Chronic Urticaria and Autoimmunity
Chronic Urticaria and Autoimmunity
CU is defined as hives lasting longer than 6 weeks. Currently, it is thought that up to 50% of CU is caused by autoimmune mechanisms. Autoantibodies to the high affinity IgE receptor are the most commonly identified offender, activating mast cells, basophils, and the complement system, resulting in the wheal and flare reaction. CU is hypothesized to occur because of a predisposition in the patient to develop autoimmune diseases. In concordance with this hypothesis, additional autoimmune diseases are observed in patients with CU. Thyroid disease, particularly hypothyroidism, is the most common additional autoimmune disease diagnosed. Furthermore, thyroid disease may directly exacerbate CU severity by activating the complement system. Other autoimmune diseases that occur more frequently in patients with CU include RA, SLE, vitiligo, pernicious anemia, celiac disease, and Sjörgen's syndrome. In case reports, CU has been identified as part of a larger autoimmune phenotype. These associations support the theory that patients who develop CU do so because of an innate propensity to mount autoimmune reactions. Treatment of thyroid disease has been reported in the literature to have varying effects on CU, as it has been demonstrated to induce remission and alternatively to have no effect on the clinical symptoms of CU. Autoimmune diseases occurring in patients with CU, especially thyroid disease, may be an important therapeutic target, but further studies are needed to establish the role of treatment on the clinical course of CU.
Conclusion
CU is defined as hives lasting longer than 6 weeks. Currently, it is thought that up to 50% of CU is caused by autoimmune mechanisms. Autoantibodies to the high affinity IgE receptor are the most commonly identified offender, activating mast cells, basophils, and the complement system, resulting in the wheal and flare reaction. CU is hypothesized to occur because of a predisposition in the patient to develop autoimmune diseases. In concordance with this hypothesis, additional autoimmune diseases are observed in patients with CU. Thyroid disease, particularly hypothyroidism, is the most common additional autoimmune disease diagnosed. Furthermore, thyroid disease may directly exacerbate CU severity by activating the complement system. Other autoimmune diseases that occur more frequently in patients with CU include RA, SLE, vitiligo, pernicious anemia, celiac disease, and Sjörgen's syndrome. In case reports, CU has been identified as part of a larger autoimmune phenotype. These associations support the theory that patients who develop CU do so because of an innate propensity to mount autoimmune reactions. Treatment of thyroid disease has been reported in the literature to have varying effects on CU, as it has been demonstrated to induce remission and alternatively to have no effect on the clinical symptoms of CU. Autoimmune diseases occurring in patients with CU, especially thyroid disease, may be an important therapeutic target, but further studies are needed to establish the role of treatment on the clinical course of CU.
