The incidence of postpartum thyroid disease (PPTD) is between 5-10%. It is a transient illness requiring no therapy in the majority, but in a minority may require treatment, and cause short and long term morbidity. Risk factors for PPTD are the presence of thyroid peroxidase antibody (TPOAb), previous PPTD and type 1 diabetes mellitus. PPTD may present in several forms – a biphasic illness with thyrotoxic and hypothyroid phases in 34%; but a thyrotoxic (21%) or a hypothyroid phase (45%) may occur alone. The thyrotoxic phase occurs early, is usually self limiting and occasionally requires treatment with beta blockers. The hypothyroid phase occurs later, is often symptomatic and may require thyroxine therapy. About a third of women who become hypothyroid will need thyroxine permanently. In the longer term, about half of these women with PPTD will become clinically or subclinically hypothyroid. PPTD is an autoimmune disease which occurs during a period of immune rebound following pregnancy induced immune modulation. Pro-inflammatory Th1 responses give way to a Th2 pattern to accommodate the growing foetus. There is evidence to suggest that this hormone induced transition specific to pregnancy, is affected in those who develop PPTD. The roles of leptin, cortisol and TGF beta have been investigated. Foetal microchimerism also has been suggested as a possible mechanism for PPTD. The role of TPOAb remains unresolved – it probably is only a marker of thyroid autoimmunity without a significant pathogenetic role. The diagnosis of PPTD is straightforward. Technetium scans may be needed rarely to differentiate PPTD from Graves’ disease. The question of screening remains unresolved primarily due to the lack of a sensitive tool and guidance as to the timing of screening. We recommend further study of causative mechanisms, the course of the illness and screening strategies in different ethnic groups from different areas.
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