What is Hashimoto's thyroiditis?
In a nutshell, Hashimoto's autoimmune thyroiditis is an autoimmune disease characterized by the presence of a goiter and thyroid antibodies are circulating in the blood. They can present in patients that have normal thyroid function or hypothyroidism. It is the most common cause of goitrous hypothyroidism in areas of the work in which dietary iodine is plentiful. Use the thyroid glossary for terms that are unfamiliar.
Hashimotos Key Points:
1. The presence of TPO or TG antibodies only indicates there is about a 4 % chance per year a patient may develop hypothyroidism based on TFTs and clinical scenario. There is about 55% chance of hypothyroidism over 13 years that a patient with baseline TSH is 2.5 to 4.0.
2. The TPO and TG antibodies generally represent a genetic predisposition/marker but not a disease in it's self. A person does not acquire predisposition for new antibodies since we are born with all the predisposition for antibodies we will have at birth, including the abnormal ones.
3. The level of TPO And TG only reflects a quantity of the antibody and not an activity which is determined by finding hypothyroidism. Therefore repeated measurements are not indicated once antibodies are positive unless during a pregnancy.
4. We general cannot recommend a particular diet or lifestyle change or supplement or medication to improve the antibodies or their potential effects because as of yet there are no convincing randomized placebo controlled studies to show efficacy.
5. There is no clinically proven treatment to change or eliminate these antibodies since they are representing genetic changes. Thyroid hormone medication does not "fix" this condition and should only be used for patients with hypothyroidism / borderline hypothyroidism planning pregnancy.
Who was Hashimoto?
Hashimoto is the first name of the Japanese medical scientist Hashimoto Hakaru. He graduated from medical school in 1907. while he worked in a surgical department, he examined tissue samples and goiter of 4 middle-aged woman. Their goiters caught his attention because they had many lymphoid cells present. In 1912 he published a paper Kojyosen rinpa -setu sho-teki henka ni kansuru kenkyu houkoku (Report on Lymphomatous Goiter). Many years later in the 1920's the paper was reviewed in American medical books and renamed Hashimotos thyroiditis.
The reduced hormone synthesis found in Hashimoto's disease is due to apoptosis of thyroid cells. More than 90% of the thyroid gland must be destroyed before primary hypothyroidism develops. The presence of lymphocytes (B and T lymphocytes) in the thyroid and circulating thyroid antibodies indicate that Hashimoto's disease is an autoimmune thyroid disorder. Autoimmune thyroiditis is characterized by thyroid cell apoptosis which leads to thyroid follicular cell destruction.
Genetic factors: there is an increased frequency in patients with Down's syndrome and gonadal dysgenesis. There is a polygenetic susceptibility and therefore difficult to to demonstrate formal allele linkages.
Pregnancy: Maternal microchimerism may contribute to the immune manipulation. This disease is postpartum Hashimoto's thyroiditis expect that it is usually transient. Some patients develop permanent thyroid failure in the early years after pregnancy.
Iodine and drugs: iodine and iodine containing medications such as amiodarone can cause autoimmune thyroiditis in susceptible patients. This is a different mechanism than the direct blockade of and destruction of the thyroid by iodine.
Irradiation: Thyroid antibodies become more prevalent after exposure to low doses of radioiodine. An example of this would be the Chernobyl nuclear disaster. It is not known if this actually causes hypothyroidism.
Age: As patients get older, the prevalence of Hashimoto's increases as well.
Infection: There is no direct evidence that infections cause autoimmune thyroiditis in humans, but there are many animal models that suggests this does occur.
A goiter is the hallmark of classic Hashimoto's disease. It develops gradually and can be found by ultrasound or routine examination by a physician. Sometimes the gland increases in size rapidly and can be sometimes associated with some pain and tenderness, mimicking de Quervain's or subacute thyroiditis. Otherwise the condition follows a painless thyroiditis picture. This goiter may remain unchanged for many years or gradually enlarge over a period of years. The end result, after decades, may be atrophic autoimmune destruction of the thyroid gland. Patients are initially with normal thyroid function, but hypothyroidism is a manifestation that may develop over several years in some but not all patients with Hashimoto's. Most studies suggest that the presence of co-existing Hashimoto's disease may be a favorable prognostic indicator in patients with papillary thyroid cancer. Hashimotos is the most common etiology (cause of) primary hypothryroidism.
There is no one "gold standard" way to diagnose Hashimoto's. Classically, blood tests will show a pattern of thyroid hyperfunction (low TSH, but normal Free T4) when the goiter first develops, followed by normal thyroid function, and then later on hypothyroidism (high TSH , low Free T4 develops). The diagnosis is confirmed by the presence of thyroid autoantibodies in the blood, usually at high levels. Thyroid peroxidase antibodies (TPO) are more common that thyroglobulin antibodies. Sometimes a Hashimoto's gland will have a particular appearance on thyroid ultrasound testing. Ultrasound testing is only appropriate to evaluate patients with goiters or compressive
In most patients, no treatment is needed for these antibodies are not usually directly tied to clinical symptoms. The presence of autoantibodies does not always immediately cause hypothyroidism and the goiter is usually small at time of diagnosis. The presence of the antibodies mainly indicates a genetic predisposition to developing primary hypothyroidism. Hashimoto's thyroiditis is characterized clinically by gradual thyroid failure, with or without goiter formation, due primarily to autoimmune-mediated destruction of the thyroid gland. There has been no randomized placebo controlled diet, lifestyle, or supplement that has been shown to change the progression of this disease. If pregnancy is not an issue, usually a thyroid function test is indicated at least once yearly to find hypothyroidism. There is no clinically proven treatment to change the effects / levels of the antibodies. The main reason for treatment is to replace the thyroid hormone by levothyroxine and/or liothyronine medication if hypothyrodism develops or alleviate symptoms of a goiter.
In one study, after follow-up of 13 years, prevalence of hypothyroidism in women with positive antibodies was 55.2% when baseline TSH was 2.5-4.0 mIU/mL
Walsh JP, et al. Thyrotropin and Thyroid Antibodies as Predictors of Hypothyroidism: A 13-Year, Longitudinal Study of a Community-Based Cohort Using Current Immunoassay Techniques. J Clin Endocrinol Metab. 2010;95:1095-1104.
Garber JR, et al. Clinical Practice Guidelines for Hypothyroidism in Adults: Cosponsored by the American Association of Clinical Endocrinologists and the American Thyroid Association. Thyroid. 2012;22:1200-1235.