These results indicate that (1) more than half the patients who developed hypothyroidism within 6 months after 131I treatment for Graves' disease recovered spontaneously, (2) TSAb activity might play some role in the recovery of transient hypothyroidism, and (3) the development of transient hypothyroidism may influence long-term thyroid function.

No abstract

These results indicate that (1) the TBII index and TSAb activity decreased over a period of more than 2 years after 131I therapy for Graves' disease, and (2) the TBII index before treatment may influence the long-term outcome of 131I therapy.

Intercellular adhesion molecule (ICAM-1), a ligand for lymphocyte function-associated antigen-1 (LFA-1), plays an important role in a variety of immune-mediated mechanisms such as lymphocyte attachment to cultured Graves' thyroid cells. We report the detection of a soluble form of the ICAM-1 molecule (sICAM-1) in sera from patients with Graves' disease (GD) and other thyroid disorders. The mean (+/- SD) sICAM-1 concentration in 28 euthyroid control subjects was 1931 +/- 681 pmol/L. The mean sICAM-1 concentration in 25 untreated hyperthyroid patients with GD was significantly elevated (3065 +/- 890 pmol/L), and decreased significantly (2489 +/- 845 pmol/L) after treatment with antithyroid drugs and/or 131I. Of 14 GD patients who had been in remission following administration of antithyroid drugs, 12 had recurrent disease. In 10 of the 12 patients in whom GD recurred, the sICAM-1 concentration (3807 +/- 796 pmol/L) increased significantly. The mean sICAM-1 concentration in patients with hypothyroidism due to chronic thyroiditis (n = 15:2895 +/- 569 pmol/L) was significantly elevated over that of control subjects, and not different from untreated hyperthyroid patients. The mean sICAM-1 concentration in patients with subacute thyroiditis (n = 13: 3036 +/- 441 pmol/L) was significantly elevated, while the mean sICAM-1 concentration in patients with nodular goiter (n = 10: 2318 +/- 490 pmol/L) was within the normal range. These results indicate that mean serum sICAM-1 concentration was significantly elevated in patients with untreated GD, and it decreased after treatment and increased at the time of recurrence. Therefore, the elevated serum concentration of sICAM-1 in patient with GD probably reflects ongoing immune processes.

From studies of binding of 51Cr-labeled T cells to human thyroid monolayers, we have postulated the existence of tissue "homing-like" receptors on thyroid cells in patients with Graves' disease (GD). In this study we have investigated whether the CD44 (Hermes-1) protein, well known as a putative human lymphocyte homing receptor, is expressed on thyroid cells in patients with GD, and if so whether its expression is influenced by interferon-gamma (IFN-gamma). Cell surface CD44, as well as CD54 (ICAM-1), another putative homing receptor, antigens were analyzed by flow cytometry and immunohistochemistry. CD44 and CD54 were both expressed on thyroid cells from untreated patients with GD, which, in the case of CD44, appeared as two peaks. IFN-gamma treatment enhanced the expression of the CD54 protein on Graves' thyroid cells and inhibited the expression of the larger of the two CD44 peaks, but not the other. Only small amounts of CD44 and CD54 were detected on normal thyroid cells, neither of which was affected by IFN-gamma. The CD44 protein was also demonstrated on both GD and normal thyroid cells by immunohistochemistry. These findings suggest that CD44, and possibly CD54, may induce putative adhesion pathways that lead to the homing of lymphocytes to the thyroid in patients who develop Hashimoto's thyroiditis and Graves' disease.