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Hashimoto's thyroiditis is named after the physician who first described the disease. In this condition, the thyroid is classically infiltrated by white blood cells known as lymphocytes, and is easily diagnosed on biopsy. Hashimoto disease is an autoimmune process, and is seen predominantly in women. In this disease, the body mounts a renegade attack on parts of the thyroid tissue. Blood tests are available to measure antibodies (in particular thyroperoxidase antibodies- TPO antibodies) that point to the diagnosis in the right clinical setting. Hashimoto's disease tends to run in families, and does have a genetic susceptibility (HLA-DR3 and HLA DR5 are the most commonly associated alleles). Because of the infiltration of lymphocytes into the thyroid tissue, the normal architecture and function of the gland is lost, rendering the patient with Hashimoto's hypothyroid, a process which occurs gradually. On examination, the thyroid gland is usually enlarged and painless. Rarely, patients with Hashimoto's disease become transiently hyperthyroid as the destruction of the gland allows for rapid release of thyroid hormone from the dying cells. This phase is short lived, and progresses to overt hypothyroidism.
As mentioned, the diagnosis can be made by biopsy, however, clinical history along with a blood test confirming hypothyroidism plus the addition of anti-TPO antibodies and a thyroid scan (if needed) also secures the diagnosis in most cases. Treatment involves starting thyroid hormone replacement (Synthroid, Levoxyl) to maintain a TSH level (thyroid stimulating hormone) within the normal range. If the thyroid is large enough to cause symptoms of compression (difficultly swallowing, hoarseness, wheezing), surgery to debunk or remove the gland may be considered if the gland dose not shrink on replacement therapy. Further information on Hashimoto's disease hypothyroidism can be found in the Hashimoto's Thyroiditis and Hypothyroidism articles.
In regard to your question about heart disease, the relationship is more related to replacement therapy of the thyroid hormones than with Hashimoto's itself. As the gland starts to lose function, hypothyroidism can result. Hypothyroidism is treated by replacing the inappropriately low, or absent endogenous thyroid hormone with a synthetic equivalent taken daily by mouth (Synthroid or Levoxyl, for example). Should a patient be over-replaced, the high dose of hormones can result in palpitations, irregular heartbeat, and over time, a weakened heart. It can also result in osteoporosis. If the hormone is under-replaced, it can exacerbate heart failure, change cholesterol profiles to become more unfavorable and slow heart rates down. Naturally, if Hashimoto's resulting in hypothyroidism remains untreated completely, this can also occur.
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"Pathogenesis of Hashimoto's thyroiditis (chronic autoimmune thyroiditis)"