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.
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