Hashimoto’s thyroiditis is an inflammatory disorder which is autoimmune in origin. It is also known as chronic autoimmune thyroiditis, as lymphocytic infiltration is seen in the thyroid. Hurthle cell formation is also seen.
Generally it is asymptomatic in mild and moderate disease conditions but the symptoms are noticeable as the condition worsens. Some common symptoms are mentioned below :
Routine thyroid function tests and thyroid antibody tests are the blood tests used to diagnose Hashimoto’s thyroiditis. The thyroid peroxidase antibody test is more sensitive than the thyroglobulin antibody test and is the preferred test for confirming autoimmune thyroid disease. If a thyroid nodule is present, an ultrasound examination may be performed . In patients with a dominant nodule, a fine-needle aspiration biopsy should be performed to exclude malignancy.
In patients with Hashimoto’s thyroiditis, the goal of treatment is to maintain level of thyroid hormones throughout the life. This can be achieved by administering a proper dose of levothyroxine sodium orally. Dietary supplement of selenium along with levothyroxine sodium is also recommended by the FDA. Gluten-free diet is also proved to reduce the level of circulating anti-thyroid peroxidise and other thyroid-related serum antibodies .
Patients with hypothyroidism need lifelong thyroid hormone replacement. Euthyroid patients with Hashimoto’s thyroiditis may have an increased risk of developing hypothyroidism and rarly hyperthyroidism. Though unusual, patients with chronic thyroiditis may change from a hypothyroid to a euthyroid state or to a hyperthyroid state because of the development of stimulating thyroid stimulating hormone (TSH) receptor autoantibodies of Graves disease .
In a prospective study of 82 women with subclinical hypothyroidism followed over a mean of 9.2 years, risk factors for overt thyroid failure were identified based on initial evaluation. The incidence of overt hypothyroidism was increased in patients positive for thyroperoxidase antibodies (58.5% vs 23%) and impaired thyroid reserve (53% vs 38%), as determined by the degree increase in T3 levels after thyroid-releasing hormone (TRH) administration.
Inflammation of the thyroid gland due to this autoimmune disease leads to insufficient amount of thyroid hormones (T3 and T4) in the body which is responsible for metabolism . Excess intake of iodine may impart toxicity to thyrocytes, induce thyroglobulin antigenicity and block the hormone synthesis by the thyroid gland.
Hashimoto’s thyroiditis can affect all age groups including children. It is approximately 7 times more common in women, with its peak onset usually between the ages of 30 to 50 years. On an average 1 in 1000 people are affected by this disease. It is prevalent in geographic areas where dietary iodine intake is high .
Though there are no sufficient studies reporting the mechanism of induction of the condition by excess iodine in the body, the same may be explained by the oxygen free radical release mechanism upon the enzymatic reaction of thyroid peroxidise and thereby increasing the immunogenicity of thyroglobulin .
In Hashimoto’s thyroiditis gradual destruction of follicles in the thyroid gland occurs when antibodies are produced against thyroglobulin and thyroid peroxidase. Activation of cytotoxic T-lymphocytes followed by cell-mediated immune response is the major cause for thyrocyte destruction. The thyroid gland becomes enlarged and lobulated. Antibodies such as TSH receptor-blocking antibodies, anti-thyroid peroxidise and antithyroglobulin can be found in the systemic circulation.
Glandular hyperplasia results due to the decreased ability of the thyroid gland to produce hormones. Also, the replacement of normal cells by fibrous and lymphoid tissue occurs. Histopathological studies indicate the presence of diffuse lymphocyte infiltration by both B cells and cytotoxic T cells . In patients with Hashimoto’s thyroiditis, thyrocytes express the Fas gene, which causes thyroid apoptosis by interaction with the Fas ligand present on the surface of the thyrocyte.
Hashimoto’s thyroiditis is named after the Japanese discoverer, Hakaru Hashimoto. It is the most common cause of primary hypothyroidism . Family history of this autoimmune disease, selenium deficiency, stress and smoking are the major contributing factors for this disease. Hashimoto’s thyroiditis is initiated by environmental factors in genetically predisposed persons.
Hashimoto’s thyroiditis is an autoimmune thyroid disorder that occurs when the immune system attacks the thyroid gland. It can be seen in all age groups including children but more common in women of age group 30 to 50 years. Though it cannot be prevented, it can be managed well by maintaining thyroid hormone levels in your body.
Destruction of thyroid gland due to autoimmune response of the body is the major cause for Hashimoto’s thyroiditis, leading to inadequate level of thyroid hormones in your body. It is prevalent in geographic areas where dietary iodine intake is high.
Common symptoms of the disease are dry skin, weight gain, cold intolerance, voice hoarseness, pressure symptoms in the neck from thyroid enlargement, tiredness, weight gain and hair thinning. Other symptoms are depression, sleeplessness, memory loss, deafness, constipation, joint pain, muscle pain, slow heart beat and irregular periods in women.
Thyroid hormone levels in the body are obtained by blood tests. An ultrasound uses sound waves to show pictures of your thyroid on a monitor. A thyroid scan shows how well your thyroid is working. You may be given a dye before the pictures are taken to help caregivers see the pictures better. Fine needle biopsy is a procedure where a small needle is used to take a sample of your thyroid gland for tests .
Maintaining the normal thyroid hormone level in the body is the basis of treatment. In addition, gluten-free diet and intake of dietary selenium also help to reduce the level of circulating thyroid specific antibodies.