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Departments of Immunology (A.M., H.D.) and Internal Medicine (A.M.), Erasmus University Medical Center, 3015 GD Rotterdam, The Netherlands; and Department of Internal Medicine (A.B.), Medical Center Rijnmond Zuid, 3075 EA Rotterdam, The Netherlands
Correspondence: Address all correspondence and requests for reprints to: A. F. Muller M.D., Department of Internal Medicine, Diakonessenhuis Utrecht, Bosboomstraat 1, 3508 TG, Utrecht, The Netherlands. E-mail: amuller{at}diakhuis.nl
Postpartum thyroiditis is a syndrome of transient or permanent thyroid dysfunction occurring in the first year after delivery and based on an autoimmune inflammation of the thyroid. The prevalence ranges from 5–7%. We discuss the role of antibodies (especially thyroid peroxidase antibodies), complement, activated T cells, and apoptosis in the outbreak of postpartum thyroiditis. Postpartum thyroiditis is conceptualized as an acute phase of autoimmune thyroid destruction in the context of an existing and ongoing process of thyroid autosensitization. From pregnancy an enhanced state of immune tolerance ensues. A rebound reaction to this pregnancy-associated immune suppression after delivery explains the aggravation of autoimmune syndromes in the puerperal period, e.g., the occurrence of clinically overt postpartum thyroiditis. Low thyroid reserve due to autoimmune thyroiditis is increasingly recognized as a serious health problem. 1) Thyroid autoimmunity increases the probability of spontaneous fetal loss. 2) Thyroid failure due to autoimmune thyroiditis—often mild and subclinical—can lead to permanent and significant impairment in neuropsychological performance of the offspring. 3) Evidence is emerging that as women age subclinical hypothyroidism—as a sequel of postpartum thyroiditis—predisposes them to cardiovascular disease. Hence, postpartum thyroiditis is no longer considered a mild and transient disorder. Screening is considered.
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