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THYROIDAL RESPONSE TO AN INCREASE OR DECREASE OF ENDOGENOUS TSH IN PATIENTS WITH HYPERTHYROIDISM AND ITS CORRELATION WITH TSH BINDING INHIBITING IMMUNOGLOBULIN
Author(s) -
Katakura M.,
Koizumi Y.,
Aizawa T.,
Takasu N.,
Yamada T.,
Yukimura Y.,
Nagata H.
Publication year - 1986
Publication title -
clinical and experimental pharmacology and physiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.752
H-Index - 103
eISSN - 1440-1681
pISSN - 0305-1870
DOI - 10.1111/j.1440-1681.1986.tb00919.x
Subject(s) - medicine , endocrinology , graves' disease , thyroid , antibody , immunology
SUMMARY 1. One hundred and twenty‐one patients with hyperthyroidism of Graves' disease were treated with antithyroid drugs for 3 years and thyroidal response to an increase or decrease of TSH and the serum thyroid stimulating immunoglobulin (TSI) activity were studied in relation to the presence or absence of TSH binding inhibiting immunoglobulin (TBII). 2. TBII activity was positive in 83% of untreated patients but decreased gradually with time during antithyroid drug therapy. Thyroidal radioactive iodine uptake (RAIU) was suppressed by T 3 in 86 of 121 treated patients but 16% of suppressible patients had TBII activity. Thyroidal RAIU was not suppressed by T 3 in 35 treated patients, and 19 of 35 unsuppressible patients had TBII activity but other 16 patients did not. When suppressible and unsuppressible patients were combined, suppression of serum T 4 and thyroidal RAIU by T 3 tended to be less in the presence of TBII activity. 3. TSI activity was detected in the sera of untreated patients but did not correlate with TBII activity. TSI activity was undetectable after treatment for 3 years irrespective of presence or absence of TBII activity and T 3 ‐suppressibility. 4. TSH, T 4 and T 3 elevation in response to 500 μg thyrotropin releasing hormone (TRH) was normal in all treated patients irrespective of presence or absence of TBII activity and T 3 ‐suppressibility. 5. It is suggested that in vivo thyroidal responsiveness to an increase or decrease of endogenous TSH did not correlate with the presence or absence of TBII activity after long‐term therapy with antithyroid drugs.