The function of the immune system is to protect the body from foreign substances that may attack it and potentially cause harm. Antibodies are made by the body to destroy these harmful substances. When you have an autoimmune disorder, your body makes antibodies to part of your body itself and it may destroy body tissues that are needed for normal function. Usually autoimmune diseases have a genetic component and need to have an environmental trigger. This section will address common autoimmune diseases that lead to hypothyroidism.
Hashimoto's thyroiditis, also called chronic lymphocytic thyroiditis or autoimmune thyroiditis, is the most common cause of hypothyroidism in the United States and in areas of the world where iodine is considered sufficient. Two percent of the United States's population has been estimated to have Hashimoto's, with up to 10 percent of women over the age of 55 and 3 percent of men affected by subclinical hypothyroidism. Hashimoto's is less often seen in children.
A person with subclinical hypothyroidism has elevated TSH levels, but T4 and T3 levels are normal. With full-blown Hashimoto's, there are circulating thyroid antibodies, a loss of thyroid follicular cells, diffuse lymphocytic infiltration of the thyroid, and the inability to make enough thyroid hormone. In some people, a goiter or noticeable swelling over the thyroid is also present.
Are there any genetic or environmental factors that will cause Hashimoto's?
According to the American Academy of Family Physicians, thyroid autoimmunity is inherited as a dominant trait. One may also need environmental triggers, such as excessive iodine consumption (the disease prevalence is in proportion to the intake of the population), radiation exposure from nuclear accidents, infection, stress, or pregnancy to develop Hashimoto's, but these triggers have not been shown to be conclusive.
Autoimmune diseases have characteristic symptoms of the body's own immune response, making antibodies that, over time, destroy its own tissue. In most cases of Hashimoto's thyroiditis, antibodies form that attack thyroid peroxidase (TPO) or thyroglobulin (Tg). Thyroid peroxidase is an enzyme in the thyroid that is involved in thyroid hormone production. Thyroglobulin is the protein that combines with iodine to make thyroid hormones.
If your doctor suspects Hashimoto's disease, she may order lab work to determine the presence of thyroglobulin antibody (TgAb) and thyroper-oxidase antibody (TPOAb). Some people may have the antibodies without Hashimoto's disease. These people are at a higher risk of developing thyroid disease, so they should be periodically checked. Testing for TSH and T4 is needed to confirm the diagnosis of Hashimoto's and in order to select the correct therapy.
An antibody is a protein component of the immune system that circulates in the blood, recognizes foreign substances like bacteria and viruses, and neutralizes them. After exposure to a foreign substance, called an antigen, antibodies continue to circulate in the blood, providing protection against future exposures to that antigen.
Symptoms of Hashimoto's disease can be vague. During the stages of subclinical hypothyroidism, there most likely will be no symptoms at all. The body is able to keep up with making thyroid hormone, but the pituitary gland needs to send more TSH to the thyroid for this to happen. This is why TSH is elevated at this stage of the disease.
As time goes on, the thyroid is not able to produce enough T4, and classic symptoms of hypothyroid may develop. As patients feel the slowing of their metabolism, they may complain of fatigue, heavy menstrual bleeding in women, weight gain, and hair and nail changes. Hair may become thin and break easily, and skin may become very dry. Patients may also notice an increased sensitivity or intolerance to cold.
As these symptoms may reflect other problems, patients may not report them to their physician. Women in childbearing years need to report a family history of thyroid problems to their physician and have their thyroid hormone levels checked.
Treatment of Hashimoto's consists of thyroid hormone replacement. Usually this is in the form of T4. Patients may be asked by their physicians to have periodic laboratory testing of TSH and T4 values. Over time, with progression of the disease, higher doses of replacement are likely.
If Hashimoto's disease is not treated, complications may be severe. Goiter, heart disease, heart failure, osteoporosis, and depression may develop. In women of childbearing age, infertility, miscarriage, and birth defects may also occur. Myxedema coma is a rare but life-threatening problem. This medical emergency occurs when the slowing of metabolism leads to confusion and decreased blood pressure, heart rate, breathing, and blood sugar. The patient's lips and tongue may be swollen and they may have puffiness around the face. Emergency help is needed.
Atrophic thyroiditis or Ord's disease is not widely covered in the literature. It has been described historically as another type of autoimmune thyroiditis without goiter. Recent studies by Allan Carlé, MD, PhD, in the Journal of Clinical Endocrinology and Metabolism classify Ord's disease and Hashimoto's as extremes of the same disease with a normal distribution of thyroid volumes.
Postpartum thyroiditis can develop into a form of Hashimoto's thyroiditis. Antiperoxidase antibodies are typical. Postpartum thyroiditis can follow three courses:
Transient hyperthyroidism: This is where the mother develops hyperthyroidism that resolves.
Transient hypothyroidism: Transient hypothyroidism follows transient hyperthyroidism. Hyperthyroidism develops, followed by hypothyroidism, and then the condition resolves.
Hypothyroidism: It is not unusual for women that have had hypothyroidism in the postpartum period progress with the disease process to full-blown hypothyroidism. In this case, the therapy would be the same as for Hashimoto's.