Hashimotos thyroiditis, also known as chronic lymphocytic thyroiditis and Hashimotos disease, is an autoimmune disease in which the thyroid gland is gradually destroyed. Early on, symptoms may not be noticed. Over time, the thyroid may enlarge, forming a painless goiter. Some people eventually develop hypothyroidism with accompanying weight gain, fatigue, constipation, depression, hair loss, and general pains. After many years the thyroid typically shrinks in size. Potential complications include thyroid lymphoma. Furthermore, because it is common for untreated patients of Hashimotos to develop hypothyroidism, further complications can include, but are not limited to, high cholesterol, heart disease, heart failure, high blood pressure, myxedema, and potential pregnancy problems.Hashimotos thyroiditis is thought to be due to a combination of genetic and environmental factors. Risk factors include a family history of the condition and having another autoimmune disease. Diagnosis is confirmed with blood tests for TSH, T4, and antithyroid autoantibodies. Other conditions that can produce similar symptoms include Graves disease and nontoxic nodular goiter.Hashimotos thyroiditis is typically treated with levothyroxine. If hypothyroidism is not present, some may recommend no treatment, while others may treat to try to reduce the size of the goiter. Those affected should avoid eating large amounts of iodine; however, sufficient iodine is required especially during pregnancy. Surgery is rarely required to treat the goiter.Hashimotos thyroiditis affects about 5% of Caucasians at some point in their lives. It typically begins between the ages of 30 and 50 and is much more common in women than men. Rates of the disease appear to be increasing.
Risk factors
The strong genetic component is borne out in studies on monozygotic twins, with a concordance of 38–55%, with an even higher concordance of circulating thyroid antibodies not in relation to clinical presentation (up to 80% in monozygotic twins). Neither result was seen to a similar degree in dizygotic twins, offering strong favour for high genetic aetiology. Medications that influence thyroid function
Certain medications or drugs have been associated with altering and interfering with thyroid function. Of these drugs, there are two main mechanisms of interference that they can have.One of the mechanisms of interference is when a drug alters thyroid hormone serum transfer proteins. Estrogen, tamoxifen, heroin, methadone, clofibrate, 5-flurouracile, mitotane, and perphenazine all increase thyroid binding globulin (TBG) concentration. Androgens, anabolic steroids such as danazol, glucocorticoids, and slow release nicotinic acid all decrease TBG concentrations. Furosemide, fenoflenac, mefenamic acid, salicylates, phenytoin, diazepam, sulphonylureas, free fatty acids, and heparin all interfere with thyroid hormone binding to TBG and/or transthyretin.The other mechanism that medications can utilize to interfere with thyroid function would be to alter extra-thryoidal metabolism of thyroid hormone. Propylthiouracil, glucocorticoids, propanolol, iondinated contrast agents, amiodarone, and clomipramine all inhibit conversion of T4 and T3. Phenobarbital, rifampin, phenytoin and carbamazepine all increase hepatic metabolism. Finally, cholestryamine, colestipol, aluminium hydroxide, ferrous sulphate, and sucralfate are all drugs that decrease T4 absorption or enhance excretion. HLA genes
The first gene locus associated with autoimmune thyroid disease was major histocompatibility complex (MHC) region on chromosome 6p21. It encodes HLAs.