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Hashimoto's thyroiditis

Hashimoto's thyroiditis, the most common form of thyroiditis, is an autoimmune disease where the body's own antibodies fight the cells of the thyroid. Also known as Hashimoto's disease, it is named after the Japanese physician, Hakaru Hashimoto (1881–1934) of the medical school at Kyushu University, who first described it to medicine in 1912. It is four times more common among women than men, and runs in families, with the HLADR5 gene most strongly implicated (conferring a relative risk of 3) in the UK. The genes implicated vary in different ethnic groups. more...

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In many cases, Hashimoto's thyroiditis usually results in hypothyroidism, although in its acute phase, it can cause a transient hyperthyroid state.

Physiologically, antibodies to thyroid peroxidase and/or thyroglobulin cause gradual destruction of follicles in the thyroid gland. Accordingly, the disease can be detected clinically by looking for these antibodies in the blood. It is also characterised by invasion of the thyroid tissue by leukocytes, chiefly T-lymphocytes.

Treatment is by daily thyroxine, with the sodium salt of thyroxine liothyronine given when the need to raise levels of circulating thyroxine is urgent.

Symptoms of Hashimoto's thyroiditis include symptoms of hypothyroidism and a goitre.

In European countries an atrophic form of autoimmune thyroiditis (Ord's thyroiditis) is more common than Hashimoto's thyroiditis.

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Postpartum thyroiditis - Tips from Other Journals
From American Family Physician, 4/1/92

Postpartum thyroiditis is a syndrome characterized by transient thyrotoxicosis, with a low thyroid radioactive iodine uptake followed by a hypothyroid phase. The syndrome occurs during the first year after delivery. Normal thyroid function is restored in most patients. Roti and Emerson review postpartum thyroiditis to delineate the pathophysiology, diagnosis and treatment.

In most studies, postpartum thyroiditis has been reported to occur in 3.9 to 8.2 percent of women. However, a marked variability occurs in the incidence rate. Some regions of Britain have an incidence rate as high as 16.7 percent, while New York and Thailand have reported rates of less than 2 percent.

The clinical course of postpartum thyroiditis consists of three sequential phases: thyrotoxic, hypothyroid and recovery. The syndrome usually presents with a thyrotoxic state that occurs one to three months after delivery and lasts for one to two months. Postpartum thyroiditis is distinguished from Graves' disease by a decreased radioactive iodine uptake. Thyrotoxicity is followed by a hypothyroid state that appears three to six months after delivery. Both thyrotoxic and hypothyroid states have few symptoms, except for fatigue; thus, the condition may go unrecognized. The most common physical sign in both stages is a painless enlargement of the thyroid gland.

Women with antithyroid antibodies or a history of goiter are more likely to develop postpartum thyroiditis. Many patients have underlying Hashimoto's thyroiditis, and women with Graves' disease develop postpartum thyroiditis more frequently than women in the general population. Thyroid antibody titers decrease during pregnancy with a nadir at term and a rise after delivery, possibly explaining the temporal relationship between delivery and postpartum thyroiditis. A strong correlation is not apparent between postpartum thyroiditis and other autoimmune disorders, such as rheumatoid arthritis and Sjogren's syndrome.

In a woman presenting with fatigue, palpitations, emotional lability or thyroid enlargement during the first year after delivery, postpartum thyroiditis should be considered. The usual thyroid screening tests, as well as radioactive iodine uptake scan and antithyroid antibody titers, should be performed. No therapy is warranted during the thyrotoxic phase, except beta blockers for symptomatic relief. During the hypothyroid stage, thyroid replacement should only be given if symptoms are severe. Many women are in the recovery phase when their symptoms are recognized.

All women with postpartum thyroiditis should have long-term follow-up, because hypothyroidism may recur in up to 23 percent of patients. Recurrent hypothyroidism may develop two to four years after the initial presentation. Iodine may also increase the incidence of hypothyroidism, so excess iodine intake should be discouraged in patients with postpartum thyroiditis. (Journal of Clinical Endocrinology and Metabolism, January 1992, vol. 74, p. 3.)

COPYRIGHT 1992 American Academy of Family Physicians
COPYRIGHT 2004 Gale Group

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