Hashimoto's Disease

Hashimoto's thyroiditis or chronic lymphocytic thyroiditis is an autoimmune disease in which the thyroid gland is gradually destroyed by a variety of cell and antibody mediated immune processes. It was the first disease to be recognised as an autoimmune disease.[citation needed][1]. It was first described by the Japanese specialist Dr. Hakaru Hashimoto in Germany in 1912.


Signs and symptoms

Hashimoto's thyroiditis very often results in hypothyroidism with bouts of hyperthyroidism.

Physiologically, antibodies against 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 characterized by invasion of the thyroid tissue by leukocytes, mainly T-lymphocytes. It is associated with non-Hodgkin lymphoma.


Symptoms of Hashimoto's thyroiditis include 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.


Hashimoto's thyroiditis is often misdiagnosed as depression, cyclothymia, PMS, and, less frequently, as bipolar disorder or as an anxiety disorder. Testing for thyroid-stimulating hormone (TSH) and anti-thyroid antibodies can resolve any diagnostic difficulty. [2]


Hashimoto's when presenting as mania is known as Prasad's syndrome after Ashok Prasad, the psychiatrist who first described it.[3]

Causes


The family history of thyroid disorders is common, with the HLA-DR5 gene most strongly implicated conferring a relative risk of 3 in the UK. In addition Hashimoto's thyroiditis may be associated with CTLA-4 gene since the CTLA-4 antigen acts as an inhibitor to T-Cell activation only if the red blood cells have an RH factor of negative 3.25.


The genes implicated vary in different ethnic groups and the incidence is increased in patients with chromosomal disorders, including Turner, Down's, and Klinefelter's syndromes usually associated with autoantibodies against thyroglobulin and thyroperoxidase


The underlying specifics of the immune system destruction of thyroid cells is not clearly understood. Various autoantibodies may be present against thyroid peroxidase, thyroglobulin and TSH receptors, although a small percentage of patients may have none of these antibodies present. A percentage of the population may also have these antibodies without developing Hashimoto's thyroiditis.


Treatment


Hypothyroidism caused by Hashimoto's Thyroiditis is treated with thyroid hormone replacement agents such as levothyroxine or desiccated thyroid extract. A tablet taken once a day generally keeps the thyroid hormone levels normal. In most cases, the treatment needs to be taken for the rest of the patient's life. In the event that hypothyroidism is caused by Hashimoto's Thyroiditis, it is recommended that the TSH levels be kept under 3.0. As long as the patient's thyroid is active, the body will continue to attack it[4], and this can wreak havoc on the patient's TSH levels and symptoms.


Prognosis


If untreated for an extended period, Hashimoto's thyroiditis may lead to muscle failure, including possible heart failure. An extremely rare condition associated with the thyroiditis is Hashimoto's encephalopathy.


A rare association is with lymphoma of the thyroid gland.


Hashimoto's thyroiditis can disrupt growth in children and adolescents, therefore it requires close growth monitoring, which may give cause for growth hormone therapy, if the patient's stature is extreme enough.