Introduction
rheumatoid arthritis, cancers, Graves’ disease, hypothyroid, autoimmune diseases, hyperthyroidism, autoimmunity
RHEUMATOID ARTHRITIS, CANCERS, INFLAMMATORY BOWEL DISEASE, PROLIFERATION, HYPOTHYROID, AUTOIMMUNE DISEASES, HYPERTHYROIDISM, MYASTHENIA GRAVIS, REMISSION, MULTIPLE SCLEROSIS, AUTOIMMUNITY
Graves’ disease (GD) is the most common cause of hyperthyroidism and approximately 3% of women and 0.5% of men develop GD in their lifetime (Antithyroid drugs (ATDs) are essential in the treatment of GD. They suppress the production of thyroid hormones by inhibiting the enzymes involved in their synthesis, such as thyroxine and triiodothyronine. Presently, treatment strategies primarily rely on ATDs or radioactive iodine (RAI) therapy to reduce thyroid hormone production. However, there is a need for greater attention to be paid to the underlying immunological mechanisms involved in GD, such as the role of T and B cells in autoimmunity (The TRAb level is a useful predictor for remission and relapse of patients at the end of the course of ATDs therapy. Patients with persistent elevation of TRAb level are unlikely to achieve remission, with relapse rates approaching 80–100%. On the other hand, patients with low or undetectable TRAb have a higher probability of achieving permanent remission, with relapse rates approaching 20–30% (The high relapse rate after ATD withdrawal implies that patients may need to resume ATD or resort to definitive treatment such as RAI or total thyroidectomy. Successful thyroid ablation by RAI or total thyroidectomy necessitates lifelong thyroid hormone replacement therapy. However, a small percentage of levothyroxine-treated patients (about 5–10%) experience persistent hypothyroid symptoms despite normal serum TSH levels (Azathioprine (AZA) is a synthetic purine analog with immunosuppressive properties that is commonly used to treat autoimmune diseases such as rheumatoid arthritis, inflammatory bowel disease, multiple sclerosis, myasthenia gravis, and certain cancers. AZA interferes with the metabolism of purine nucleic acid, which is essential for lymphoid cell proliferation following antigenic stimulation, resulting in the inhibition of cellular immunity and antibody responses (