Chronic urticaria/angioedema and Graves' disease: Coexistence of 2 antireceptor antibody-mediated diseases
2001; Elsevier BV; Volume: 108; Issue: 5 Linguagem: Inglês
10.1067/mai.2001.119161
ISSN1097-6825
AutoresCarla Irani, Nancy Gordon, Burton Zweiman, Arnold I. Levinson,
Tópico(s)Coagulation, Bradykinin, Polyphosphates, and Angioedema
ResumoThe pathogenesis of autoimmune diseases typically involves interference with the function or destruction of tissues by autoantibodies or autoreactive T cells. Graves' disease and some cases (20% to 30%) of chronic idiopathic urticaria (CIU) are exceptions. Anti–thyroid-stimulating hormone receptor (TSHR) antibodies and anti-FcϵRI antibodies, respectively, function as agonists in these 2 conditions. Although autoimmune thyroid disease has been associated with chronic urticaria, there have been no reports describing the coexistence of anti-FcϵRI antibodies, chronic urticaria, and Graves' disease in the same patient. We report the case of a 53-year-old woman with CIU/angioedema since the age of 21 years who was diagnosed with Graves' disease at the age of 49 years. Graves' disease was diagnosed on the basis of tachycardia, weight loss, ophthalmopathy, a thyroid-stimulating hormone level of <0.1 μIU/mL (normal range, 0.5-6.9), and a serum T4 level of 20.7 μg/dL (normal range, 4.7-11.4). The thyroid scan revealed an enlarged gland with diffuse increased uptake of iodine at 2 and 24 hours. The patient received radioactive iodine and is currently euthyroid on Synthroid. She still requires chronic antihistamine therapy for control of her urticaria/angioedema. Using a standard protocol,1Zweiman B Valenzano M Atkins P. Characteristics of histamine-releasing activity in the sera of patients with chronic idiopathic urticaria.J Allergy Clin Immunol. 1996; 98: 89-98Abstract Full Text Full Text PDF PubMed Scopus (92) Google Scholar we screened the patient's serum for anti-FcϵRI antibodies on unmodified and lactic acid–treated (IgE-stripped) basophils obtained from normal donors. The patient's serum induced a 46% basophil histamine release from IgE-stripped basophils (normal range, 2.4% to 7.6%), consistent with the presence of anti-FcϵRI antibodies in this assay system.1Zweiman B Valenzano M Atkins P. Characteristics of histamine-releasing activity in the sera of patients with chronic idiopathic urticaria.J Allergy Clin Immunol. 1996; 98: 89-98Abstract Full Text Full Text PDF PubMed Scopus (92) Google Scholar The pathogenesis of CIU is not completely understood, but mast cell activation is thought to be of major importance. Antibodies reactive with FcϵRI, the high-affinity IgE receptor, have been found in the serum of some patients (30% to 40%) with CIU.2Sabroe R Poon E Orchard G. Cutaneous inflammatory cell infiltrate in chronic idiopathic urticaria: comparison of patients with and without anti-FcepsilonRI or anti-IgE antibodies.J Allergy Clin Immunol. 1999; 103: 484-493Abstract Full Text Full Text PDF PubMed Google Scholar These autoantibodies have the potential to cross-link FcϵRs on mast cells and basophils. This leads to the release of granule constituents, such as histamine, and the production of proinflammatory lipid mediators, chemokines, and cytokines.3Kinet J-P. The high affinity IgE receptor (Fc epsilon RI): from physiology to pathology.Annu Rev Immunol. 1999; 17: 931-972Crossref PubMed Scopus (860) Google Scholar Smaller subsets of patients with CIU who lack anti-FcϵRI antibodies have anti-IgE antibodies that cross-link FcϵRIs occupied by IgE. Thyroid autoimmunity—in particular, Hashimoto's thyroiditis—and chronic urticaria have been associated in many reports,4Leznoff A Sussman GL. Syndrome of idiopathic chronic urticaria and angioedema with thyroid autoimmunity: a study of 90 patients.J Allergy Clin Immunol. 1989; 84: 66-71Abstract Full Text PDF PubMed Scopus (333) Google Scholar along with a high titer of antimicrosomal antibodies and/or antithyroglobulin antibodies. In a subset of these patients, urticaria was controlled with thyroxine treatment. Despite the clinical association between thyroid autoimmunity and CIU, a cause-and-effect relationship has not yet been proved. In the case of Graves' disease, the inflammatory cells in the thyroid produce cytokines, such as TNF-α, that help maintain the intrathyroidal autoimmune process.5Weetman AP. Medical progress: Graves' disease.N Engl J Med. 2000; 343: 1236-1248Crossref PubMed Scopus (876) Google Scholar Interestingly, there is a significant upregulation of TNF-α in the keratinocytes of patients with urticaria6Hermes B Prochazka A-K Haas N. Upregulation of TNF-alpha and IL-3 expression in lesional and uninvolved skin in different types of urticaria.J Allergy Clin Immunol. 1999; 103: 307-314Abstract Full Text Full Text PDF PubMed Google Scholar that is not restricted to the lesional sites. To our knowledge, this is the first report of the coexistence of chronic urticaria and anti-FcϵRI antibodies with an autoimmune disease mediated by a different antireceptor antibody. Although there is no homology between the protein sequences of TSHR and FcϵRI, it is not known whether their 3-dimensional structures could give rise to a shared conformational B cell epitope. It would be interesting to determine whether patients with Graves' disease have anti-FcϵRI antibodies in the absence of CIU. 1/8/119161
Referência(s)