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Results for “THYROCALCITONIN”

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At least 19 recordsLinked to original sources
PubMed1980

Spinal cord injury: effect of thyrocalcitonin on calcium, magnesium and phosphorus in paraplegic rats.

Calcium, magnesium and phosphorus balances were studied in 20 paraplegic rats (T5) fed ad libitum an 18% casein diet. Ten of the paraplegic animals were treated daily with 4MRC (Medical Research Council) units of thyrocalcitonin. Ten sham-operated rats served as controls. Spinal cord transection caused an immediate increase in urinary excretion of calcium, 550 +/- 70 micrograms/24 hr, compared with controls levels, 257 +/- 85 micrograms/24 hr. Paraplegia also resulted in an elevated excretion of fecal calcium, 39 +/- 5 mg/24 hr, phosphorus, 42 +/- 7 mg/24 hr, and magnesium, 4.6 +/- 0.8 mg/24 hr, compared with that of controls, 26 +/- 6 mg/24 hr, 32 +/- 6 mg/24 hr and 2.7 +/- 0.8 mg/24 hr for calcium, phosphorus and magnesium, respectively. Administration of thyrocalcitonin to paraplegic rats further increased urinary excretion of calcium, 835 +/- 186 micrograms/24 hr. However, fecal losses of calcium, 19 +/- 5mg/24 hr, phosphorus, 31 +/- 6mg/24 hr, and magnesium, 2.6 +/- 0.4mg/24 hr, which were elevated following spinal cord transection, were markedly reduced after thyrocalcitonin treatment. As a result, balances of these compounds, which were depressed in rats following spinal cord transection, were "normalized" after treatment with thyrocalcitonin. It would seem, therefore, worthwhile to study the effect of thyrocalcitonin in spinal cord injured humans in an effort to determine whether or not it would be helpful in improving mineral balances.

Animals↗
PubMed1982

[Serum results following experimental fracture alignment and thyrocalcitonin treatment (author's transl)].

Serum alkaline phosphatase activity, serum calcium and phosphorus concentrations were determined during bone healing under treatment of thyrocalcitonin. The right tibiae of 160 albino rats were osteotomized. Of these, 80 were treated with thyrocalcitonin. During the 50-day observation period, the calcium level in the thyrocalcitonin-treated sample never differed significantly from that of the control group. However, the alkaline phosphatase activity and the serum phosphorus level significantly differed from the control levels (P less than 0.05) during 4 days of observation. The increased serum alkaline phoshatase activity--a sign of osteoblastic activity--suggests that thyrocalcitonin may aid in osteogenesis and bone healing.

Alkaline Phosphatase↗
PubMed1982

[Experimental studies on the effect of thyrocalcitonin on secondary bone healing (author's transl)].

The effect of thyrocalcitonin on secondary bone healing was studied in 180 Sprague-Dawley-rats. The right tibia of all the rats was osteotomized. Half of the animals was treated with thyrocalcitonin. Until the 60th postoperative day, the increase in 99mTc-methylendiphosphonate activity was measured and significant differences in ratios were noted. Between the postoperative days 10 to 25, there was a significant difference in the impulse quotients between the thyrocalcitonin and untreated rats (P less than 0.05). These results indicate that thyrocalcitonin may aid in secondary bone healing.

Animals↗
PubMed1968

Medullary carcinoma and thyrocalcitonin.

Seven patients with medullary carcinoma of the thyroid were investigated, and the thyrocalcitonin activity of the primary tumours, metastatic deposits, and the serum was estimated.Medullary carcinomas of the thyroid with amyloid stroma contain 100 to 600 times more thyrocalcitonin than normal thyroid tissue, and lymph nodes with metastatic deposits are equally rich in the hormone. High values of thyrocalcitonin are also found in the blood of these patients. Medullary carcinoma of the thyroid with amyloid stroma is the first disease to be recognized in which there is hypersecretion of thyrocalcitonin.

Adenocarcinoma, Papillary↗
PubMed1992

[Malignant endocrine tumor of the pancreas associated with high blood thyrocalcitonin levels].

A case of thyrocalcitonin-secreting endocrine tumour of the pancreas is reported. Endocrine pancreatic tumours are neoplasias evolving over a long period; most of them are multisecreting, usually with a predominant secretion responsible for clinical symptoms. In this particular case the retrospective diagnosis of a thyrocalcitonin-secreting tumour of the pancreas was made by immunocytochemical study of the pancreatectomy specimen. One year after pancreatectomy, the persistence of clinical signs and a plasma thyrocalcitonin level higher than 25,000 pg/ml led to the discovery of a liver metastasis. An immunocytochemical study of the segmental hepatectomy specimen showed a single population of thyrocalcitonin-secreting cells identical with those found in the pancreatic tumour. In this context, radioimmunological assays of peptides and immunocytochemistry seem to be the best diagnostic methods.

Aged↗
PubMed1975

Stimulation of thyrocalcitonin secretion by ethanol in patients with medullary thyroid carcinoma--an effect apparently not mediated by gastrin.

We have compared the effects of oral and intravenous ethanol on the secretion of both thyrocalcitonin and gastrin in five patients with medullary carcinoma of the thyroid. Ethanol caused a moderate rise in plasma thyrocalcitonin to 316% +/- 343% of baseline when given intravenously and to 197% +/- 106% of baseline when given orally. Only oral ethanol caused a measurable rise in serum gastrin levels. Serum calcium did not change significantly from baseline during either oral or intravenous administration. The results suggest that stimulation of thyrocalcitonin secretion by ethanol is not secondary to increased secretion of gastrin nor to the induction of hypercalcemia. Neither oral nor intravenous ethanol appears to be as effective as intravenous pentagastrin in testing for the presence of medullary carcinoma.

Administration, Oral↗
PubMed1987

Thyrocalcitonin-containing cells in the Di George anomaly.

The Di George syndrome is an anomaly characterized by the complete or partial absence of derivatives of the third and fourth pharyngeal pouches often associated with defective development of the third, fourth, and sixth aortic arches leading to absence or hypoplasia of the thymus and parathyroid glands and to cardiovascular anomalies. The fifth pharyngeal pouch, often considered a part of the fourth pouch, gives rise to the ultimobranchial body (UB), which becomes incorporated into the thyroid gland and is thought to be the source of thyroid C cells. Robinson suggested that complete or partial absence of the UB should be considered a part of the Di George anomaly. To substantiate this theory, the thyroid glands of 11 patients with the Di George syndrome and 11 age-matched control infants were examined immunohistochemically using the immunoperoxidase technique for presence or absence of thyrocalcitonin (TC)-containing cells. Only three of 11 patients with the Di George syndrome had TC-containing cells in their thyroid glands (27 per cent), and nine of 11 control infants had these cells (82 per cent). It is concluded that thyroid C cell deficiency is present in most patients with Di George anomaly, suggesting a relationship between these cells and development of derivatives of the third through fifth visceral pouches. Furthermore, there is a spectrum of deficiency of thyroid C cells in these individuals comparable with the spectrum of partial to complete absence of third and fourth pharyngeal pouch derivatives regarding thymus and parathyroid glands. Immunostaining for TC of the lungs of all infants with the Di George syndrome and control infants revealed similar numbers of thyrocalcitonin-containing cells in both groups. Asynchronous development of thyroid and lung thyrocalcitonin-containing cells in those with the Di George syndrome favors the theory that the latter develop independently of derivatives of the third through fifth visceral pouches. This study further supports a neural crest origin of the Di George anomaly and strengthens the concept that the Di George anomaly is a neurocristopathy.

Calcitonin↗
PubMed1987

Plasma thyrocalcitonin and parathyroid hormone concentrations in early neonatal hypocalcaemia.

During the first week of life serum calcium, phosphorus, magnesium, immunoreactive thyrocalcitonin hormone, and parathyroid hormone concentrations were determined daily in 36 preterm and 29 small for gestational age, full term, healthy infants. Preterm babies with early neonatal hypocalcaemia had significantly higher concentrations of serum thyrocalcitonin hormone in the first four days of life than normocalcaemic preterm babies. Parathyroid hormone concentrations were similar in hypocalcaemic and normocalcaemic infants. In contrast, in the full term group no significant differences were detected in thyrocalcitonin hormone and parathyroid hormone patterns between hypocalcaemic and normocalcaemic subjects. This suggests two different pathogeneses for early hypocalcaemia in low birthweight infants. Hyperthyrocalcitoninaemia seems to be the main determining factor in preterm infants, while a non-hormonal pathogenesis should be considered in full term infants who are small for gestational age.

Calcitonin↗