Familial studies of autoimmune thyroiditis.
Explore the source record for details and available documents.
Biomedical subjects
Publications and source records attributed to R Hall.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
The TSH responses to the catecholamine depleting agent monoiodotyrosine (1 g po) and the dopamine receptor blocking drug metoclopramide (10 mg po) have been compared in euthyroid and hypothyroid subjects. Both drugs lead to a prompt and significant rise in TSH levels (peak values at 60-75 min) which is very much greater in hypothyroid than euthyroid subjects. The findings lend further support to the inhibitory role of dopamine in the control of TSH release in man, since TSH release follows either dopamine depletion with monoiodotyrosine or dopamine receptor blockade with metoclopramide.
Explore the source record for details and available documents.
Explore the source record for details and available documents.
Female PVG/c rats, thymectomized on weaning and given 4 courses of whole body irradiation to a total dose of 1000 rads, developed experimental autoimmune thyroid disease (EAITD) as assessed by histological evidence of thyroiditis and circulating levels of antithyroglobulin antibodies. Hypothyroidism resulted. Induction of the disease was associated with a highly significant fall in T lymphocyte numbers. Eight weeks after their last dose of irradiation the animals commenced treatment with Cyclosporin A (10 mg/kg rat/day, intragastrically) and were treated for varying time intervals thereafter. The reversal of the T lymphocyte helper: suppressor ratio on Cyclosporin A therapy was associated with a significant improvement in the disease process. The alterations in the T cell subsets and in the disease lasted only as long as the drug was administered and thereafter reverted towards that seen in the control groups of animals receiving no treatment.
Several Graves' sera were simultaneously assessed in a bioassay based on the ability of porcine thyroid cells to organify 125I and in a radioreceptor assay for TSH receptor binding activity. Both assay systems were sensitive to 1 mcU/ml (final concentration) of unlabelled bovine TSH. Six Graves' sera were studied in detail over a wide (0-1.0 mcl sera) dose response range in repeat determinations. Two sera exhibited parallel binding and stimulating. However, two sera revealed significant inhibition of 125I-TSH binding prior to the demonstration of stimulation and the other two sera showed stimulatory capabilities before significant binding was evident. IgG was prepared from one serum by ammonium sulphate precipitation and chromatography on Sepharose 6B and then subjected to preparative isoelectric focusing. The isoelectric distribution of the two activities were found to be identical with major peaks of activity at pl=9.5 and pl=8.5. In summary: 1) each Graves' sera exhibits different dose-response curves with respect to binding and stimulation, 2) at certain concentrations of sera, only binding or stimulation were evident, 3) neither assay was consistently more sensitive for the presence of Graves' immunoglobulins, 4) for one Graves' sera, binding and stimulation could not be separated by isoelectric focusing. These studies would suggest each Graves' immunoglobulin has inherently different characteristics in its interaction with the TSH receptor.
In the course of a population study of thyroid dysfunction in pregnancy and the post-partum period, 65 women, considered to be antibody-positive (microsomal and thyroglobulin), and 82 antibody-negative women were assessed for postnatal depression at 6-8 weeks post partum. The women were also assessed for the development of post-partum thyroid dysfunction. Of the 147 women, 22 met DSM-III criteria for major depression. The presence of autoantibodies showed little association with depressed mood but there was a minor association of postnatal depression with actual thyroid dysfunction in that incidence of the latter condition was higher in depressed women (Raskin scale P less than 0.01; Edinburgh scale P less than 0.05; Montgomery-Asberg scale P less than 0.1). Three of eight mothers with thyroid dysfunction had major depression and were depressed on all three scales.