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Postpartum Endocrine Disorders

Posted by on Dec. 15, 2008 at 11:38 AM
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Endocrine Disorders

Postpartum thyroid dysfunction can occur any time in the first postpartum year. Clinical or laboratory dysfunction occurs in 5-10% of postpartum women and may be caused by primary disorders of the thyroid, such as postpartum thyroiditis (PPT) and Graves disease, or by secondary disorders of the hypothalamic-pituitary axis, such as Sheehan syndrome and lymphocytic hypophysitis.

Postpartum thyroiditis

PPT is a transient destructive lymphocytic thyroiditis occurring within the first year after delivery.


PPT develops 1-8 months postpartum and is an autoimmune disorder in which microsomal antibodies of the thyroid play a central role. PPT has 2 phases: thyrotoxicosis and hypothyroidism.

  • Thyrotoxicosis occurs 1-4 months postpartum and is always self-limited. The condition is caused by the increase release of stored hormone as a result of disruption of the thyroid gland.
  • Hypothyroidism arises between the fourth and eighth month postpartum.

Risk factors for development of PPT include a positive antithyroid antibody test finding, history of PPT, and family or personal history of other thyroid or autoimmune disorders.


Approximately 4% of women develop transient thyrotoxicosis in the postpartum period. Of these, 66-90% return to a euthyroid state; 33% progress to hypothyroid. Approximately 2-8% of women develop hypothyroidism in the postpartum period. A third of these patients experience transient thyrotoxicosis, whereas 10-30% go on to develop permanent thyroid dysfunction.

Morbidity and mortality

Patients with high antithyroid antibody levels during pregnancy, multiparity, and history of spontaneous abortions are at high risk for permanent hypothyroidism. Having developed PPT, these women are at significant risk for recurrent disease after subsequent pregnancies.


Patients with thyrotoxicosis may report fatigue, palpitations, heat intolerance, tremulousness, nervousness, and emotion liability. Patients in the hypothyroid phase often complain of fatigue, dry skin, coarse hair, cold intolerance, depression, and memory and concentration impairment. Because many of these symptoms are mild and nonspecific and are often associated with the normal postpartum state, PPT may go undiagnosed.


On examination, a patient may have tachycardia, mild exophthalmos, and a painless goiter.


The first laboratory test to be performed should be the thyroid-stimulating hormone (TSH) test. TSH is decreased during the thyrotoxicosis stage and increased during the hypothyroid phase. If the TSH level is abnormal, check thyroid stimulating antibodies, free thyroxine index (FTI), and radioactive iodine uptake (RIU) in order to distinguish this disorder from Graves disease. In PPT, RIU is low, thyroid-stimulating antibodies are undetectable, and FTI is high.

A thorough, cost-effective screening test for PPT does not exist; therefore, limit screening to high-risk patients such as those with previous PPT or other autoimmune disorders.


No treatment is available to prevent PPT.

Thyrotoxicosis phase: No treatment is required for the thyrotoxicosis phase unless the patient's symptoms are severe. In this case, a beta-blocker is useful. For example, propranolol can be started at 20 mg every 8 hours and can be doubled if the patient remains symptomatic. Propylthiouracil (PTU) has no role in the treatment of PPT because the disorder is caused by the release of hormone from the damaged thyroid and is not secondary to increased synthesis and secretion.

Hypothyroid phase: Since the hypothyroid phase of PPT is often transient, no treatment is required unless necessitated by the patient's symptoms. Treatment is with thyroxine (T4) replacement. T4 is most often given for 12-18 months, then gradually withdrawn. The starting dose is 0.05-0.075 mg, which may be increased by 0.025 mg every 4-8 weeks until a therapeutic level is achieved.

Postpartum Graves disease

Postpartum Graves disease is not as common as PPT, but it accounts for 15% of postpartum thyrotoxicosis. Similar to classic Graves disease, postpartum Graves disease is an autoimmune disorder characterized by diffuse hyperplasia of the thyroid gland caused by the production of antibodies to the thyroid TSH receptor, resulting in increased thyroid hormone production and release. No clinical features distinguish postpartum Graves disease from Graves disease in other settings; therefore, diagnosis and management of this disorder is beyond the scope of this article (see Graves Disease).

Lymphocytic hypophysitis

Lymphocytic hypophysitis is a rare autoimmune disorder causing pituitary enlargement and hypopituitarism, leading to a decrease in TSH and to hypothyroidism. Symptoms include headache, visual field deficits, difficulty lactating, and amenorrhea. Diagnosis requires histopathologic examination. Most patients do not require transsphenoidal hypophysectomy, so diagnosis is based on history, physical, diagnostic imaging, and the temporal relationship to pregnancy. Identification of the disorder becomes clearer as the pituitary reverts to its normal size and recovers some of its normal function. During the acute phase of this disease, hormone replacement is often necessary.

Sheehan syndrome

Sheehan syndrome is the result of ischemia, congestion, and infarction of the pituitary gland, resulting in panhypopituitarism caused by severe blood loss at the time of delivery. Patients have trouble lactating and develop amenorrhea, as well as symptoms of cortisol and thyroid hormone deficiency. Treatment is with hormone replacement in order to maintain normal metabolism and response to stress.

Mother Mary had an unassisted birth and breastfed Jesus.

by on Dec. 15, 2008 at 11:38 AM
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