Q&A

Postpartum Thyroiditis

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In conjunction with the American Society of Endocrine PAs (ASEPA), Clinician Reviews will be bringing you practical information about topics in endocrinology that may help you to better understand and manage patients with diabetes, thyroid disorders, and other metabolic conditions. In this month’s column, ASEPA Immediate Past President Scott Urquhart, PA-C, discusses postpartum thyroiditis.


 

Q: I frequently counsel patients on family planning, pregnancy expectations, and postpartum concerns. Would you please discuss the specifics of postpartum thyroiditis?

Postpartum thyroiditis (PPT) affects about 5% to 10% of postpartum patients, as evidenced by biochemical thyroid dysfunction. It usually presents during the first three to nine months postpartum.

The condition may present as transient hyperthyroidism, transient hypothyroidism, or hyperthyroidism resolving to transient or permanent hypothyroidism. Only one-quarter to one-third of women experience both the hyperthyroid and hypothyroid phases; one-third of patients will have only a thyrotoxic or hypothyroid phase.

Those who are at risk for or develop PPT have underlying autoimmune thyroid disease (eg, Hashimoto’s thyroiditis). During pregnancy, the maternal immune system is partially suppressed; it rebounds dramatically after delivery, leading to increased risk for autoimmune thyroid disease in patients with thyroid peroxidase antibodies (TPOAb).

Q: How do I know if my patients are at risk for thyroid disease during or following pregnancy?

We need to ascertain who is at risk for PPT so we can appropriately evaluate and screen for the condition. It is important to educate your patients prior to or during pregnancy about the risk, timeline of occurrence, and signs/symptoms of PPT.

If possible, I recommend discussing this with patients in the family-planning stages. It would be helpful to ask the prospective mother about a family history of hyperthyroid or hypothyroid disease (eg, Grave’s disease or Hashimoto’s thyroiditis). It’s also important to inquire about other autoimmune diseases in the patient or in her family.

Other autoimmune conditions that increase the risk for thyroid disease are: systemic lupus erythematosus, rheumatoid arthritis, pernicious anemia, vitiligo, type 1 diabetes, and Addison’s disease. Of note, patients with type 1 diabetes are three times more likely than those without that condition to develop PPT.

Q: Which tests will provide the best information about risk for or presence of PPT? When should I order such tests?

The thyroid-stimulating hormone (TSH) assay is the most sensitive laboratory test for thyroid function in a patient with a normal pituitary-thyroid axis. Testing for TPOAb is the best available screening tool for postpartum thyroiditis, being widely available, economical, and reproducible. Studies evaluating the utility of TPOAb have demonstrated a sensitivity of 46% to 89%, with a specificity of 91% to 98%. Depending on the timeline of the postpartum presentation, an elevated or low TSH level in conjunction with positive TPOAb is pathognomonic for PPT.

If the prospective or expectant mother has a personal or family history of an autoimmune disease, it would be a good idea to obtain a baseline TSH level and TPOAb. If unobtainable beforehand, a baseline TSH during pregnancy is prudent, since many of the signs and symptoms of hyper/hypothyroidism can be similar to those seen in “normal” pregnancy. A normal TSH in the face of elevated TPOAb increases the patient’s likelihood of developing Hashimoto’s thyroiditis or PPT. The best time to check TPOAb is before pregnancy or after delivery, since these antibodies can decrease or even normalize during pregnancy.

Q: Since PPT can be elusive, how might one clinically evaluate the postpartum patient?

The reasons for missed diagnosis of PPT are twofold. First, it results from women reporting few to no symptoms or simply “writing off” the signs and symptoms, thinking they’re related to the significant emotional/physical demands of caring for the new baby. Second, there is a lack of clinician recognition regarding the risk factors, clinical presentation, and frequency of PPT. Since one-third of the hyperthyroidism of PPT is asymptomatic or unreported by patients, it’s easy to see how clinicians can be uncertain whether postpartum anxiety, insomnia, palpitations, increased heart rate, and fatigue reflect thyrotoxicosis or “new mother demands.” Similarly, fatigue, constipation, impaired concentration/memory, weight gain, and depression can be interpreted as hypothyroidism or the emotional and physical challenges of infant care. Since either hyperthyroid or hypothyroid symptoms can be subtle, PPT goes undiagnosed—and therefore, untreated.

Here is an example to provide a clearer understanding:

PPT can go from hyperthyroid to hypothyroid over a four- to six-month period. I like to refer to this evolving process in its three phases to foster understanding of what is going on not only symptomatically but biochemically as well. The first phase starts with a bout of hyperthyroidism from an increased release of thyroid hormone (T4 and/or T3) as a result of nonpainful/nontender thyroid inflammation.

During this first phase, it’s unfortunate that many new mothers’ symptoms are “written off” as the anxieties associated with being a new mother. If a TSH is not ordered, the woman may feel that the clinician is correct in the assessment and that this is all a natural part of the postpartum period. If her hyperthyroid symptoms worsen, she is unlikely to seek follow-up care for fear of being deemed an “anxious mother,” and as a result, the correct diagnosis is missed.

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