Hashimoto’s disease is an autoimmune thyroid disorder, characterized by the production of antibodies in response to thyroid antigens (antibody producing) and the replacement of normal thyroid structures with lymphocytes and lymphoid germinal centers.
Chronic lymphocytic thyroiditis, or Hashimoto’s thyroiditis, was first described by the Japanese physician Hashimoto in 1912.
This disease shows a marked hereditary pattern but it is 20 times more common in women than in men. It occurs most frequently between 30 and 50 years of age but may arise in young children.
The thyroid, typically enlarged, pale yellow, and lumpy on the surface, shows dense lymphocytic infiltration, and the remaining thyroid tissue frequently contains small empty follicles.
The goiter (gradual painless enlargement of the thyroid gland) is usually asymptomatic (no symptoms), but sometimes patients complain of dysphagia (difficulty in swallowing) and a feeling of local pressure.
Thryroiditis is the general term used to describe three different disorders in which the thyroid becomes inflamed. Most commonly, the inflammation takes the form of a chronic, progressive disease known as chronic lymphocytic thyroiditis or Hashimoto’s disease. This condition may be so mild that it may go unnoticed for many years, but eventually it may destroy so much thyroid tissue that hypothroidism develops.
Hashimoto’s disease appears to be an inherited condition. As with Grave’s disease, one probably must inherit a gene or set of genes to be able to inherit this disorder.
It is most commonly diagnosed after the age of 40, for this is when patients usually become hypothyroid. The body’s immune system seems to play a role in the production of the thyroid inflammation and tissue destruction that occurs in chronic lymphocytic thyroiditis.
Substances known as autoantibodies, made by certain white blood cells called lymphocytes, appear in the blood in this condition. It is most likely that these antibodies have the capacity to damage thyroid tissue. When enough tissue has been destroyed, the thyroid hormone production falls below normal, and symptoms of hypothyroidism appear.
In its very early stages, the thyroid inflammation probably will be so mild that at first nothing will appear to be wrong. The first indication of a problem may be a goiter - a gradual painless enlargement of the thyroid gland.
During this period, the thyroid gland is becoming infiltrated with lymphocytes, which start gradual thyroid destruction and scarring that result in subsequent thyroid failure. If the function of the thyroid decreases to the point that the gland can no longer make a normal amount of thyroid hormone, symptoms of hypothyroidism appear, and the patient may begin to look and feel sick for the first time. At this point, the destruction of the thyroid may be so extensive that very little normal thyroid tissue remains.
Essentially, the diagnosis of Hashimoto’s disease is based on finding thyroid antibodies in the blood. The level of these often increases as the disease progresses. In the late stages when all the thyroid gland has been destroyed, the level of the auto-antibodies may fall to low or undetectable levels.
There is no safe and reliable way of modifying the faulty immunological system that mistakenly believes that your thyroid cells are “foreign.” Thus, the basic cause of Hashimoto’s thyroiditis is not treated.
If the patient had a temporary phase of Hashitoxicosis (Hashimoto’s + toxic + condition), a beta-blocker and/or antithyroid medication, such as carbimazole, may be given for a short time.
If the gland becomes uncomfortably painful, a short course of corticosteroids may be used in subacute viral thyroiditis.
In general, the treatment is the management of the consequences of thyroid failure, although a goiter is sometimes prevented from becoming larger or is reduced in size by giving thyroxine.
The essential step is the prevention of hypothyroidism when this is imminent or the correction of hypothyroidism when this has developed. The best treatment is replacement therapy with thyroxine.
Occasionally, surgery is required, particularly if there is any possibility that the goiter is due to cancer and not to Hashimoto’s disease. This difficulty may arise when the thyroid feels very hard or is enlarged unevenly, but usually a needle biopsy will resolve this diagnostic difficulty.
What tests need to be done to diagnose which disorder is involved, or to rule out some other disease?
How much of the thyroid has been destroyed?
Are there any complications to this condition as it progresses?
Will any treatment be recommended?
Will thyroxine be prescribed? What are the side effects? Will this be required for life?
What can be expected from lifelong hormone therapy?
Are there any signs or symptoms that should be reported immediately?