Postpartum thyroiditis

doi:10.1016/j.beem.2004.03.008

Best Practice & Research Clinical Endocrinology & Metabolism

Volume 18, Issue 2, June 2004, Pages 303-316

https://doi.org/10.1016/j.beem.2004.03.008 Get rights and content

Abstract

Postpartum thyroiditis (PPT) is the occurrence, in the postpartum period, of transient hyperthyroidism and/or transient hypothyroidism, with most women returning to the euthyroid state by 1 year postpartum. The prevalence of PPT varies from 1.1 to 16.7%, with a mean prevalence of 7.5%. Women with type I diabetes mellitus have a three-fold increase in the prevalence of PPT. PPT is an autoimmune disorder which is a transient form of Hashimoto's thyroiditis occurring postpartum as a consequence of the immunologic flare following the immune suppression of pregnancy. Women experience symptoms in both the hyperthyroid and hypothyroid phase, but the association between PPT and postpartum depression remains undefined. Approximately 25% of women with a history of PPT will develop permanent hypothyroidism in the ensuing 10 years. Treatment for the hyperthyroid phase, when required, is a short dose of beta-blockers. Women with a TSH greater than 10 mU/l, or between 4 and 10 mU/l with symptoms or attempting pregnancy, require thyroid hormone replacement. Whether or not to screen for PPT remains controversial.

Section snippets

Definition

The classical case of PPT is the occurrence in the postpartum period of transient hyperthyroidism followed by transient hypothyroidism, with a return to the euthyroid state by 1 year postpartum. Hyperthyroidism always predates hypothyroidism and occurs between 2 and 6 months postpartum. The hypothyroid phase can occur at any time between 3 and 12 months following delivery. By convention, hypothyroidism which occurs more than 1 year postpartum, is not defined as PPT.

PPT has a variety of clinical

Prevalence

The prevalence of PPT varies dramatically, ranging from 1.1 to 16.7%. Explanations for the variation include differences in study design (in particular the frequency and duration of screening postpartum), whether or not screening was initiated during pregnancy or began postpartum, differences in how PPT was defined, and inherent geographical differences. Figure 1 illustrates the prevalence of PPT in studies in which screening was performed a minimum of twice postpartum and extended until at

Etiology

PPT is an autoimmune disorder which occurs during the first year following delivery, a time of immunological rebound following the immunosuppression of pregnancy. The association of PPT with thyroid antibodies, distinct T-cell abnormalities, and a pathological picture consistent with thyroiditis combine to provide strong evidence of the immunological basis of PPT. Other evidence supporting an autoimmune etiology includes an increased incidence of HLA DR-3, 4 and 5 in women who develop PPT.26.,

Diagnosis

The two major diseases that present with hyperthyroidism in the postpartum period are PPT and Graves' disease. In both entities TSH is suppressed and free T4 and T3 levels may be elevated. Both entities can present shortly after delivery, and are associated with enlargement of the thyroid and the presence of thyroid peroxidase antibodies. The presence of exopthalmos, a bruit, or TSH receptor antibody positivity is typically diagnostic of Graves' disease. However, infrequently, women with PPT

Postpartum depression—relation to PPT and thyroid antibodies

Whether or not PPT, or the mere presence of thyroid antibodies in euthyroid women, is associated with postpartum depression remains an unresolved question. Approximately 10 studies have investigated these issues with varying results. In the next two paragraphs I will review the articles published by the two major research groups that have focused on this topic.

Harris and colleagues have published a number of manuscripts exploring the interaction between the thyroid and depression. Their first

Permanent hypothyroidism and PPT

The majority of women with PPT return to the euthyroid state by the end of the first postpartum year. This is consistent with the pathological findings, which indicate a diffuse or focal lymphocytic infiltrate, but little to no follicular atrophy or fibrosis. Postpartum thyroiditis occurs in women with a predilection to autoimmune thyroiditis, as indicated by the presence of thyroid antibodies, distinct T-cell changes, and specific HLA predilections. It is therefore not surprising that

Prevention of PPT

Two studies have attempted to prevent the occurrence of PPT by intervening with various therapies in women who are thyroid-antibody positive. The rationale for preventing PPT includes preventing the symptoms that accompany the hyperthyroid and hypothyroid phase. Furthermore, by preventing PPT one can theoretically forestall, or perhaps even prevent, the occurrence of permanent primary hypothyroidism.

Kampe et al. conducted the first prevention study in 1990.⁵⁵ Fifty-eight Swedish women who were

Treatment of postpartum thyroiditis

The majority of women in the hyperthyroid phase of PPT do not require intervention as the severity of the hyperthyroidism is typically mild, and the time course rarely exceeds a couple of months. Symptomatic women are effectively managed with a short course of beta-blockers titrated based on symptom severity. Figure 3 provides a step-by-step algorithm regarding treatment decisions, and monitoring frequency, of PPT.

Whether or not to treat women in the hypothyroid phase of PPT is complex and

Screening for postpartum thyroiditis

The controversy regarding whether or not to screen for PPT has become more intense as the effect of subtle hormonal abnormalities both on the ability to maintain the pregnancy until term, as well as the impact on the intellectual development of the unborn child, has become better defined. Clearly, a decision regarding screening for PPT cannot look at the impact of PPT in isolation, but must be a component of a cost-effective decision analysis that evaluates all of the untoward effects of

Conclusion

In conclusion, PPT impacts one out of every 14 women in the postpartum period and is associated with symptoms in both the hyperthyroid and hypothyroid phase. The ability to select women with a greater than 50% chance of developing PPT (based on the presence of a high titer of thyroid antibodies in the first trimester of pregnancy) presents a unique model to further our understanding of the immune alterations which allows for maternal acceptance of the fetal allograft, as well as deepen our

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