Hakaru Hashimoto is a Japanese physician who was first to describe the condition in a German paper in 1912. Hashimoto’s thyroiditis is an inflammation of the thyroid gland and sometimes referred to as Hashimoto’s disease, chronic lymphocytic thyroiditis and autoimmune thyroiditis.
Hashimoto’s thyroiditis results from the malfunction of the immune system. The thyroid antibodies attack the thyroid gland causing swelling and inflammation. The healthy cells and tissue are slowly destroyed and the gland is not able to produce enough thyroid hormones to maintain the body’s metabolism.
In the early stages of the disease some individuals may experience intermittent and temporary phases of overactive and underactive thyroid function. This short term event characterized by an abnormally high increase in thyroid hormone levels is called hashitoxicosis. The patient will have hyperthyroid symptoms such as nervousness, trembling and temporary rapid weight loss.
The disease progresses gradually and many people aren’t aware they have it until the enlarged gland forms a goiter. Goiter is an abnormal enlargement of the thyroid gland. In some individuals it could be seen and felt as a swelling in the front of the neck. In people with Hashimoto’s disease the goiter is normally painless and it could take weeks or even years to form.
The antibodies are produced when foreign substances, called antigens are present in the body, each antibody is active against only one type of antigen. The antibody will combine with the antigen and make it inactive.
There are two types of antibodies associated with Hashimoto’s disease:
- Antithyroperoxidase antibodies (TPO Ab) that sometimes is also called microsomal antibodies and act against thyroid peroxidas. Thyroid peroxidase (TPO) is an enzyme made in the thyroid gland. Without functional thyroid peroxidase the iodine taken up by the thyroid gland is not added to thyroglobulin and then as a result the production of thyroid hormones is absent or reduced. In most affected individuals, hypothyroidism occurs and the thyroid gland becomes enlarged building a goiter in an attempt to compensate for reduced hormone production.
- Antithyroglobulin antibodies (Tg Ab) act against a protein called thyroglobulin, which is found in thyroid cells. Thyroglobulin constitutes the storage form of T3 and T4 thyroid hormones within the thyroid gland. As the result of action of the Tg antibodies, lymphocytic destruction of thyroid tissue may occur.
Simple thyroid blood testing can be performed to determine the presence and level of antibodies. A negative test is normal and means no antibodies are detected. If the higher level of antibodies are measured the more likely autoimmune process to be initiated.
Significantly elevated or high thyroid antibodies are most frequently found in Hashimoto’s and Grave’s diseases. In Hashimoto’s thyroiditis the antithyroglobulin antibodies, or antithyroid peroxidase antibodies, or both combined may be present at the same time.
There are some other medical conditions such as hypothyroidism, myxedema, Systemic lupus erythematosus (SLE), thyroid cancer, thyrotoxicosis, rheumatoid arthritis, pernicious anemia, autoimmune collagen vascular disease and type 1 diabetes where the level of thyroid antibodies is mild to moderately elevated.
High normal or low positive thyroid antibodies can also be present in pregnant women and in healthy people. It means that there is a risk that eventually the person may develop hypothyroidism or autoimmune disease.
Hashimoto’s disease can result in hypothyroidism
While the exact mechanism of the autoimmune thyroiditis remains unknown, it is stated in current research that the genetic predisposition combined with environmental triggers initiate the autoimmune response to the thyroid gland. About 80% of the susceptibility to develop an autoimmune thyroid disease (AITD) is attributed to genetic factors, while environmental factors contribute to 20%.
Most people with Hashimoto’s disease don’t have any symptoms initially. As disease progresses some patients can experience hyperthyroid symptoms due to excess of thyroid hormone coming into the blood strem as the thyroid gland becomes destructed during the autoimmune attack.
These periods of thyroid hormone release and hyperthyroid symptoms are usually followed by times when a person has hypothyroid symptoms. Some people with Hashimoto’s seem to never get their thyroid levels stable and their doctors are constantly trying to adjust the dose of thyroid medication ignoring the fact that autoimmune attack on the thyroid gland is in progress.
When the thyroid cannot produce enough thyroid hormones to meet the body’s needs, the person becomes hypothyroid. Hashimoto’s thyroiditis has become the most common cause of hypothyroidism in North America and other industrialized countries. The disease occurs six times more frequently in women than in men (female/male ratio 6:1).
Hypothyroid symptoms are varied because there are thyroid hormone receptors in virtually every tissue of the body. Often a subclinical hypothyroidism occurs first then progresses to a persistent hypothyroidism and requires thyroid hormone replacement. In most cases Hashimoto’s thyroiditis is a permanent condition that can not be reversed and needs a life-long treatment.
There is a new approach in treating the Hashimoto’s disease as an autoimmune condition using the modulation of the immune system. The goal of the treatment is to stop autoimmune attack on your thyroid by calming down and balancing the immune system, and to heal the inflammation. As a result, the autoimmune condition may become stable and it prevents the thyroid gland from further destruction. If caught early, the level of antibodies can fall before causing permanent damage allowing to preserve the thyroid gland.
Other very successful treatment is a holistic nutritional approach that is based on identifying and removing dietary triggers of Hashimoto’s disease, healing leaky gut syndrome, optimizing digestion and using whole foods to support immune system and correct nutritional deficiencies.
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