ISSN 1470-3947 (print) | ISSN 1479-6848 (online)

Endocrine Abstracts (2008) 16 P165

Chemokine CXCL10 gene polymorphisms in Addison's disease

Dilek Sadet1, Marissa Penna-Martinez1, Alina Kurylowicz3, Jane Paunkovic2, Heinrich Kahles1, Patrick Brück1, Klaus Badenhoop1 & Elizabeth Ramos-Lopez1

1Division of Endocrinology, Diabetes and Metabolism, Department of Internal Medicine I, Frankfurt am Main, Germany; 2Department of Nuclear Medicine, Medical Center, Zajecar, Serbia; 3Department of Endocrinology, Medical Research Center, Polish Academy of Science, Warsaw, Poland.

Background and aims: CXC chemokine ligand 10 (CXCL10) also known as chemokine interferon γ inducible protein (IP-10) is a CXCR3 chemokine belongs to a group of structurally related molecules, that induce the chemotaxis of diverse leukocyte subtypes including activated T-helper 1 lymphocytes, natural killer cells and monocytes. In patients with Hashimoto’s thyroiditis, type 1 diabetes mellitus and Graves’ disease high levels of CXCL10 ligand in serum have been found. Therefore, we investigated the role of CXCL10 gene polymorphisms in patients with Addison’s disease (AD) and in patients with Graves’ disease (GD).

Materials and methods: Patients from Germany with Addison’s disease (n=174), Graves’ disease (n=171) and healthy controls (HC: n=285) were genotyped for the CXCL10_89 and for the CXCL10_90 (AD: n=183; GD: n=82) polymorphism within the CXCL10 gene. Additionally patients with Graves’ disease and healthy controls from Poland (GD: n=181; HC: n=147) and Serbia (GD: n=177; HC: n=151) were genotyped for the CXCL10_89 polymorphism using real time PCR.

Results: In patient with Addison’s disease, the CXCL10_89 (G/A) heterozygosity was more frequent (58.6 vs 46.7%) while the (G/G) homozygosity rate (25.9 vs 36.5%) was found less than in healthy controls (P=0.031). No differences were observed in the genotype-frequencies for CXCL10_90 and CXCL10_89 polymorphisms in Graves’ disease.

Conclusion: CXCL10_89 gene polymorphism was significantly associated with Addison’s disease in the German population but not with Graves’ disease. Our results point out that CXCL10 could be a candidate gene in the pathogenesis of Addison’s disease. Nevertheless, functional studies are underway to put these findings into physiological contexts.

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