Autoimmune thyroid disease (flajani-parry-graves-von basedow disease): Etiopathogenesis, clinical manifestations and diagnosis

Abstract

Autoimmune thyroid disease is the most common organ-specific autoimmune disorder affecting 2-5 % of the population in Western countries. Graves-Basedow disease is the most frequent form of hyperthyroidism in iodine sufficient countries; while the exact etiology of thyroid autoimmunity is not known, interaction between genetic susceptibility and environmental factors appears to be of fundamental importance to initiate the process of thyroid autoimmunity. The identified autoimmune thyroid disease susceptibility genes include immune-modulating genes, such as the Major Histocompatibility Complex, Cytotoxic T Lymphocyte Antigen-4, CD40 molecule, Protein Tyrosine Phosphatase-22, TSH receptor and Thyroglobulin. The exact nature of the role environmental factors play in Graves-Basedow disease is still not well known, but the involvement of several factors such as: iodine diet, drugs, stress, and infections has been reported. In Graves-Basedow disease the lymphocytic infiltration of the thyroid leads to activation of TSH Receptor (TSHR)-reactive B-cells that secrete TSHR stimulating antibodies causing hyperthyroidism. These antibodies bind to TSH receptors on the surface of thyroid follicular cells, leading to continuous and uncontrolled thyroid stimulation, associated with excess synthesis of the thyroid hormones T4 and T3, and thyroid hypertrophy. Graves-Basedow disease includes thyrotoxicosis, goiter, exophthalmos, and pretibial myxedema when fully expressed, but can occur with one or more of these features.