PROGNOSTIC VALUE OF SUPPRESSED THYROTROPIN LEVEL AND POSITIVE THYROTROPIN-RECEPTOR ANTIBODY ACTIVITY IN GRAVES' DISEASE WITH LONG-LASTING CLINICAL REMISSION

1997 ◽  
Vol 3 (3) ◽  
pp. 113-117 ◽  
Author(s):  
Hassan M. Heshmati, MD ◽  
Alain Chevalier, MD ◽  
Hossein Gharib, MD, FACE ◽  
Jérôme Clerc, MD ◽  
Christian Boutteville, MS ◽  
...  
Thyroid ◽  
1998 ◽  
Vol 8 (2) ◽  
pp. 119-124 ◽  
Author(s):  
VALDO MICHELANGELI ◽  
CATHY POON ◽  
JONATHON TAFT ◽  
HARVEY NEWNHAM ◽  
DUNCAN TOPLISS ◽  
...  

1998 ◽  
pp. 281-285 ◽  
Author(s):  
M Akuzawa ◽  
M Murakami ◽  
M Yamada ◽  
T Satoh ◽  
H Shimizu ◽  
...  

Clinical evaluation was conducted to ascertain whether thyrotropin receptor antibody (TRAb) in the normal range may still be involved in the regulation of thyroid function after prolonged treatment for Graves' disease. All patients (n = 33) were treated with antithyroid drugs for an average of 10.6 years and were under euthyroid conditions in which normal blood levels of tri-iodothyronine (T3) were significantly correlated with blood thyrotropin (TSH) levels, but not with titers of TRAb. A significant correlation was observed between TRAb titer and thyroid-stimulating antibody (TSAb) activity. In contrast, this correlation was not found in normal subjects. After administration of T3 (75 microg daily for 8 days), the patients showed increased levels of T3 with concomitant suppression of TSH levels. Under these conditions, linear regression analysis showed significant correlations of TRAb titer and TSAb activity with 24-h thyroid radioiodine uptake (r = 0.641 and 0.621 respectively, P < 0.01), in contrast to declining blood thyroxine levels. Moreover, the immunoglobulin G (IgG) of the patients precipitated to a greater extent than IgG from normal subjects a peptide consisting of the amino acid sequence near the terminus of the human TSH receptor. These findings indicated that TRAb at normal levels possessed significant unremitting activities on thyroid function despite long-term treatment in euthyroid patients with Graves' disease.


1986 ◽  
Vol 113 (4) ◽  
pp. 493-499 ◽  
Author(s):  
U. Di Mario ◽  
A. Scardellato ◽  
W.J. Irvine ◽  
L. Kennedy ◽  
M. Kadlubowski ◽  
...  

Abstract. Activated T cells, T-cell subsets, thyrotropin receptor antibodies and immune complexes were evaluated in 31 patients with newly diagnosed Graves' disease. Activated T cells were assayed by monoclonal antibodies against early (4F2) and late activation surface lymphocyte antigens (different epitopes of class II antigens). In comparison with the normal population, Graves' patients showed a significant decrease in the suppressor cytotoxic T-cell subset. Significant increases of 4F2-positive cells (70% of patients studied), class II antigen-positive cells (65%), thyrotropin receptor antibodies (93%), Clq-immune complexeses (44%) and conglutinin-immune complexes (37%) were observed. A significant inverse correlation between the increase in 4F2-positive cells and thyrotropin receptor antibody values was also observed. Lymphocytes from Graves' patients were cultured in the presence of thyrotropin receptor antibody-positive or -negative sera, with or without mitogen stimulation. Thyrotropin receptor antibodies were shown not to interfere with the expression of activation antigens in cultured cells. The different patterns of humoral and cellular immune phenomena may indicate the existence of either different stages of Graves' disease or a heterogeneity of the immunopathogenesis in different patients.


1991 ◽  
Vol 38 (4) ◽  
pp. 429-433 ◽  
Author(s):  
KAZURO KAISE ◽  
NOBUKO KAISE ◽  
KATSUMI YOSHIDA ◽  
HIROSHI FUKAZAWA ◽  
KOKI MORI ◽  
...  

1991 ◽  
Vol 125 (5) ◽  
pp. 491-493 ◽  
Author(s):  
V. Fonseca ◽  
M. Thomas ◽  
G. Dusheiko

Abstract. We measured thyrotropin receptor antibodies in serum obtained from 2 groups of patients participating in clinical trials of recombinant interferon-α 2b for viral hepatitis. Group I: Patients with hepatitis B (N=8), received interferon 5×106 units thrice weekly for 4 months. Group II: Patients with non-A, non-B hepatitis (N=16) were randomized to receive interferon in a dose of either 0.25×106 or 3×106 U thrice weekly for 6 months and then crossed over to receive the other dosage schedule for a further 6 months. None of the patients developed thyrotoxicosis. Thyrotropin receptor antibody activity was detectable within the "normal range" (<10 U/l) in 6 patients prior to treatment. In Group I, thyrotropin receptor antibodies became detectable in 6 patients on treatment, in 4 of whom it was 10 U/l. In Group II, thyrotropin receptor antibody activity was unchanged on low-dose interferon, but on the higher dose became detectable in 9 patients, in 7 of whom it was >10 U/l. We conclude that treatment with interferon is associated with the development of thyrotropin receptor antibodies in a large proportion of patients. It is possible that in some patients treated with higher doses of interferon the increase in thyrotropin receptor antibody activity may be sufficient to induce hyperthyroidism.


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