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Postpartum Thyroiditis and Chronic Thyroiditis With Transient Thyrotoxicosis

Chronic thyroiditis with transient thyrotoxicosis is a disorder in which a self-limited episode of thyrotoxicosis is associated with a histologic picture of chronic lymphocytic thyroiditis. Ongoing production of thyroid hormone is negligible and the RAIU is decreased. The syndrome occurs in patients of any age and mainly in women. Manifestations of thyrotoxicosis are usually mild but may be severe. The thyroid is nontender, firm, symmetric, and slightly or moderately enlarged.

The etiology, pathogenesis, and pathophysiology of this disorder are unclear. Viral antibody titers show no characteristic patterns. It is presumed that thyrotoxicosis results from leakage of hormone from the gland, as in subacute thyroiditis. Low values for the RAIU, in turn, reflect hormonal suppression of TSH secretion and not increased plasma iodine, since urinary iodine excretion is not greatly elevated. Some degree of postpartum thyroditis.

Thyrotoxicosis in CT/TT usually abates within 2 to 5 months, and the thyrotoxic phase may be followed by a hypothyroid phase. The latter is usually self-limited.

Postpartum thyroiditis is a variant of CT/TT which occurs after pregnancy. This disorder develops within 2 to 6 months after delivery in 5 to 6 percent of otherwise normal women and in about one-fourth of women with insulin-dependent diabetes mellitus. Such patients usually have a small goiter and a family history of thyroid disease and may have postpartum depression. Within the first 2 to 3 months post partum, transient symptoms of thyrotoxicosis, such as fatigue, palpitations, emotional lability, and heat intolerance, are likely. Laboratory findings include elevated serum levels of T₄ and T₃, suppressed TSH, elevated titers of antithyroid antibodies, and a low RAIU. Patients may undergo a subsequent hypothyroid phase (from 4 to 8 months post partum) associated with a low serum T₄ level, elevated TSH, and high titers.

In the thyrotoxic phase, this disorder can be differentiated from Graves' disease by demonstration of a depressed RAIU and the absence of increased urinary iodine excretion. The latter finding also excludes the jodbasedow syndrome. When these data are available, the disorder must be differentiated from other causes of thyrotoxicosis with a low RAIU, principally subacute thyroiditis. Lack of tenderness or nodularity of the thyroid and absence of marked elevation of the ESR tend to exclude the latter diagnosis. Patients with either functioning ectopic thyroid tissue or thyrotoxicosis factitia.

Since the thyroid is not hyperfunctioning in this disorder, measures used in the treatment of hyperthyroidism are useless.