The Long Acting Thyroid Stimulator (LATS) in Thyrotoxicosis

Abstract

For some time evidence has accumulated regarding the association of thyrotoxicosis with autoimmune phenomena. Varying degrees of the lymphadenoid changes characteristic of Hashimoto’s disease are commonly observed in the glands of patients with thyrotoxicosis and a high incidence of antibodies to thyroglobulin and the thyroid cytoplasmic antigen can be demonstrated. In addition, 30% of patients have gastric parietal cell antibodies while the association with pernicious anaemia, a well established autoimmune disorder, is much greater than would be expected by chance. Furthermore, among the first degree relatives of patients with Hashimoto’s disease there are many cases of hyperthyroidism. A notable advance in this field was provided by the work of Adams and Purves (1957) who established a new assay for pituitary TSH depending upon the release of radioisotope from the thyroid of guinea pigs prelabelled with ¹³¹I. Whereas injection of TSH led to an increase in blood radioactivity reaching a maximum by 2 to 3 h, Adams and Purves found that the serum of patients with Graves’ (Basedow’s) disease caused a rise in blood ¹³¹I which was maximal at 7 h or later. The assay was improved by McKenzie (1958) using mice. The active component has been termed the ‘long acting thyroid stimulator’ (LATS).