Autoimmune diseases include more than eighty distinct disorders in which the immune system attacks certain cells or cellular components of one’s own body. Autoimmune diseases may be systemic in which cellular components of several different organs are affected. An example is systemic lupus erythematosus (SLE) in which the nuclear component of cells which comprise tissues of the lungs, skin, are affected. Autoimmune diseases may also be organ-specific. For instance, the autoimmune thyroid diseases primarily target the thyroid gland causing it to be underactive or overactive.
Some disorders, such as multiple sclerosis (MS) and neuropathy, appear to have subtypes, some disorders having and some not having an autoimmune origin. Diseases with an autoimmune origin show evidence of autoantibodies and immune generated cell destruction. Hyperthyroidism may also occur as an autoimmune disease or as a disorder with no evidence of autoimmunity. While 85% to 95% of all cases of hyperthyroidism are caused by autoimmunity and are, in fact, Graves’ disease, other causes of hyperthyroidism include thyroid nodules, genetic mutations, and underlying pituitary disorders.
Furthermore, some autoimmune diseases occur as a primary disease or as a cluster of symptoms, which occur in the presence of other autoimmune diseases. For instance, Sjögren’s Syndrome a disease which primarily affects the oral and auditory glands is present in many patients with autoimmune thyroid disease. Sjögren’s Syndrome may also occur as a primary disease in which salivary, gastric and vaginal glands are affected.
Autoimmune diseases are caused by a combination of genetic and environmental factors. Typically, patients do not have genes for a specific autoimmune disease. They have a certain cluster of genes, which make them susceptible to developing a number of different autoimmune diseases. This means that these individuals may or may not develop an autoimmune disease. Genetically predisposed individuals may develop autoantibodies that appear in their blood but never cause symptoms of disease. In fact, most everyone has natural occurring autoantibodies.
The immune system genes associated with Graves’ disease in Caucasians are HLA B8, DR3, and DQ1. However, this haplotype or combination of alleles is also seen in several other autoimmune diseases including type 1 diabetes and celiac disease. That’s why patients who develop Graves’ disease have a better chance of developing these other autoimmune diseases than normal individuals.
Certain environmental triggers are known or suspected to cause disease development in these genetically susceptible individuals. For example, the rubella virus has been linked to the development of insulin dependent or juvenile diabetes mellitus, which is also known as type 1 diabetes. Silica is associated with autoimmune scleroderma and sunlight is known to trigger or exacerbate symptoms in SLE.
