The 9th National Conference on Endocrinology, sponsored by the Chinese Medical Association, was held in Dalian from August 26-29, 2010. Chinese and foreign scholars reported the latest research progress and made in-depth reviews in the fields of thyroid diseases, hypothalamic-pituitary disorders, sex hormones and post-transplantation management, obesity and metabolic syndrome. Only selected highlights in the field of thyroid disorders are presented below. The significance of immunological properties of thyroid autoantibodies in AITD Common autoimmune thyroid diseases (AITD) include Graves’ disease (GD), Hashimoto’s thyroiditis (HT), etc. Antibodies associated with AITD include thyrotropin receptor antibody (TRAb), thyroglobulin antibody (TgAb), and thyroid peroxidase antibody (TPOAb). The thyroglobulin (Tg) gene is a susceptibility gene for AITD and TgAb can be detected in animal models of spontaneous autoimmune thyroiditis.TPOAb has antibody-dependent cell-mediated cytotoxic effects and complement-dependent cytotoxic effects. Studies in mice and humans suggest that the production of TgAb may precede TPOAb. Epidemiological investigations have shown that in people without a history of thyroid disease, those with positive serum thyroid autoantibodies (TgAb and TPOAb) are more likely to have abnormal thyroid function than those with negative. and TPOAb levels are significantly higher in hypothyroid patients than in HT patients with normal thyroid function. So, can the disease process in HT patients be predicted by antibody titers alone? The answer is no. The pathogenicity of the autoantibody response also depends on its immunological properties: IgG subtype distribution, affinity, recognized antigenic determinants, etc. HT is dominated by IgG1 and IgG4 subtypes, and increased levels of serum IgG2, serum TgAb IgG1 subtype, and TPOAb IgG4 subtype may be risk factors for disease progression in HT patients. affinity of TgAb may also be related to HT disease progression, and TgAb may undergo affinity maturation under constant stimulation by Tg, and at similar antibody titers, affinity may help predict HT disease progression. Studies have shown that AITD patients recognize different antigenic determinants than non-AITD patients and that there are differences in the Tg antigenic determinants recognized by HT and GD. In addition, antibody immunological properties are important in identifying patients with GD alone and GD combined with HT. In conclusion, antibody immunological characteristics (antibody titer, IgG subtype distribution, affinity, recognized antigenic determinant clusters) can help to reveal the mechanism of AITD, facilitate early diagnosis of the disease, and have important implications in autoimmune thyroid diseases. Immune interventions in Graves’ disease Graves’ disease is an autoimmune disease whose clinical symptoms are not limited to the thyroid but are a multisystem syndrome with symptoms including hyperthyroidism (hyperthyroidism) combined with infiltrative proptosis, Graves’ ophthalmopathy, and mucinous edema. Since the first discovery of gamma globulin, which resembles the function of thyroid stimulating hormone, by Adams and Purves in 1956, many scholars have been working to explore the role and place of immune intervention therapy in Graves’ disease. Hormonal drugs and immunosuppressive agents are mostly used in autoimmune diseases such as systemic lupus erythematosus (SLE), rheumatoid arthritis (RA), and dry syndrome (SS) to suppress the immune response and reduce the inflammatory response. According to the literature, massive glucocorticoid shock therapy for Graves’ hyperthyroidism and hyperthyroidism combined with infiltrative proptosis does not have a better overall prognostic benefit than antithyroid drug therapy, which is consistent with the available clinical observations. In contrast, intravenous glucocorticoids for Graves’ ophthalmopathy and limited mucinous edema were well tolerated by patients, with few side effects and effective treatment. Immunosuppressants – Rituximab reduces the immune response by inhibiting the response of mature B lymphocytes. Numerous studies have shown that immunosuppressants are effective in the treatment of autoimmune diseases, and clinical studies have been conducted on their use in Graves’ disease. In fact, hormonal and immunosuppressive therapies for autoimmune diseases only target the non-specific antibody-mediated inflammatory response rather than the pathogenesis of the disease. To further investigate immune interventions for Graves’ disease, animal models of Graves’ disease are mostly used. Chen Chunrong et al. observed that co-expression of recombinant adenoviral vectors [thyroid stimulating hormone receptor (TSHR), interleukin (IL)-4/IL-12] significantly reduced the specific immune response to Th2 antigens and induced Graves’ hyperthyroidism, but had no significant disease-inducing effect on Th1 antigens. In summary, glucocorticoids are ineffective in the treatment of Graves’ disease; glucocorticoids and immunosuppressants are effective in Graves’ ophthalmopathy, limited mucinous edema, and hematologic abnormalities, but they target nonspecific inflammatory responses rather than pathogenesis; and adenoviral vectors have some immune intervention therapeutic effect, which provides a basis for further clinical studies. Current status and confusion in the application of antithyroid drugs Antithyroid drugs (ATDs) have been used in the treatment of hyperthyroidism for more than half a century and remain the cornerstone of hyperthyroidism treatment, especially for Graves’ hyperthyroidism. The course of treatment is generally divided into three phases: the initial treatment phase, the reduction phase, and the maintenance phase, and the total course of treatment is generally 1.5 to 2 years. So how to choose the right medication for hyperthyroidism? There are two main categories of ATD drugs commonly used in clinical practice: thioureas (propylthiouracil: PTU) and imidazoles (methimazole: MMI). Clinical studies have shown that MMI and PTU have similar mild to moderate adverse effects, while PTU has multiple lethal adverse effects. PTU can cause severe liver failure and death in adults and children, has a higher incidence of granulocyte deficiency than MMI, and has a higher risk of anti-neutrophil cytoplasmic antibody (ANCA)-associated vasculitis. Therefore, in general, MMI is the first-line drug for hyperthyroidism, while PTU is used as a second-line drug in cases of allergy or intolerance to MMI. Common adverse effects of ATD are rash, pruritus, granulocytopenia, liver injury, arthralgia, gastrointestinal reactions, abnormal taste and smell, granulocyte deficiency, and ANCA vasculitis. Longer treatment cycles for hyperthyroidism and long-term drug therapy increase the risk of adverse reactions. Adverse drug reactions often lead to treatment failure: on the one hand, physicians are concerned about serious adverse reactions, resulting in inadequate doses; on the other hand, any minor adverse reactions can lead to reduced compliance and thus affect treatment. Thus, failure of antithyroid drug therapy is often due to inadequate dosing or poor patient cooperation. Therefore, physicians should explain to patients, obtain their cooperation, and follow up regularly 2-4 weeks after medication administration to adjust the dosage in a timely manner. In special cases, such as hyperthyroidism during pregnancy, PTU is given during the first 3 months of pregnancy. mMI, PTU as a class D pregnancy drug, can cause hypothyroidism and malformation in newborns, and should be applied only after its beneficial effects on pregnant women are confirmed. In addition, hyperthyroid heart disease (hyperthyroid heart) and sudden death are the main causes of death in patients with hyperthyroidism, and patients with hyperthyroid heart failure are often combined with liver damage, therefore, the safety of medication is crucial. On the one hand, heart failure, infection and other serious stress reactions reduce the efficacy of ATD; on the other hand, increasing the dose of ATD is likely to cause systemic adverse reactions in the blood and liver and aggravate the disease. Obviously, there is a contradiction between “long-term adverse drug reactions” and “ultimate benefit of adherence to treatment” – ATD adverse reactions reduce patient compliance, and ATD cannot meet the needs of patients with hyperthyroidism and hyperthyroid heart disease in pregnancy. The contradiction between “long-term adverse effects” and “ultimate benefit of adherence” is that ATD decreases patient compliance and ATD does not meet the medication requirements of patients with hyperthyroidism in pregnancy and hyperthyroid heart disease. This therapeutic paradox poses a dilemma in clinical practice and is a question that endocrinologists need to consider.