Hashimoto' Thyroiditis

Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is attacked by a variety of thyroid antibody until destroyed completely. Most of patients will end with serious hypothyroidism. It was the first disease to be recognized as an autoimmune disease. It was first described by the Japanese specialist Hakaru Hashimoto in Germany in 1912.

Signs and symptomsHashimoto's thyroiditis very often results in hypothyroidism with bouts of hyperthyroidism. Symptoms of Hashimoto's thyroiditis include Myxedematous psychosis, weight gain, depression, mania, sensitivity to heat and cold, paresthesia, fatigue, panic attacks, bradycardia, tachycardia, high cholesterol, reactive hypoglycemia, constipation, migraines, muscle weakness, cramps, memory loss, infertility and hair loss.

The thyroid gland may become firm, large, and lobulated in Hashimoto's thyroiditis, but changes in the thyroid can also be nonpalpable. Enlargement of the thyroid is due to lymphocytic infiltration and fibrosis rather than tissue hypertrophy. Physiologically, antibodies against thyroid peroxidase (TPO) 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 characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. It is associated with non-Hodgkin lymphoma.

Diagnosis is made by detecting elevated levels of anti-thyroid peroxidase antibodies in the serum.

Given the relatively non-specific symptoms of initial hypothyroidism, Hashimoto's thyroiditis is often misdiagnosed as depression, cyclothymia, PMS, chronic fatigue syndrome, fibromyalgia and, less frequently, as ED or an anxiety disorder. On gross examination, there is often presentation of a hard goitre that is not painful to the touch; other symptoms seen with hypothyroidism, such as periorbital myxedema, depends on the current state of progression of the response, especially given the usually gradual development of clinically relevant hypothyroidism. Testing for thyroid-stimulating hormone (TSH), Free T3, Free T4, and the anti-thyroglobulin antibodies (anti-Tg), anti-thyroid peroxidase antibodies (anti-TPO) and anti-microsomal antibodies can help obtain an accurate diagnosis. Earlier assessment of the patient may present with elevated levels of thyroglobulin owing to the transient thyrotoxicosis as inflammation within the thyroid causes damage to the integrity of thyroid follicle storage of thyroglobulin; TSH is concomitantly decreased.

Ultrasound imaging of the thyroid gland (right lobe longitudinal) in patient with Hashimoto Thyroiditis.This exposure of the body to substantial amounts of previously isolated thyroid enzymes is thought to contribute to the exacerbation of tolerance breakdown giving rise to the more pronounced symptoms seen later in the disease as thyroperoxidase and thyroglobulin are further exposed to without. Lymphocytic infiltration of the thyrocyte-associated tissues often leads to the histologically significant finding of germinal center development within the thyroid gland.

Hashimoto's when presenting as mania is known as Prasad's syndrome after Ashok Prasad, the psychiatrist who first described it.

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