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Autoimmune Thyroid DiseasePostpartum Thyroiditis

Certain diseases affecting the function of the thyroid gland occur when an individual's immune system fails to recognize particular thyroid proteins as "self" and reacts to the proteins as if they were foreign. This usually triggers both humoral and cellular immune responses. As a result, antibodies to these proteins are generated, which then alter thyroid function. Two common autoimmune diseases with opposite effects on thyroid function are Hashimoto's disease and Graves' disease. In Hashimoto's disease, the thyroid gland is infiltrated by lymphocytes, and elevated levels of antibodies against several components of thyroid tissue (e.g., antithyroid peroxidase and antithyroglobulin antibodies) are found in the serum. The thyroid gland is destroyed, resulting in hypothyroidism. In Graves' disease, stimulatory antibodies to the TSH receptor activate thyroid hormone synthesis, resulting in hyperthyroidism (see text for details).

A third, fairly common autoimmune disease is postpartum thyroiditis, which usually occurs within 3 to 12 months after delivery. The disease is characterized by a transient thyrotoxicosis (hyperthyroidism) often followed by a period of hypothyroidism lasting several months. Many patients eventually return to the euthyroid state. Often only the hypothyroid phase of the disease may be observed, oc curring in more than 30% of women with antibodies to thyroid peroxidase detectable preconception. The disease is also observed in patients known to have Graves' disease. The postpartum occurrence of the disorder is likely due to increased immune system function following the suppression of its activity during pregnancy.

It has been estimated that 5 to 10% of women develop postpartum thyroiditis. Of these women, about 50% have transient thyrotoxicosis alone, 25% have transient hypothyroidism alone, and the remaining 25% have both phases of the disease. The prevalence of the disease has prompted a clinical recommendation suggesting that thyroid function (serum T4, T3, and TSH levels) be surveyed postpartum at 2, 4, 6, and 12 months in all women with thyroid peroxidase antibodies or symptoms suggestive of thyroid dysfunction. Patients who have experienced one episode of postpartum thyroiditis should also be considered at risk for recurrence after pregnancy.

Treatment for thyrotoxicosis commonly involves inhibiting thyroid hormone synthesis and secretion. Thion-amides are a class of drugs that inhibit the oxidation and organic binding of thyroid iodide to reduce thyroid hormone production. Some drugs in this class also inhibit the conversion of T4 to T3 in the peripheral tissues. Thyroid hormone replacement is required to treat hypothyroidism.

disorder caused by antibodies directed against the TSH receptor in the plasma membranes of thyroid follicular cells. These antibodies bind to the TSH receptor, resulting in an increase in the activity of adenylyl cyclase. The consequent rise in cAMP in follicular cells produces effects similar to those caused by the action of TSH. The thyroid gland enlarges to form a diffuse toxic goiter, which synthesizes and secretes thyroid hormones at an accelerated rate, causing thyroid hormones to be chronically elevated in the blood. Feedback inhibition of thyroid hormone production by the thyroid hormones is also lost.

Less common conditions that cause chronic elevations in circulating thyroid hormones include adenomas of the thyroid gland that secrete thyroid hormones and excessive TSH secretion caused by malfunctions of the hypothala-mic-pituitary-thyroid axis. The disease state that develops in response to excessive thyroid hormone secretion, called hyperthyroidism or thyrotoxicosis, is characterized by many changes in the functioning of the body that are the opposite of those caused by thyroid hormone deficiency.

Hyperthyroid individuals are nervous and emotionally irritable, with a compulsion to be constantly moving around. However, they also experience physical weakness and fatigue. Basal metabolic rate is increased and, as a result, body heat production is increased. Vasodilation in the skin and sweating occur as compensatory mechanisms to dissipate excessive body heat. Heart rate and cardiac output are increased. Energy metabolism increases, as does appetite. However, despite the increase in food intake, a net degradation of protein and lipid stores occurs, resulting in weight loss. All of these changes can be reversed by reducing the rate of thyroid hormone secretion with drugs or by removal of the thyroid gland by radioactive ablation or surgery.

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