From the Guidelines
For patients with suspected hyperthyroidism, particularly those with type 1 diabetes, it is essential to test for antithyroid peroxidase and antithyroglobulin antibodies soon after diagnosis, as their presence is predictive of thyroid dysfunction, including hyperthyroidism, as noted in the 2018 study 1. When evaluating patients for hyperthyroidism, several key points must be considered:
- The presence of thyroid autoantibodies, such as antithyroid peroxidase (TPO) and antithyroglobulin (TG) antibodies, can identify patients at increased risk for thyroid autoimmunity, as discussed in the 2005 American Diabetes Association statement 1.
- Thyroid function tests, including TSH, free T4, and free T3 levels, should be performed after metabolic control has been established for several weeks, and at any time clinical thyroid dysfunction is suspected, as recommended in the 2005 statement 1.
- The US Preventive Services Task Force (USPSTF) found no direct evidence that treatment of thyroid dysfunction based on risk level alters final health outcomes, highlighting the need for individualized care, as noted in the 2015 USPSTF recommendation statement 1.
- The most critical antibody tests for hyperthyroidism diagnosis and monitoring include thyroid stimulating immunoglobulin (TSI), TPOAb, and TgAb, which help identify autoimmune causes like Graves' disease, and TSH receptor antibodies (TRAb), which are highly specific for Graves' disease diagnosis. Key considerations in the management of hyperthyroidism include:
- Comprehensive evaluation and treatment should be initiated in patients with suppressed TSH and elevated T4/T3 levels, as recommended in the 2005 statement 1.
- Treatment is generally recommended for patients with a TSH level that is undetectable or less than 0.1 mIU/L, particularly those with overt Graves' disease or nodular thyroid disease, as discussed in the 2015 USPSTF recommendation statement 1.
- Patients with previously normal TSH levels may be rechecked every 1–2 years or obtained at any time the growth rate is abnormal, as recommended in the 2005 statement 1.
From the Research
Antibody Labs for Hyperthyroidism
- The diagnosis and management of Graves' disease, a common cause of hyperthyroidism, involve the detection of thyroid-stimulating hormone receptor autoantibodies (TRAbs) 2.
- TRAbs play a crucial role as pathogenic antibodies in both the diagnosis and management of Graves' disease, and their detection has become an essential clinical laboratory marker 2.
- The use of thionamides, such as methimazole and propylthiouracil, is a common medical treatment for Graves' hyperthyroidism, but a relatively high proportion of patients relapse after thionamide withdrawal 3.
- Other possible medical treatments for hyperthyroidism include iodine and compounds containing iodine, perchlorate, lithium, β-adrenergic antagonists, and glucocorticoids 3.
- The choice of treatment for hyperthyroidism depends on the underlying diagnosis, the presence of contraindications to a particular treatment modality, the severity of hyperthyroidism, and the patient's preference 4.
Treatment Options
- Methimazole (MMI) and propylthiouracil (PTU) are two commonly used antithyroid medications for the treatment of hyperthyroidism caused by Graves' disease 5.
- MMI 30 mg/d has been shown to be more effective than PTU 300 mg/d and MMI 15 mg/d in normalizing serum free T4 (FT4) levels in patients with severe hyperthyroidism 5.
- However, PTU is not recommended for initial use due to its higher risk of adverse effects, such as mild hepatotoxicity 5.
- Radioactive iodine ablation of the thyroid gland is the most widely used treatment for hyperthyroidism in the United States 4.
Antibody Response
- High doses of antithyroid drugs, such as MMI and PTU, have been shown to decrease thyroid-stimulating antibody (TSAb) activity and antithyroid microsomal (MCHA) titers in patients with Graves' disease 6.
- The decrease in MCHA titers was associated with a decrease in free T4 values, indicating a reduction in thyroid hormone production 6.
- However, the titers of MCHA did not change significantly in patients with Hashimoto's thyroiditis treated with MMI or PTU plus T4 6.