Postpartum thyroiditis

Drugs (amiodarone, radiocontrast media, lithium, a-interferon) Silent thyroiditis (including postpartum)... 

Painless (silent, lymphocytic, postpartum) thyroiditis is a common cause of thyrotoxicosis its etiology is not fully understood and may be heterogeneous autoimmunity may underlie most cases. 

Treatment-related altered serum th5Toid hormone levels indicate that chlorine dioxide and chlorite may exert toxic effects that are mediated through the neuroendocrine axis. Changes in thyroid hormones have been reported in laboratory animals that were either directly exposed to chlorine dioxide (repeated doses as low as 9 mg/kg/day), or exposed to chlorine dioxide or chlorite via their mothers (maternal doses of chlorine dioxide and chlorite as low as 13 and 9 mg/kg/day, respectively) during pre- and postpartum development (Bercz et al. 1982 Carlton and Smith 1985 Carlton et al. 1987, 1991 Mobley et al. 1990 Orme et al. 1985). 

Secondary hypothyroidism, or pituitary hypothyroidism, is the consequence of impaired thyroid-stimulating hormone (TSH) secretion and is less common than primary hypothyroidism. It may result from any of the causes of hypopituitarism (e.g., pituitary tumor, postpartum pituitary necrosis, trauma). Patients with secondary hypothyroidism exhibit undetectable or inappropriately low serum TSH concentrations. In secondary hypothyroidism, a normal thyroid gland lacks the normal level of TSH stimulation necessary to synthesize and secrete thyroid hormones. Such patients usually also have impaired secretion of TSH in response to exogenous thyrotropin-releasing hormone (TRH) administration. 

The manifestations of hyperthyroidism depend on the severity of the disease, the age of the patient, the presence or absence of extrathyroidal manifestations, and the specific disorder producing the thyrotoxicosis. Of the various types of hyperthyroidism, only two are common Graves disease and toxic multinodular goiter. Less common causes include toxic adenoma and postpartum thyroiditis, among others. 

The second patient had other risk factors for autoimmune thyroid disease, and the association was probably coincidental, but the episode may have been precipitated by low estrogen concentrations, as is hypothesized in postpartum thyroiditis. 

Browne-Martin K, Emerson CH. Postpartum thyroid dysfunction. Clin Obstet Gynecol 1997 40 90-101. 

Since its description in 1975, painless (sUent, lymphocytic, postpartum) thyroiditis has been recognized as a common cause of thyrotoxicosis and may represent up to 15% of cases of thyrotoxicosis in North America. The etiology is not fully understood and may be heterogeneous. The triphasic course of this illness mimics that of painful thyroiditis. Most patients present with mild thyrotoxic symptoms. Lid retraction and lid lag are present but exophthalmos is absent. The thyroid gland may be diffusely enlarged but thyroid tenderness is absent. 

The 24-hour RAIU wiU be suppressed to less than 2% during the thyrotoxic phase of painless thyroiditis. Antithyroglobuhn and antimicrosomal antibody levels are elevated in more than 50% of patients. Painless thyroiditis frequently occurs during the immediate postpartum period, and individual patients may experience recurrence of the disease with subsequent pregnancies. Patients with mild hyperthyroidism and painless thyroiditis should be reassured that they have a self-hmited disease. Adrenergic symptoms may be ameliorated with propranolol. Antithyroid drugs are not indicated because they do not decrease the release of preformed thyroid hormone. 

TSH is required for normal thyroid secretion. Thyroid atrophy and decreased thyroid secretion follow pituitary failure. Pituitary insufficiency may be caused by destruction of thyrotrophs by either functioning or nonfunctioning pituitary tumors, surgical therapy, external pituitary radiation, postpartum pituitary necrosis (Sheehan s syndrome), infiltrative processes of the pituitary such as metastatic tumors, tuberculosis, histiocytosis, and autoimmune mechanisms. In all these sitnations, TSH deficiency most often occurs in association with other pituitary hormone deficiencies. 

Momotani N, Noh J, Ishikawa N, Ito K. Relationship between silent thyroiditis and recurrent Graves disease in the postpartum period. J CUn Endocrinol Metab 1994 79 285-289. 

Stagnaro-Green A. Recognizing, understanding, and treating postpartum thyroiditis. Endocrinol Metab CUn North Am 2000 29 417-430, ix. 

Stagnaro-Green A (2002) Clinical review 152 Postpartum thyroiditis. Clin Endocrinol Metab, 87 4042-4047. 

Thyroid Hypofunction Hypothyroidism is the most common disorder of thyroid function. It can be divided into patients who have a failure of the thyroid gland to produce sufficient thyroid hormone (primary hypothyroidism) and patients in which pituitary or hypothalamic disease is associated with impaired TSH stimulation (central or secondary hypothyroidism). Worldwide, primary hypothyroidism is caused most often by iodine deficiency. In areas where iodine is sufficient, chronic autoimmune thyroiditis (Hashimoto s thyroiditis) accounts for most cases. Other causes include postpartum thyroiditis, surgical removal, or radioactive iodine ablation of the gland. Hypothyroidism present at birth (cretinism) is the most common preventable cause of mental retardation in the world. 

AITD have high concentrations of circulating thyroid autoantibodies (Arai et ai, 2000 Carle et aL, 2006 Feldt-Rasmussen, 1996), for the most part the disorder appears to be the consequence of tissue damage initiated by T lymphocytes (Weetman and McGregor, 1994). Measurement of autoantibodies against thyroid peroxidase (TPO-Ab) and thyroglobulin (Tg-Ab) has for many years been a major tool in the diagnosis of autoimmune thyroid diseases, such as Hashimotos thyroiditis, primary myxedema and postpartum thyroiditis (Feldt-Rasmussen et ai, 1991 Feldt-Rasmussen, 1996). 

Women who have recendy been pregnant comprise an important subpopulation that is frequendy studied to elucidate the prevalence of hypothyroidism. While there are no large population-based reports to date, there are considerable data on the frequency of hypothyroidism in relatively small groups of patients. Postpartum lymphocytic thyroiditis results in transient hypothyroidism, with up to one quarter of patients eventually becoming permanently... 

Hypothyroidism thus remains a significant source of morbidity in the American population. Within this iodine-replete population, relatively small differences in iodine intake do not appear to significantly affect the prevalence of this disorder. Although the risk of hypothyroidism associated with postpartum thyroiditis is significant, the most important subpopulation at risk for hypothyroidism appears to be the elderly. 

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