Serial Changes in Thyroid-Stimulating Antibody and Thyrotropin Binding Inhibitor Immunoglobulin at the Time of Postpartum Occurrence of Thyrotoxicosis in Graves' Disease*
- 1 August 1987
- journal article
- research article
- Published by The Endocrine Society in Journal of Clinical Endocrinology & Metabolism
- Vol. 65 (2) , 324-330
- https://doi.org/10.1210/jcem-65-2-324
Abstract
Thyroid-stimulating antibody (TSAb) and TSH binding inhibitor immunoglobulin (TBII) were measured serially in 10 patients with Graves' disease at the time of postpartum onset (n = 2) or relapse (n = 8) of Graves' thyrotoxicosis and in 5 patients with Graves' disease who were in remission and had no postpartum relapse of Graves' thyrotoxicosis. TSAb was measured by a sensitive cAMP accumulation assay using FRTL-5 cells, and TBII was determined by radioreceptor assay. In no patient with either recurrent or new onset postpartum hyperthyroidism did the serum free T3 index (FT3I) rise before the free T4 index (FT4I). Of the 10 patients who had postpartum thyrotoxicosis, concomitant increases in serum FT4I and FT3I, and TSAb and TBII were observed in only 1 patient. Increases in TSAb and TBII after those in FT4I and FT3I occurred in 6 patients. In 1 patient, an increase in TBII was associated with the occurrence of thyrotoxicosis, but TSAb increased 1 month later. In the other 2 patients, a TSAb increase was followed by the development of thyrotoxicosis, but TBII increased later. In 3 of these 10 patients, the increased serum FT4I and FT3I values decreased spontaneously, whereas the TSAb and TBII levels increased continuously. No positive test or increase in TSAb or TBII was found in the 5 patients with Graves' disease who did not have a postpartum relapse of thyrotoxicosis. These data indicate that postpartum initiation of Graves' thyrotoxicosis is not always associated with an increase in circulating anti-TSH receptor antibodies and that such parameters are poor indicators of thyroid function. Intrathyroidal humoral or cell-mediated immunological mechanisms may also be involved in mediating thyrotoxicosis in Graves' disease.Keywords
This publication has 15 references indexed in Scilit:
- EVIDENCE THAT THYROID-STIMULATING ANTIBODY IS PRODUCED IN THE THYROID GLANDThe Lancet, 1984
- Immunoglobulin G inhibitor of thyroid-stimulating antibody is a cause of delay in the onset of neonatal Graves' disease.Journal of Clinical Investigation, 1983
- THYROID AUTOANTIBODY SYNTHESIS BY CULTURES OF THYROID AND PERIPHERAL-BLOOD LYMPHOCYTES .1. LYMPHOCYTE MARKERS AND RESPONSE TO POKEWEED MITOGEN1983
- Aggravation of Thyrotoxicosis in Early Pregnancy and after Delivery in Graves' Disease*Journal of Clinical Endocrinology & Metabolism, 1982
- Postpartum Recurrence of Hyperthyroidism and Changes of Thyroid-Stimulating Immunoglobulins in Graves' Disease*Journal of Clinical Endocrinology & Metabolism, 1980
- Clinical Significance of Assay of Thyroid-Stimulating Antibody in Graves' DiseaseAnnals of Internal Medicine, 1980
- Zoological Specificity of Human Thyroid-Stimulating Antibody*Journal of Clinical Endocrinology & Metabolism, 1978
- CHANGES OF SERUM IMMUNOGLOBULINS IGG, IGA, IGM, AND IGE DURING PREGNANCY1978
- MEASURMENT OF CIRCULATING THYROID MICROSOMAL ANTIBODIES BY THE TANNED RED CELL HAEMAGGLUTINATION TECHNIQUE: ITS USEFULNESS IN THE DIAGNOSIS OF AUTOIMMUNE THYROID DISEASESClinical Endocrinology, 1976
- Assessment of Thyroid Function by the Combined Use of the Serum Protein-Bound Iodine and Resin Uptake of131I-TriiodothyronineJournal of Clinical Endocrinology & Metabolism, 1965