The incidence of Hashimoto’s thyroiditis, also referred to as goitrous autoimmune thyroiditis, is estimated to be equivalent to that of Grave’s disease. Although first discovered one hundred years ago, the pathophysiology of this disease has not yet been completely defined. Patients present with varying degrees of symptoms and may present euthyroid. Studies have found associations between genetic predisposition, environmental factors and co-occurrence of other autoimmune disorders within patients with autoimmune thyroiditis. This has further impeded advances to clearly define the mechanisms associated with autoimmune thyroiditis as there are a number of potential confounding factors which are not shared by all patients. Concern has been raised suggesting that iodination of salt led to the emergence or increase in prevalence of autoimmune thyroiditis. In regions where chronic excess consumption of iodine occurs, studies have not found an association between iodine intake and prevalence of this disorder. Furthermore, autoimmune thyroiditis patients with low thyroid levels of iodine are at risk of developing hypothyroidism. Therefore iodine therapy is indicated in patients with autoimmune thyroiditis to preserve normal function of the thyroid, unless the patient has goiter. Patients receiving iodine therapy must be monitored closely to ensure the condition does not exacerbate.
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