Abstract
The origin of hyperthyroidism in Graves’ disease was displayed demonstrating the complexity of the processes. The role of stimulating TSH receptor antibodies is the one factor for the production of increased thyroidal T3 and T4. The T3 and T4 formation in colloid-embedded thyroglobulin and the activities of thyroidal deiodinases [type 1 (DIO1) and type 2 (DIO2)] play a crucial role in that. The findings of different authors were summarized with respect to highlighting the role of tissue-specific deiodinase activities. Apart from the results of experimental studies, the clinical results were brought to the front. The role of tissue-specific type 2 deiodinase activity was demonstrated according to thyroid function, the presence of autoantibodies against thyroid peroxidase (TPO), thyroglobulin (Tg) and TSH receptor. Autoantibodies against human eye muscle membrane and cytosol antigens had influencing effects on tissue-specific DIO2 activities, and the antieye muscle antibody immunoglobulin isotypes were associated with eye muscle enlargements. Antithyroid drug (ATD) therapy demonstrated relevant effects on tissue-specific DIO2 activities, which were manifested in the alterations of thyroid hormone levels. An asymptomatically appearance of autoantibodies against peptides corresponding to amino acid sequence of DIO2 was detected associating with thyroid hormone and anti-TPO, anti-Tg and TSH receptor antibody levels during the therapy.