Autoimmunity and hypothyroidism.

Abstract

Hypothyroidism can be induced by various diseases. An autoimmune cause accounts for approximately 90% of adult hypothyroidism, mostly due to Hashimoto's disease. The majority of Hashimoto patients are women aged between 20 and 60 years old and nearly 10% show overt hypothyroidism. With time euthyroid patients progress to hypothyroidism and thus the prevalence of hypothyroidism is higher in elderly patients. Especially at 3 to 8 months postpartum, the prevalence of hypothyroidism is very high, up to 2-4%, but more than 90% of these cases are transient. Autoimmune destructive mechanisms, such as antibody dependent cytotoxicity, K and NK cell cytotoxicity, T lymphocyte cytotoxicity and lymphokine cytotoxicity, have been studied in vitro, but the most important factor in vivo is still unknown. A recent finding is that thyroid stimulation blocking antibody (TSBAb) may induce primary atrophic hypothyroidism. This antibody not only blocks TSH-induced cAMP production but also blocks TSH-induced DNA synthesis and iodine uptake in cultured thyroid cells. The prevalence of TSBAb in patients with primary atrophic hypothyroidism varies in different studies, from 0 to 47%. Reports on the relationship between TSBAb and TSH-binding inhibitory immunoglobulin (TBII) detected by radioreceptor assay are conflicting. The prevalence of TSBAb in patients with goitrous hypothyroidism is also controversial, varying from 0 to 20%. Transient hypothyroidism is observed frequently in the postpartum period and in the post-thyrotoxic phase of pregnancy-unrelated silent thyroiditis. Maternal TSBAb causes transient neonatal hypothyroidism when the activity is more than 1500 i.u./litre. The blocking and stimulatory types of anti-TSH receptor antibodies may both react with the same epitope(s) of TSH-receptor related antigens but the exact mechanisms that lead to the different effects are unknown. In some patients, including those with Graves' disease, stimulating and blocking antibodies co-exist and thyroid function may change from hyperthyroidism to hypothyroidism, or vice-versa, depending on the balance of stimulatory and blocking activities. Hypothyroidism in Graves' disease after treatment is thought to be induced in two ways: autoimmune thyroid destruction and the predominant appearance of TSBAb. Dietary iodine restriction is helpful in allowing recovery from hypothyroidism in more than half of the patients with spontaneously occurring primary hypothyroidism in Japan. Submaximal doses of T3 may be useful in differentiating transient from persistent hypothyroidism, since spontaneous recovery is detected by an increase of serum T4.(ABSTRACT TRUNCATED AT 400 WORDS)