At a Glance

Postpartum thyroid dysfunction, also known as postpartum thyroiditis (PPT), affects approximately 4-10% of postpartum women. PPT often occurs in stages, with thyrotoxicosis appearing first, followed by hypothyroidism. Not all women experience both stages of PPT. Approximately one-third of women with postpartum thyroid dysfunction exhibit both stages of the disease, whereas one-third of women have only a thyrotoxic or hypothyroid stage.

The thyrotoxic stage of PPT usually occurs 1-4 months after delivery and lasts approximately 1-3 months. This stage of PPT is often missed, because symptoms so closely mimic post pregnancy symptoms (i.e., fatigue, insomnia, anxiety, palpitations, and irritability), making it difficult to diagnose. Women will often present with the hypothyroid stage, which usually occurs 4-8 months after delivery and lasts approximately 9-12 months. Symptoms include fatigue, weight gain, and depression. Most women regain normal thyroid function within 12-18 months of the onset of symptoms, but about 20% of women who experience the hypothyroid stage remain hypothyroid.

Other symptoms of hypothyroidism include brittle fingernails; coarsening and thinning of hair; puffy eyes; pale, dry skin; weakness; and constipation. Symptoms expressing themselves later in the course of the disease are hoarseness; menstrual disorders; puffy hands, face, and feet; thickening of the skin; thinning of eyebrows; increased cholesterol levels; muscle and/or joint aches and stiffness; slowed speech; and decreased hearing.

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Other symptoms of hyperthyroidism include loss of concentration, nervousness, tremor, heat intolerance, excessive sweating, palpitations, muscle weakness, and enlarged thyroid gland.

PPT is believed to be an autoimmune disorder similar to Hashimoto’s thyroiditis. The exact cause of postpartum dysfunction is unknown. However, it is speculated to be the result of modification to the immune system required during pregnancy. PPT is associated with the development of antithyroid antibodies (antithyroid peroxidase (TPO) and antithyroglobulin (TgAb) antibodies. Women with autoimmune disorders, positive antithyroid antibodies, history of previous thyroid dysfunction, history of previous PPT, or family history of thyroid dysfunction are more likely at risk for developing PPT. Approximately 20% of women who have PPT develop the disease with subsequent pregnancies.

PPT should be differentiated from lymphocytic hypophysitis. Lymphocytic hypophysitis can also occur postpartum and may cause TSH deficiency along with one or more pituitary hormones, including ACTH. It can be distinguished from PPT by blood tests. Lymphocytic hypophysitis will have normal TSH levels with low FT4 levels, whereas PPT will have increased TSH levels with low FT4.

What Tests Should I Request to Confirm My Clinical Dx? In addition, what follow-up tests might be useful?

Diagnosis of PPT involves thyroid function tests, as well as thyroid antibody tests. In 65-85% of patients with PPT, thyroid peroxidase antibody (TPOAb) and TgAb concentrations are elevated, but TPOAb is the more sensitive. TSH and T4 should also be ordered. In the hyperthyroid stage of the disease, TSH levels are low, whereas T4 is high. In the hypothyroid stage of the disease, TSH levels are high, whereas T4 is low. In women who experience both stages of the disease, serum T4 levels may be low for several days to weeks before serum TSH levels rise above normal range.

During the hyperthyroid stage of the disease, a radioactive iodine uptake (RAIU) test may be performed (if the mother isn’t breast-feeding) to distinguish PPT from Grave’s disease. RAIU is decreased in women with PPT.

Are There Any Factors That Might Affect the Lab Results? In particular, does your patient take any medications – OTC drugs or Herbals – that might affect the lab results?

Interferences may obscure the diagnosis of PPT or complicate the monitoring of the effectiveness of thyroid replacement therapy.

Autoantibodies or heterophilic antibodies can interfere with thyroid function testing. Interferences caused by heterophilic antibodies can sometimes be detected by simply using a different manufacturer’s method. Tests in which dilutions are acceptable, such as total T4, total T3, or TSH, but not free T4 or free T3, may be checked for linearity of response.

Phenytoin, carbamazepine, aspirin, and furosemide competitively inhibit hormone protein binding and acutely increase free T4, resulting in a reduction in total T4. Eventually, a normal equilibrium is reestablished in which free T4 levels normalize at the expense of lower T4 levels.

Heparin stimulates lipoprotein lipase, liberating free fatty acids that inhibit total T4 protein binding and elevate free T4.

Glucocorticosteroids and dopamine can lower total T3 and inhibit TSH production. This interaction is of particular concern in sick, hospitalized patients in whom the elevated TSH level in primary hypothyroidism may be obscured.

Propranolol has an inhibitory effect on T4 to T3 conversion.

Liver disease, androgens, and nephrotic syndrome decrease thyroxine binding globulin (TBG) decreasing total thyroid hormones. Estrogens increase TBG, increasing total thyroid hormones.

Methods that use fluorescent tags may be affected by the presence of fluorophore-related therapeutic or diagnostic agents.

What Lab Results Are Absolutely Confirmatory?

It has been suggested that the best confirmation of hypothyroidism is an evaluation of response to a trial administration of thyroxine supplement in patients with symptoms of hypothyroidism.

What Tests Should I Request to Confirm My Clinical Dx? In addition, what follow-up tests might be useful?

In selecting analytes to diagnose PPT or monitor replacement therapy, one should remain aware that thyroxine binding is increased in pregnancy and decreased in liver disease, by androgens, and in nephrotic syndrome; concomitant use of highly protein bound drugs and systemic illness can alter test levels.

In general, serum TSH levels are less affected by binding issues than T3 and T4 levels. T3 and T4 circulate in the body bound to TBG; transthyretin, formally known as thyroxine binding prealbumin; and serum albumin and binding will be affected by changes in any of these binding components. Shifts toward total T3 or T4 will decrease available free T3 and free T4, the active forms of the hormones. Theoretically, free T3 or free T4 are not affected analytically by binding. However, in reality, all of the free methods are binding protein dependent to varying extents.

Are There Any Factors That Might Affect the Lab Results? In particular, does your patient take any medications – OTC drugs or Herbals – that might affect the lab results?

TSH or free T4 levels may be diagnostically misleading during transition periods of unstable thyroid function. Unstable thyroid status is seen with thyroiditis, including PPT. These transition periods may also occur in the early phase of treating hyper- or hypothyroidism or changing the dose of thyroxine supplement. It takes 6-12 weeks for pituitary TSH secretion to reequilibrate to the new thyroid hormone status.

Increased estrogen levels in pregnancy cause an increase in TBG, elevating free T4.