Increased serum anti-carbonic anhydrase II antibodies in patients with Graves' disease


Alver A., Mentese A., Karahan S. C., Erem C., Keha E. E., Arikan M. K., ...Daha Fazla

EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES, cilt.115, sa.5, ss.287-291, 2007 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 115 Sayı: 5
  • Basım Tarihi: 2007
  • Doi Numarası: 10.1055/s-2007-960498
  • Dergi Adı: EXPERIMENTAL AND CLINICAL ENDOCRINOLOGY & DIABETES
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.287-291
  • Anahtar Kelimeler: Hashimoto's thyroiditis, Graves' disease, anti-CA II antibody, anti-CA I antibody, CHRONIC-PANCREATITIS, AUTOANTIBODIES, MICE
  • Karadeniz Teknik Üniversitesi Adresli: Evet

Özet

Carbonic anhydrase II (CA II) has an important role in thyroid hormone synthesis via regulating iodide (I-) transport across thyroidal cell membranes and the existence of autoantibodies against CA I and/or CA II have been shown in sera from patient with various autoimmune diseases such as Sjogren's Syndrome, Systemic Lupus Erythmatosus, type 1 diabetes, primary biliary cirrhosis and ulcerative colitis. The aim of this study was to investigate the presence of anti-CA I and CA II antibodies in autoimmune thyroid disease and the relationships between the autoantibodies and other clinical parameters. We studied 40 autoimmune thyroid patients (20 Hashimoto's thyroiditis, HT and 20 Graves' disease, GD) and 21 healthy control subjects. Serum anti-CA I and CA II antibodies were screened by ELISA. Positive rate of anti-CA II (25 %) antibody was significantly higher in GD patients as compared to HT patients and control subjects (p < 0.05). There were no significant changes in positive rate of anti-CA I antibody. In addition, a significant correlation between serum anti-CA antibodies titers and other studied clinical parameters was not found. The results suggest that anti-CA II antibodies may be involved in the pathogenesis of GD.