Some concepts are essential for understanding the autoimmune Hashimoto’s thyroiditis, the most common cause of hypothyroidism.
The immune system is the body’s means of protection against microorganisms, such as bacteria or viruses, and other “foreign” substances. It is composed of two major parts. One component, B lymphocytes, produces antibodies, proteins that attack “foreign” substances and cause them to be removed from the body; this is called the humoral immune system. The other component consists of special white blood cells called T lymphocytes, which can attack “foreign” substances directly; this is called the cellular immune system. The immune response also involves proteins called cytokines, chemical messengers that pass messages between cells.
Normally, the immune system can distinguish between “self” and “not self” and only attacks those tissues that it recognizes as “not self”. This is usually the desired response, but not always.
Autoimmune disorders are diseases caused by the body producing an inappropriate immune response against its own tissues. Sometimes the immune system will cease to recognize one or more of the body’s normal constituents as “self” and will create autoantibodies – antibodies that attack to its own cells, tissues, and/or organs. This induces inflammation, causes damage and leads to autoimmune diseases. The cause of autoimmune diseases is unknown, but there seems to be a common genetic predisposition to their development.
Autoimmune disorders fall into two general types: those that damage many organs (systemic autoimmune diseases, such as systemic lupus erythematosus, Sjogren’s syndrome, rheumatoid arthritis, polymyalgia rheumatic, Horton’s disease, ankylosing spondylitis, Behcet’s disease, Wegener’s granulomatosis, Goodpasture’s syndrome) and those where only a single organ or tissue is directly damaged by the autoimmune process, such as Hashimoto’s thyroiditis (thyroid), celiac disease, Crohn’s disease and ulcerative colitis (GI tract), Addison’s disease (adrenal), type 1 diabetes mellitus (pancreas islets), primary biliary cirrhosis, primitive sclerosing cholangitis, autoimmune hepatitis (liver), multiple sclerosis, Guillan-Barré syndrome (nervous system). (Click Here)
The Gluten-Thyroid connection is part of this autoimmune context. I will discuss that later.
Anti-thyroid Antibodies
The integrity of the thyroid function is checked by its functional and autoimmune aspect.
Thyroid peroxidase (TPO) is a key enzyme that helps the reaction which adds iodine to thyroglobulin, an essential protein necessary to producing the thyroid hormones. TPO function is stimulated by TSH. The presence of an autoimmune system disorder can cause disruptions in the enzyme activity and in how the thyroglobulin is produced. Studies show that 90 % of people with hypothyroidism are producing antibodies to thyroid tissue.
Auto-immune Hashimoto’s thyroiditis is characterized by the presence in the blood of increased number of thyroid antibodies: thyroid peroxidase antibodies (anti-TPO, also named anti-microsomal antibodies), and thyroglobulin antibodies. Those antibodies react against proteins in the thyroid gland and initiate an inflammatory reaction causing attack and gradually destruction of the thyroid cells, which leads the thyroid gland to become underactive. Autoimmune destruction of the thyroid gland is believed to be caused by an immune response, both humoral and cells mediated.
Thyroid autoantibodies are found more frequently in females and its prevalence increases with age.
The identification of anti-TPO and/or anti-thyroglobulin antibodies during screening can lead to the diagnosis of subclinical thyroid disease, or asymptomatic euthyroid state but with the potential autoimmune and possible future thyroid failure. It is therefore important to perform both assays simultaneously.
Antibody production may be confined to lymphocytes within the thyroid, and therefore serum of some patients with Hashimoto’s disease may have normal concentration (not raised) for one or both thyroid antibodies (it concerns only a small percentage of patients). This confirms why both have to be tested. However, the autoantibodies may develop over time and repeated testing should be done.
The presence of thyroid autoantibodies substantially contributes to the pathogenesis of Hashimoto’s disease and of other thyroid disorders, such as primary myxedema, Graves’ disease, as well as thyroid cancers.
The rate of anti-thyroid peroxidase (anti-TPO) is considered normal if it is less than 35 IU/mL in adults, and that of anti-thyroglobulin antibodies if less than 20 IU/mL, these standards can vary between laboratories.
Only a small number (3%) of people with no evidence of disease may have anti-thyroid antibodies. This number may reach 15% in patients over 60 years, particularly among women. The doctor will have to track the individual’s health over time. While most may never experience thyroid dysfunction, a few may develop it.
But having anti-thyroid antibodies does not necessary mean that one has thyroid disease. They are also present in a smaller percentage of serum from non-autoimmune thyroid disorders, such as Sjogren’s syndrome, lupus, rheumatoid arthritis, pernicious anemia, Addison’s disease, celiac disease, alopecia areata. However, 5 to 50 percent of people with these conditions can also have a concurrent autoimmune thyroid disease.
Two other types of thyroid antibodies may be found in autoimmune thyroiditis: the immunoglobulins that stimulate the TSH receptor in the cells of the thyroid (TSI antibodies), which are the cause of hyperthyroidism in Graves’ disease (or Basedow-Graves disease), and anti-TSH receptor antibodies. (Click Here)