Hashimoto's Thyroiditis (Autoimmune Thyroiditis)
Hashimoto’s thyroiditis, also called autoimmune thyroiditis and chronic lymphocytic thyroiditis, is a chronic inflammatory autoimmune disease. The cells of the thyroid gland releases thyroglobulin. Thyroglobulin is a large protein molecule containing iodine. Normally thyroglobulin is broken down into the thyroid hormones which are then released at a controlled rate into the blood stream. This rate is monitored and regulated by the pituitary gland through the release of TSH – thyroid stimulating hormone. However, this does not occur in Hashimoto’s Thyroiditis. In this case, the T cells react with an antigen in the thyroid cell membrane, destroying it and triggering the uncontrolled release of thyroglobulin. Antibodies are then immediately formed against the overflow of thyroglobulin and the thyroid cell membranes. Depending on how the antigens react with the TSH receptors, they can either block them, rendering the gland unresponsive to the TSH or the opposite effect can occur, where they mimic them, overriding normal control. The result is either Thyroid deficiency in the first case, or overactivity in the second. It is unknown as to why one response occurs in some people and the opposite effect in others.
An autoimmune reaction to proteins in the thyroid is the underlying cause of Hashimoto’s. It is not unusual for persons with autoimmune thyroid disease to have other coinciding autoimmune disorders. Approximately 25 percent of patients with Hashimoto’s may develop pernicious anemia, diabetes, hypoadrenalism, or other autoimmune diseases.
Symptoms of Hashimoto’s are as follows: thyroid gland enlargement, eventually various symptoms of hypothyroidism (fatigue, lethargy, cold intolerance, constipation, coarse, dry skin and hair)