Hashimotos thyroiditis and Graves disease have been thought to be the autoirnmune diseases having their distinct and separate clinical and pathologic features. Because of the partial and complete simi1arity in histologic feature, it has been hypothesized that Hashimoto's thyroiditis and Oraves disease may be interrelated. Several patients who had been diagnosed as Graves disease showed features of hypothyroidism, and were proven to have histologie features of Hashimotos thyroiditis in their thyroid tissue. Two meehanisms had been suggested to explain tbis phenomenon. One is that the combined Hashimotos thyroiditis in Graves' disease may become predominant with time, The other is that the amount of TSH receptor blocking antibody may increase in the course of Graves disease. Early recognition of these patients would be impartant to estabilish therapeutic plan. Futhermcee, extensive study of these patients would give more understanding of the mechanism of these diseases. Here we report 5 cases of clinically diagnosed Graves disease with pathologic features of Hashimotos thyroiditis or focal lymphocytic thyroiditis.
Autoantibodies against thyroid hormones can be detected in the sera of patients with both thyroidal and non-thyroidal disorders. These antibodies interfere with the radioimmunoassay of serum total and free thyroid hormone concentrations, resulting in a discrepancy between the measured hormone levels and clinical features. This can in turn lead to an erroneous diagnosis and patients may receive unnecessary treatment from physicians who are unaware of the presence of the autoantibodies. We experienced a woman having Hashimotos' thyroiditis with a spurious elevation of total T3 and free T3 values according to one-step analog-tracer radioimmunoassay who was had been treated as Graves' disease in past. Through the use of a polyethylene glycol precipitation method, she was subsequently revealed to have anti-triiodothyronine autoantibodies. We report this case with a review of related literature.
Hashimotos thyroiditis has been associated with a various autoimmune disorders. The immunologic mechanisms involved in the pathogenesis of these disorders have not always been thought to be the same. Although it was demonstrated that there were high prevalence of abnormal thyroid function and autoantibody in autoimmune hemolytic anemia(AIHA) and Fisher-Evans syndrome(FES), AIHA combined with Hashimotos thyroiditis is rare in Korean literature. It was suggested that a common immunologic mechanism may be involved in the pathogenesis of both disease and the possibility of multiple autoimmune syndrome might present in autoimmune hematologic disorders. We experienced a 74-year old woman with a 12-year history of a hypothyroidism due to Hashimotos thyroiditis was hospitalized with sudden development of warm AIHA with positive Direct & Indirect Coombs test and pericardial effusion. Her thyroid function test showed subclinical hypothyroidism with the maintenance dosage of levothyroxine(100pg/day). With glucocorticoid and plasmapheresis, AIHA and pericardial effusion were corrected successfully. It is suggested that the prudent immunologic study is needed for the anemia developed in patients with Hashimotos thyroiditis with or without hypothyroidism.
BACKGROUND TSH receptor blocking antibody (TRBAb) is a pathogenic factor in the vast majority of patients with primary myxedema. It has been reported that TRBAbs are found in some patients with chronic goitrous autoimmune thyroiditis (Hashimoto's thyroiditis), but the significance or the role of TRBAb in Hashimotos thyroiditis is not clear, We recently reported that hTSHR-CHO cells which express the functional human TSH receptors are more sensitive and are better in detecting functional TSH receptor antibodies in Graves patients than FRTL-5 cells. We are to investigate the biological role of TRBAb in Hashimotos thyroiditis by measuring thyroid stimulation blocking antibody (TSBAb) activities of Hashimoto's IgG's using hTSHR-CHO cells. Moreover, we are to see if there is any difference in epitope recognition between Hashimotos TRBAb and myxedema's TRBAb by measuring TSBAb activities with mutant receptor expressing cell lines, Mcl+2 and Mc 2 in those patients. METHOD: We measured TSBAb activities of IgGs from patients with primary myxedema (PM, n= 10) and those with hypothyroid (n 20) or euthyroid (n 17) Hashimoto's thyroiditis (HT) using wild type hTSHR-CHO cells (WT) and two chimeric receptor expressing cell lines, Mcl+2 and Mc2. RESULTS: TSBAb activities measured by WT were higher in hypothyroid HT than in euthyroid HT (30.0+-23.2% vs. 6.1+-28.7, p<0.05), and TSBAb-positive rate tend to be higher in the former (20%, 5/20) than in the latter (0%, 0/17, p=0.07). TRBAbs from PM (n=4) had high TBII activities and had persistent blocking activities despite of the replacement of amino acid residue 8~165 of extracellular domain of TSHR with those of rat LH/CGR (Mcl +2). However, TRBAbs from HT (n=4) had no TBII activity at all and lost blocking activities when measured with Mcl+2. CONCLUSION: TRBAbs are found in 20% of hypothyroid patients with Hashimotos thyroiditis in assay using hTSHR-CHO cells, and they seem to play a role in the development of hypothyroidism in some patients with Hashimotos thyroiditis. TRBAbs of Hashimotos thyroiditis are different in epitope recognition from TRBAbs of primary myxedema.