Abstract
Purpose of Review. Studies have been published in the field of autoimmune thyroid diseases since January 2005. The review is organized into areas of etiology, autoimmune features, autoantibodies, mechanism of thyroid cell injury, B-cell responses, and T-cell responses. Also it reviews the diagnosis and the relationship between autoimmune thyroid disease, neoplasm, and kidney disorders. Recent Findings. Autoimmune thyroid diseases have been reported in people living in different parts of the world including North America, Europe, Baalkans, Asia, Middle East, South America, and Africa though the reported figures do not fully reflect the number of people infected per year. Cases are unrecognized due to inaccurate diagnosis and hence are treated as other diseases. However, the most recent studies have shown that the human autoimmune thyroid diseases (AITDs) affect up to 5% of the general population and are seen mostly in women between 30 and 50 years. Summary. Autoimmune thyroid disease is the result of a complex interaction between genetic and environmental factors. Overall, this review has expanded our understanding of the mechanism involved in pathogenesis of AITD and the relationship between autoimmune thyroid disease, neoplasm, and kidney disease. It has opened new lines of investigations that will ultimately result in a better clinical practice.
Highlights
The principal diseases of the human thyroid gland are goiter, hyperthyroidism, hypothyroidism, autoimmune thyroiditis, and neoplasm [1]
There is genetic susceptibility to Hashimoto’s thyroiditis, and much has been learned in recent years concerning the susceptibility genes for this disorder in particular and for autoimmune thyroid disease in general [60]
Diagnosis of autoimmune thyroid diseases (AITDs) is based upon clinical features and supported laboratory investigations
Summary
The principal diseases of the human thyroid gland are goiter (diffuse or nodular), hyperthyroidism, hypothyroidism, autoimmune thyroiditis, and neoplasm [1]. The human AITDs broadly include Graves’ disease (GD) and Hashimoto’s thyroiditis (HT) which are the most common causes of thyroid gland dysfunctions and nonendemic goiter [4]. These conditions arise due to complex interactions between environmental and genetic factors [5] and are characterized by reactivity to self-thyroid antigens which are expressed as distinctive inflammatory or antireceptor autoimmune diseases [6, 7]. Graves’ disease, on the other hand, involves the binding of autoantibodies to TSH receptor which leads to stimulation It is the most common cause of thyrotoxicosis [14]. Smoking is a risk factor, and therapeutic options include local measures to combat inflammation—glucocorticoids, plasmapheresis, and immune suppressants as well as orbital radiation, decompressive surgery, and thyroid ablation [2]
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