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Results for “Long-Acting Thyroid Stimulator”

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At least 19 recordsLinked to original sources
PubMed1975

Effect of long-acting thyroid stimulator on serum concentration of luteinizing hormone in the rat.

1. The effect of long-acting thyroid stimulator (LATS) on the serum luteinizing hormone (LH) levels of the rat in pro-oestrus has been studied. 2. The injection of three out of four LATS-containing immunoglobulin G fractions caused an increase in amounts of serum LH. 3. Adrenalectomy and dexamethason suppression did not alter this response. 4. Injection of large doses of adrenocorticotrophic hormone did not produce any increase in serum concentrations of LH. 5. It is postulated that LATS may have a direct effect on the release of LH from the pituitary gland.

Adrenal Glands↗
PubMed1978

Detection and properties of TSH-binding inhibitor immunoglobulins in patients with Graves' disease and Hashimoto's thyroiditis.

TSH-binding inhibitor immunoglobulins (TBII) have been detected in patients with Graves' disease and Hashimoto's thyroiditis by using the radioreceptor assay of TSH. In untreated Graves' patients, TBII levels correlated well with thyroidal 99mTc uptake at 30 min and the grade of epithelial hyperplasia of thyroid follicles. There were many Graves' patients whose sera contained high TBII levels but no detectable bioassayable thyroid-stimulating activity (LATS), and in these patients, close correlation was observed between serum levels of TBII and bioassayable LATS-protector activity. TBII were detectable in 2 (10%) of 20 patients with Hashimoto's thyroiditis, both of whom were clinically hypothyroid. The serum or IgG fraction from one of them, however, did not contain any significant LATS, LATS-protector, or human thyroid adenylate cyclase-stimulating activity and caused inhibition of adenylate cyclase stimulation by TSH. In that patient, TBII may be acting to block TSH binding to TSH receptors, thus causing TSH unresponsiveness and hypothyroidism.

Adolescent↗
PubMed1978

An in vitro procedure for the estimation of thyroid hormone releasing factors in sera of thyrotoxic patients.

LATS containing sera and a number of Graves' disease sera stimulated T4 release from mouse thyroids in vitro as determined by RIA, thus confirming the presence of a thyroid hormone releasing factor in sera of thyrotoxic patients. The pattern of stimulation was similar to that previously shown for TSH in terms of T4 release time sequence. cAMP increase and catecholamine inhibition via alpha-adrenergic receptors. In the same in vitro system, neutralization with a human thyroid homogenate showed presence of LATS-Protector (LPA) in LATS negative thyrotoxic sera. The present study describes a simpler procedure for estimating LATS or similar activity, as compared to the McKenzie assay, and suggests identical receptor sites for TSH and other thyroid stimulators.

Animals↗
PubMed1975

Relation of thyroid-stimulating immunoglobulins to thyroid function and effects of surgery, radioiodine, and antithyroid drugs.

Thyroid-stimulating immunoglobulins (T.S.I.) have been detected in the serum of all patients with untreated Graves' disease, and in these patients the levels of T.S.I. correlated significantly with the early uptake of 131I by the thyroid. The frequency of T.S.I. in patients treated solely by antithyroid drugs, by radioiodine, or by partial thyroidectomy was 53 per cent, 50 per cent, and 17 per cent, respectively. The reduced frequency of T.S.I. in the serum of patients treated by drugs or radioiodine was probably due to spontaneous remission, but in the case of partial thyroidectomy the operation itself clearly had a dramatic effect on the serum-T.S;I. These results accorded well with the reported frequency of thyroid autonomy in similar groups of patients and suggested that thyroid-stimulating immunoglobulins were responsible for hyperthyroidism in Graves' disease.

Adenylyl Cyclases↗
PubMed1975

Hyperthyroidism in Tasmania following iodide supplementation: measurements of thyroid-stimulating autoantibodies and thyrotropin.

Serum thyroid-stimulating autoantibodies (LATS and LATS protector) and thyrotropin (TSH) concentrations were measured in the serum of 30 patients with hyperthyroidism living in Tasmania who developed their disease following correction of iodine deficiency by addition of iodate to the bread. Patients were grouped according to thyroid scan results. None of 8 patients with autonomous thyroid nodules had thyroid-stimulating autoantibodies. These were present in both of the patients with uniform thyroid scans and 14 of 20 patients (70%) with irregular scans without demonstrated localized autonomy. Serum TSH, measured by immunoassay of concentrated serum extracts, was 0.15 muU/ml or less in all patients, below the range of 0.35 to 2.60 muU/ml found in normal subjects. Only 6 (20%) of the 30 patients failed to show either localized autonomy or thyroid-stimulating autoantibodies. In most regards these patients resembled those with antonomous nodules. The findings support the conclusion that the increased incidence of phyerthyroidism in Tasmania was due to an increased supply of iodine to patients with latent hyperthyroidism whose thyroid glands, due to the presence of toxid nodule(s) or thyroid-stimulating autoantibodies, were unresponsive to control by TSH deprivation. There was no evidence for additional pathogenic mechanisms

Adult↗
PubMed1978

Do thyroid-stimulating immunoglobulins cause non-toxic and toxic multinodular goitre?

The prevalence of serum thyroid-stimulating immunoglobulins (T.S.I.) in a variety of thyroid diseases was determined in 96 patients and 35 normal controls. Significantly elevated levels of T.S.I. were found not only in patients with Graves' disease and Hashimoto's thyroiditis but also in those with non-toxic and toxic multinodular goitre, whereas patients with a single autonomously functioning thyroid nodule, with subacute thyroiditis, and with "hyperthyroiditis" had levels which did not differ from those in the controls. We postulate that non-toxic multinodular goitre, like Graves' disease, may result from increased circulating T.S.I., which in some cases may be present in sufficient concentration to cause thyrotoxicosis.

Adolescent↗
PubMed1979

Thyroid-stimulating immunoglobulins do not cause non-autonomous, autonomous, or toxic multinodular goitres.

Thyroid-stimulating immunoglobulins (TSIs) were measured by radioreceptor assay in serum from 51 patients with a multinodular goitre, divided into four groups according to thyroid function, and in 30 normal people. In 9 patients who were euthyroid and had non-autonomous thyroid function and in 6 patients who were hyperthyroid, TSI index was normal . Of 21 euthyroid patients with autonomous function only 2 had a slightly abnormal TSI index (66 in both, normal greater than or equal to 68). Another series of 15 clinically euthyroid patients also had a normal TSI index. These results suggest that TSIs do not contribute to the pathogenesis of multinodular goitre, as has been suggested by others.

Adult↗
PubMed1975

Treatment of hyperthyroidism in pregnancy with propylthiouracil and methimazole.

Twenty-one women were studied who had received propylthiouracil or methimazole during 26 pregnancies. Four of the infants had a goiter at birth, and 3 of these had neonatal thyrotoxicosis. In 2 children neonatal thyrotoxicosis was not evident at birth because of maternal antithyroid therapy. Five children had congenital defects. Two mothers were responsible for 4 of the children with abnormalities, and both mothers had been treated with thiourea drugs for long periods, ranging from 7 to 11 years. The majority of children who are exposed to these drugs in utero appear to have no subsequent ill effects. However, prolonged therapy with these agents may be undesirable.

Abnormalities, Drug-Induced↗