Lesson 3: Autoimmune Thyroid Disease
Autoimmune Thyroid Disorders
The various autoimmune thyroid disorders or AITDs include Graves’ disease, which is autoimmune hyperthyroidism, Hashimoto’s thyroiditis and idiopathic thyroid failure, which cause autoimmune hypothyroidism, and Hashitoxicosis. All of these disorders are considered to be overlapping syndromes.
Patients with both Graves’ disease and Hashimoto’s thyroiditis may experience periods of Hashitoxicosis especially as they move between hypothyroidism and hyperthyroidism. Hashitoxicosis is primarily a condition of hypothyroidism characterized by the presence of stimulating TSH receptor antibodies, the antibodies that cause hyperthyroidism in Graves’ disease. These antibodies cause transient symptoms of hyperthyroidism whenever these antibody levels rise in sufficient amounts to cause a temporary burst of excess thyroid hormone.
Symptoms Certain symptoms tend to overlap, that is, they may occur in any of the autoimmune thyroid disorders. Overlapping symptoms include palpitations, sleep disturbances, vitiligo, an autoimmune condition characterized by patches of white unpigmented skin, weight gain, weight loss, hair loss, inability to properly regulate body temperature, mood swings, depression, irritability, digestive disturbances and cognitive changes.
Certain symptoms, such as mental fog and hair loss, are more common in hypothyroidism than hyperthyroidism, but these symptoms can occur in either disorder. Nevertheless, because symptoms overlap it can be difficult to recognize when someone has moved from hyperthyroidism to hypothyroidism without measurements of the thyroid hormones FT4 and FT3.
Autoimmune thyroid disorders also share certain features that distinguish them from other thyroid disorders. They’re all caused by thyroid antibodies, they cause changes in thyroid cells that can be studied microscopically, and they have a genetic predisposition. Patients with AITDs also show evidence that their immune cells react to various proteins found within thyroid cells. Specifically, immune reactivity demonstrated by antibody production is directed against the TSH receptor protein found on the surface of thyroid cells, the enzyme thyroid peroxidase or TPO, and thyroglobulin. Antibodies to these proteins are easily found in patients with AITDs and their presence helps with diagnosis.
Tests for TSH, FT4 and FT3, are used as screening tests to determine if hypothyroidism or hyperthyroidism are present. Thyroid antibody tests are then used to establish that the thyroid disorder is autoimmune in origin. Thyroglobulin, TPO, and TSH receptor antibodies can be found in all of the autoimmune thyroid disorders. Patients with TPO, thyroglobulin or blocking TSH receptor antibodies who are hypothyroid are diagnosed with Hashimoto’s thyroiditis or idiopathic thyroid failure. Patients with thyroglobulin, TPO or TSH receptor antibodies, especially stimulating antibodies, who are hyperthyroid are diagnosed with autoimmune hyperthyroidism or Graves’ disease.
Patients with AITD often have other autoantibodies, including antibodies to gastric parietal cells, antibodies to adrenal gland enzymes, antibodies to ovarian enzymes, antibodies to components of the pituitary gland. Patients with AITD are also more likely to have anticardiolipin antibodies. These antibodies are related to clotting disorders that cause miscarriage and stroke.
Antibodies to gliadin, the protein component of wheat, rye and barley may also be present, indicating a condition of gluten sensitivity enteropathy or celiac disease. In pregnancy, patients with thyroid antibodies, especially TPO antibodies, are two to three times more likely to have miscarriages. Women receiving fertility treatments have been found to have an increased risk for thyroid antibodies.
In addition, up to 25 percent of patients with Graves’ disease have antibodies to DNA and occasional patients have antibodies to liver mitochondria. Other autoimmune conditions that are seen more often in patients with Graves’ disease than with normal individuals include pernicious anemia, vitiligo, alopecia, angioedema or giant hives, myasthenia gravis and idiopathic thrombocytopenic purpura, a disorder causing low platelet levels.
Besides the environmental triggers discussed in the section on genetic and environmental factors, patients with hepatitis C who are on interferon are at risk for developing AITDs. Patients with HIV/AIDS also have increased risk for AITD presumably because of molecular mimicry, an ability of certain viruses, particularly retroviruses, to alter their appearance and induce autoantibody production.
