Hippokratia 2004, 8(3):112-120
M Kita, A Saratzis
Endocrinology Dpt, Hippokratio General Hospital, Thessaloniki, Greece
Abstract
Postpartum thyroiditis is a syndrome of transient or permanent thyroid dysfunction occuring in the first year after delivery and is based on an autoimmune inflammation of the thyroid. The prevalence ranges from 1,1-21,1%. The role of antibodies (especially thyroid perodixase antibodies), complement, activated T cells, and apoptosis is important 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 occurence 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 every six months.