Level Of Long-acting Thyroid Stimulator Research Articles

Relation between thyroid function and serum levels of long-acting thyroid stimulator.

Bioassays of long-acting thyroid stimulator (LATS) were performed in three groups of subjects: in normal controls, in thyrotoxic patients before and serially after 131-I treatment, and in patients with hypopituitarism. Of the untreated thyrotoxic patients, 27.7% had raised serum LATS levels initially. There was no correlation between the relapse rate after 131-I therapy and the initial or subsequent LATS titres: in particular, thyrotoxicosis sometimes recurred after an initially high LATS titre had fallen into the normal range. The distribution of the results of LATS assays in the hypopituitary patients was significantly different from that in the normal subjects; 4 out of 27 hypopituitary patients had LATS levels above the normal range, although they had no thyrotoxicosis. On the other hand, the majority of the patients with hypopituitarism, 19 out of 27, had LATS titres below the mean normal level, possibly due to deficiency of a substance we have termed pseudo LATS. These results raise doubts about a direct causative role for LATS in most cases of thyrotoxicosis.

Suppressibility of Thyroid Function Despite High Levels of Long-Acting Thyroid Stimulator

The long-acting thyroid stimulator (LATS) has been said to be the pathogenetic factor of the thyroid autonomy or hyperfunction in Graves' disease. Two patients had the ophthalmopathy and pretibial myxedema of Graves' disease occurring with Hashimoto's thyroiditis. Both patients had suppressed thyroid function in response to exogenous thyroid hormone in spite of the presence of high levels of LATS in their serums. The long-acting thyroid stimulator may not be the cause of the fixed thyroid function of Graves' disease.

Neonatal Hyperthyroidism in an Infant Born of an Euthyroid Mother

An infant with neonatal hyperthyroidism was born to an euthyroid mother previously treated for hyperthyroidism with sodium iodide I 131. Measurable levels of long-acting thyroid stimulator (LATS) were found in mother and infant. A review of previous cases of neonatal hyperthyroidism in which LATS determinations have been performed indicates the importance of LATS in the pathogenesis of this condition. Infants born of mothers with hyperthyroidism or with a history of treated hyperthyroidism should be evaluated in the neonatal period for hyperthyroidism, particularly if measurable levels of LATS have been found in the mother's serum late in pregnancy. Early treatment of neonatal thyrotoxicosis with propylthiouracil is recommended for severely affected cases.

The effect of radioablation of the thyroid gland in Graves' disease with high levels of long-acting thyroid stimulator (LATS)

Radioablation of the thyroid gland (with large doses of 131I) was attempted in thirteen carefully selected patients with Graves' disease, ophthalmopathy and (in five cases) pretibial myxedema, on the basis of previous suggestions that such therapy might ameliorate the ophthalmopathy and dermopathy. All these patients had been treated with conventional doses of 131I for their hyperthyroidism from one to eight years previously and were either euthyroid or (controlled) hypothyroid at the time of ablation. The patients were selected on the basis of persistent high titers of LATS (long-acting thyroid stimulator); the LATS and the major clinical manifestation (e.g., ophthalmopathy) had to be reasonably stable for at least one year in each patient. Because of the previous relative stability of these parameters, it was considered that each patient might act as his own control. In addition, five of these patients had circulating thyroid autoantibodies. Despite the hypothyroid status of six patients, residual thyroid parenchyma was readily demonstrable by routine means prior to attempted ablation. Complete ablation was different even with large and sometimes repeated doses of 131I. With a 1 mc. (millicurie) scanning dose, complete ablation seemed to be achieved in four patients; however with TSH (thyroid-stimulating hormone) and a 5 mc. dose, residual thyroid parenchyma was demonstrated in two of these four. In the eleven patients with such minimal residual functioning thyroid parenchyma, the twenty-four hour radioactive iodine uptake values were less than 1 per cent in each patient. Thyroxine therapy was administered to all. The longest follow-up is now two years. In none of these patients was there any significant change in the ocular manifestations or the pretibial myxedema. There were no significant changes in LATS titers. Thyroid autoanlibodies, present in five, declined in every inslance, twice to zero. Apart from the decline in thyroid auloantibodies, therefore, there has been no demonstrable effect of total or “almost total” thyroid ablation in terms of the exophthalmos, pretibial myxedema or LATS assays. The two year period may not be long enough to demonstrate that removal of the thyroid “antigen” lowers LATS titers. However the period of observation now seems long enough to suggest that removal of the thyroid “antigen” does not cause LATS to decline significantly, particularly since thyroid autoantibodies did decline significantly. If this continues to be true, either there is an antigenic stimulus for LATS in some tissue oher than the thyroid gland, or LATS arises without prior antigenic stimulation.

Observations against a causal relationship between the long-acting thyroid stimulator and ophthalmopathy in Graves' disease.

ABSTRACT An analysis was made of observations carried out in 65 patients with ophthalmopathy of Graves' disease, in an attempt to identify any statistical correlation between the level of long-acting thyroid stimulator in the blood of the patients, the severity of opthalmopathy and the incidence of preceding radioiodine therapy. Thirty-five of the sera did not give a positive response in the bioassay for the thyroid stimulator; with 17 a positive response up to 300% at 9 hr with 0.5 ml/mouse was found; and with the remaining 13 the value was greater than 300%. There was no correlation between these values and the severity of ophthalmopathy or the assessment of whether or not the eye condition was progressing at the time that serum was obtained. There was no correlation between the incidence of preceding radioiodine therapy and the severity of ophthalmopathy or the value obtained on assay of serum for the long-acting thyroid stimulator. With one additional patient, observations over a period of 15 months s...

Humoral factors in the pathogenesis of Graves' disease.

Humoral factors in the pathogenesis of Graves' disease.J M McKenzieJ M McKenziePublished Online:01 Jan 1968https://doi.org/10.1152/physrev.1968.48.1.252MoreSectionsPDF (11 MB)Download PDF ToolsExport citationAdd to favoritesGet permissionsTrack citations ShareShare onFacebookTwitterLinkedInWeChat Previous Back to Top Download PDF FiguresReferencesRelatedInformation Cited ByHyperthyroidism, Exophthalmos, and Goiter: Historical Notes on the OrbitopathyThyroid, Vol. 20, No. 3TSH Receptor AntibodiesThyroid, Vol. 17, No. 10Course of Proptosis in Patients With Graves' Disease After Endoscopic Orbital DecompressionThe Laryngoscope, Vol. 109, No. 8Thyroid DysfunctionEndocrinology and Metabolism Clinics of North America, Vol. 17, No. 3The Spectrum and Significance of Autoantibodies Reacting with the Thyrotropin ReceptorEndocrinology and Metabolism Clinics of North America, Vol. 16, No. 2Ocular Manifestations of Graves' Disease: A Review29 June 2016 | Journal of the Royal Society of Medicine, Vol. 77, No. 11Graves' ophthalmopathy. A clinical and immunologic reviewSurvey of Ophthalmology, Vol. 26, No. 1NOMENCLATURE OF THYROID-STIMULATING ANTIBODIESThe Lancet, Vol. 305, No. 7917CONGENITAL-MALFORMATION RATES AND SPONTANEOUS-ABORTION RATESThe Lancet, Vol. 305, No. 7917Association of the long-acting thyroid stimulator protector with the immunoglobulin G fraction of serum from patients with thyrotoxicosisBiochimica et Biophysica Acta (BBA) - Protein Structure, Vol. 379, No. 1Does lats cause hyperthyroidism in Graves' disease?Metabolism, Vol. 21, No. 9Current status and future prospects for research in psychosomatic medicineJournal of Psychiatric Research, Vol. 8, No. 3-435S-sulfate uptake by mouse harderian gland: Effect of serum from patients with Graves' diseaseMetabolism, Vol. 20, No. 4The lipolytic activity of long-acting thyroid stimulatorBiochimica et Biophysica Acta (BBA) - Lipids and Lipid Metabolism, Vol. 231, No. 2Characterisation of long-acting thyroid stimulator γG binding proteinBiochimica et Biophysica Acta (BBA) - Protein Structure, Vol. 229, No. 3Studies of homologous immunization with mouse harderian glandMetabolism, Vol. 20, No. 3In vitro influence of thyrotropin or long-acting thyroid stimulator on mouse thyroid membrane potentialMetabolism, Vol. 19, No. 10Thyroid gland in Graves' disease: Victim or culprit?Metabolism, Vol. 19, No. 10More about Australia Antigen and HepatitisThe Lancet, Vol. 296, No. 7668L.A.T.S.The Lancet, Vol. 296, No. 7668Stimulation of thyroid adenyl cyclase activity and cyclic adenosine 3′,5′-monophosphate by long-acting thyroid stimulatorMetabolism, Vol. 19, No. 6VI—THE THYROID GLANDThe Lancet, Vol. 295, No. 7661The nature of the interaction between thyroid stimulating γG-globulin (long-acting thyroid stimulatory) and thyroid tissueBiochimica et Biophysica Acta (BBA) - General Subjects, Vol. 208, No. 2The thyroid-stimulating properties of long-acting thyroid stimulator γG-globulin subunitsBiochimica et Biophysica Acta (BBA) - General Subjects, Vol. 192, No. 2THYROTOXICOSIS: DRUGS, SURGERY, OR RADIOIODINE?The Lancet, Vol. 294, No. 7627The distribution of the long-acting thyroid stimulator among γG-immunoglobulinsBiochimica et Biophysica Acta (BBA) - Protein Structure, Vol. 188, No. 1Iodide goiter and the pharmacologic effects of excess iodideThe American Journal of Medicine, Vol. 47, No. 1The effect of radioablation of the thyroid gland in Graves' disease with high levels of long-acting thyroid stimulator (LATS)The American Journal of Medicine, Vol. 46, No. 2EMOTION AND NON-SPECIFIC INFECTION AS POSSIBLE ÆTIOLOGICAL FACTORS IN GRAVES' DISEASEThe Lancet, Vol. 292, No. 7561LEUCOCYTE-HEXOKINASE ISOENZYMES IN DOWN'S SYNDROMEThe Lancet, Vol. 292, No. 7561 More from this issue > Volume 48Issue 1January 1968Pages 252-310 Copyright & PermissionsCopyright © 1968 by American Physiological Societyhttps://doi.org/10.1152/physrev.1968.48.1.252PubMed4865519History Published online 1 January 1968 Published in print 1 January 1968 Metrics

EVIDENCE OF A NORMALLY FUNCTIONING PITUITARY TSH SECRETION MECHANISM IN A PATIENT WITH A HIGH BLOOD LEVEL OF LONG-ACTING THYROID STIMULATOR.

A thyrotoxic woman became grossly hypothyroid after treatment with 131I. Bio-assay of her serum showed the presence of a high level of long-acting thyroid stimulator (LATS). By application of a concentration procedure which extracts TSH but not LATS, it was shown that her serum contained a high level of TSH, in addition to the LATS. After the patient had received 0.4 mg of thyroxine daily for 2 weeks, there was no change in the LATS content of her serum, but TSH was no longer detectable, nor was TSH detectable in a serum sample taken when the patient was thyrotoxic before receiving the 131I therapy. It is concluded that the patient's pituitary gland secreted TSH when the blood thyroxine level was below normal and that this secretion was stopped by the administration of thyroxine in suppressive dosage. There was no evidence of TSH secretion when the patient was in the untreated thyrotoxic state. These observations indicate that there is no defect in the control of TSH secretion in Graves' disease. This is in accord with the evidence that LATS is not of pituitary origin.

The response of hypophysectomized mice to injections of human serum containing long-acting thyroid stimulator.

Human serum, obtained from a patient with Graves’s disease and containing a high level of long-acting thyroid stimulator, elicited highly significant responses when injected into hypophysectomized mice. The mean response did not differ significantly from that elicited in a control group of intact mice. This shows that the site of action of the abnormal thyroid stimulator is not the pituitary gland and makes it likely that the material acts directly on the thyroid.