Stephen C Dreskin1, Karen Y Andrews. 1. University of Colorado Health Sciences, Denver, Colorado 80262, USA. stephen.dreskin@uchsc.edu
Abstract
PURPOSE OF REVIEW: Although it is generally accepted that thyroid autoimmunity is more prevalent in patients with chronic urticaria than in the general population, the importance of this finding is unclear. In addition, there are reports that chronic urticaria remits in some but not all patients who have evidence of thyroid autoimmunity and are treated with l-thyroxine. This review will summarize the history of this controversy and suggest a possible role for thyroid autoimmunity in the pathophysiology of chronic urticaria. RECENT FINDINGS: Important subsets of patients with chronic urticaria have autoantibodies to the high-affinity receptor for IgE (FcepsilonRI), anti-IgE, and antithyroid antibodies. Patients with chronic urticaria and biochemical evidence of thyroid autoimmunity may have active thyroid disease or may be clinically euthyroid. These patients are often poorly responsive to conventional therapy of urticaria and may have more chronic disease. New findings on the pathogenic effects of anti-FcepsilonRI auto-antibodies and of antithyroid antibodies have revealed a role for complement activation. SUMMARY: Currently, there are no compelling arguments to decide whether or not thyroid autoimmunity plays a significant role in the pathogenesis of chronic urticaria. New developments concerning a role for complement activation in the pathogenesis of chronic urticaria may, however, lead to better understanding of this phenomenon in the future.
PURPOSE OF REVIEW: Although it is generally accepted that thyroid autoimmunity is more prevalent in patients with chronic urticaria than in the general population, the importance of this finding is unclear. In addition, there are reports that chronic urticaria remits in some but not all patients who have evidence of thyroid autoimmunity and are treated with l-thyroxine. This review will summarize the history of this controversy and suggest a possible role for thyroid autoimmunity in the pathophysiology of chronic urticaria. RECENT FINDINGS: Important subsets of patients with chronic urticaria have autoantibodies to the high-affinity receptor for IgE (FcepsilonRI), anti-IgE, and antithyroid antibodies. Patients with chronic urticaria and biochemical evidence of thyroid autoimmunity may have active thyroid disease or may be clinically euthyroid. These patients are often poorly responsive to conventional therapy of urticaria and may have more chronic disease. New findings on the pathogenic effects of anti-FcepsilonRI auto-antibodies and of antithyroid antibodies have revealed a role for complement activation. SUMMARY: Currently, there are no compelling arguments to decide whether or not thyroid autoimmunity plays a significant role in the pathogenesis of chronic urticaria. New developments concerning a role for complement activation in the pathogenesis of chronic urticaria may, however, lead to better understanding of this phenomenon in the future.