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  • Title: Immunologically mediated hypothyroidism.
    Author: Dussault JH, Rousseau F.
    Journal: Endocrinol Metab Clin North Am; 1987 Jun; 16(2):417-29. PubMed ID: 3319590.
    Abstract:
    In this article, new avenues in the understanding of immunologic processes involved in hypothyroidism have been explored. The discovery of a family of TSH-R directed antibodies, including TSI-block, TGI, and TGI-block, has afforded perspectives on the etiology of autoimmune thyroid disorders. Thus, whereas TSI and TSI-block influence thyroid function, TGI and TGI-block are involved in thyroid cell proliferation and maturation. We have focused on three clinical entities that have been elucidated relatively recently--namely, silent thyroiditis, postpartum thyroiditis, and congenital hypothyroidism. Silent thyroiditis, a common form of transient thyroiditis, yields very few clinical symptoms or signs but significant alterations in biological tests, including a thyroid 131I uptake compatible with silent thyroid destruction. Although an autoimmune etiology is really not certain at this moment, it is not completely excluded. Silent thyroiditis does not usually require therapy, except in the rare cases in which symptoms are very severe. Postpartum thyroiditis, probably a special form of silent lymphocytic thyroiditis, differs from silent thyroiditis only by its relation to pregnancy and its higher rate of persistent thyroid disease. It has a high prevalence in pregnant women (5.5 to 10.2 per cent) in all populations studied, and may be responsible for a substantial proportion of cases of postpartum depression. Although the etiology is not clear, an autoimmune process seems to be involved. Although prediction of this state is difficult, a previous episode or high titers of microsomal antibodies in the first trimester show good correlations with the disease. Thyroid hormone replacement therapy is recommended for persistent disease. Congenital hypothyroidism appears to be mediated by passively transferred maternal blocking antibodies. TSI-block is likely responsible for the transient form of congenital hypothyroidism in the same way that TSI may cause transient congenital thyrotoxicosis. Passive transfer of maternal TGI-block appears to be causal in the majority of newborns with the sporadic form of congenital hypothyroidism. Early (in utero) onset of the disease could explain why 15 per cent of adequately treated infants subsequently demonstrate subtle neurologic sequelae. Because screening procedures for TGI-blocking antibodies are being made available, it should be possible to detect those potentially severe in utero cases and commence thyroid hormone replacement therapy before birth.
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