individuals with other diseases. The mean maximal TSH response in the hypercalcemic group (3.7 +/- 0.4 microU/ml) was 46% lower than in the normocalcemic group (6.8 +/- 1.2 microU/ml; p less than 0.02). Similarly, the mean maximal PRL response was 45% lower in the hypercalcemic (31 +/- 5 ng/ml) than in the normocalcemic patients (57 +/- 9 ng/ml; p less than 0.05). Feasible mechanisms behind this inhibitory influence of chronic endogenous hypercalcemia on TSH and PRL responsiveness are discussed.
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PMID:Effect of chronic endogenous hypercalcemia on prolactin and thyrotropin responsiveness in man. 644 10

The clinical and morphological aspects of occult sclerosing carcinoma of the thyroid are presented on the basis of a ten-year review of the surgically removed thyroids in Geneva and from the study of thyroid glands obtained from 133 consecutive autopsies. The 15 cases found in the surgical material represented 7.7% of all malignant thyroid tumours and one fifth of the papillary carcinomas. Occult tumours are found at a mean age of 46.6 years and predominate in women. Clinically, two thirds presented as nodular goiters, two cases as primary hyperplasia and one as primary hyperparathyroidism. Three out of 15 cases presented clinically with a cervical lymph node metastasis. Treatment was conservative in all cases and consisted of subtotal thyroidectomy and/or elective lymphadenectomy, followed by medical suppression of TSH. Follow-up in 11 cases showed a single recurrence in a cervical lymph node, while the other 10 cases have been disease free for 4 to 13 years. In the autopsy series 3 thyroid glands (2.3%) contained occult tumours, two of which were microcarcinomas. The Genevan series compares with other European and American studies but differs from the much higher incidence in the Japanese.
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PMID:[Occult papillary thyroid cancer]. 707 79

This study deals with the setting up of human serum calcitonin radioimmunoassay (hCT-RIA) using the high titer and specific antibody which was prepared by our own laboratory. The final dilution of the antibody titer was 1:1,200,000 when the binding rate of Bo/T was 30%. The antibody's affinity constant (Kd) was 2.25 x 10(11) L/M. No cross reaction was found between the antibody and the following eight different peptide hormones and proteins, viz.: TSH, T3, T4, ACTH, PTH, BGP, Insulin and Gastrin. The coefficients variation of intra and inter assay were 3.2% and 9.0%, respectively. The mean recovery rate of CT was 99.8%. The sensitivity of this assay was 9.4 pg/ml. The examination of this methodology showed that all its indices met the demands of RIA. There was no difference in the mean value of serum CT between the two sexes in 232 normal subjects, but the serum CT concentration in those aged of sixty and over of men and women, were much lower than those aged of fourty group. Mean CT concentration was low in the patients with primary osteoporosis, but were significantly higher in those suffering from medullary thyroid carcinoma, primary hyperparathyroidism crisis and chronic renal failure.
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PMID:[The setting up of human serum calcitonin radioimmunoassay and its clinical application]. 1045 98

Hyperthyroidism is frequently associated with hypercalcemia, which usually subsides after successful treatment of hyperthyroidism. Moreover, thyroid nodules are frequently detected by preoperative thyroid ultrasound in patients with primary hyperparathyroidism. Sensitised by the observation of a patient with coexisting hyperthyroidism and hyperparathyroidism we prospectively evaluated thyroid nodules in euthyroid patients with hyperparathyroidism by thyroid scintigraphy. Whereas the first patient with hyperparathyroidism was hyperthyroid the subsequent four patients with hyperparathyroidism and thyroid nodules had normal fT3 and fT4. Two patients had hypercalcemia and nephroureterolithiasis. Three patients suffered from hypercalcemia and bone pain due to osteoporosis. In the hyperthyroid patient hypercalcemia persisted after euthyroidism was achieved intact parathyroid hormone was found to be elevated. Subsequently, thyroid nodules, detected by preoperative ultrasound in four euthyroid patients with primary hyperparathyroidism, were identified as compensated hot nodules by thyroid scintigraphy. All patients underwent combined subtotal thyroidectomy and parathyroid resection. Histology showed hyperplastic parathyroid glands in one patient and a single parathyroid adenoma in four cases. Postoperatively calcium and PTH levels returned to normal and TSH levels increased in all patients. Persistence of hypercalcemia after successful treatment of hyperthyroidism should be reason for the determination of parathyroid hormone. Thyroid nodules detected by preoperative ultrasound in patients with hyperparathyroidism living in areas of iodine deficiency should be further evaluated by scintigraphy even if TSH is normal. In the case of hot thyroid nodules both parathyroid and partial thyroid resection should be performed.
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PMID:Coincidence of hot thyroid nodules and primary hyperparathyroidism. 1048 41

Primary hyperaldosteronism is associated with other endocrinology pathologies, like pheochromocytoma, Cushing's syndrome, hyperprolactinemia, primary hyperparathyroidism and a type of multiple endocrine neoplasia. Furthermore, association between hyperaldosteronism and thyroid diseases were already pointed out. Aim of the study was to value the prevalence of some thyroid diseases in a series of patients with primary hyperaldosteronism. We studied 105 consecutive patients with primary hyperaldosteronism, 43 (40.95%) with adrenal adenoma, 62 (50.05%) with bilateral adrenal hyperplasia and a control group of 223 patients with essential arterial hypertension. In all patients we tested thyroid function (FT3, FT4, TSH), thyroid antibodies (AbTPO, AbTG) and, sometimes, thyroid morphology by ultrasonography (US scan). The results of the study show that thyroid disfunction occur in 28.6% of patients with primary hyperaldosteronism and in 16.6% of patients with essential hypertension, with a statistically significative difference (chi2 = 0.012). At present, the relationship between primary hyperaldosteronism and thyroid diseases is unclear, but it can be hypothesized that there are common pathogenetic mechanisms, like an imbalance between various growth factors. Further studies are necessary to confirm the results of our study.
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PMID:[High prevalence of thyroid disfunction in primary hyperaldosteronism]. 1620 15


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