| Autor: |
Maury, C. P. J., Aittoniemi, J., Tiitinen, S., Laiho, K., Kaarela, K., Hurme, M. |
| Předmět: |
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| Zdroj: |
Journal of Internal Medicine; Oct2007, Vol. 262 Issue 4, p466-469, 4p, 1 Chart |
| Abstrakt: |
Objective. The aim of this study was to investigate whether polymorphism of the mannose-binding lectin 2 (MBL2) gene is related to the occurrence of systemic AA amyloidosis in patients with rheumatoid arthritis (RA). Methods. MBL2 structural gene polymorphisms at codon 52 (CGT→TGT, Arg→Cys; D), codon 54 (GGC→GAC, Gly→Asp; B) and codon 57 (GGA→GAA, Gly→ Glu; C), and MBL2 promoter region polymorphism at position –221 (G→C) were examined in 57 patients with RA complicated by biopsy-proven reactive amyloidosis and 51 control RA patients without amyloid. Results. A strong association was found between the presence of a structural MBL2 gene variant O (B, D or C) and the occurrence of amyloidosis in RA patients: 29 of 57 (50.9%) of the RA patients with amyloid had a variant allele compared with 12 of 51 (23.5%) of the RA patients without amyloid (OR 3.37, 95% CI 1.47–7.72; P = 0.004). Conclusion. We conclude that variant MBL2 structural genotype constitutes a significant risk factor for reactive amyloidosis in RA and that the increased risk is probably related to MBL-mediated impairment of mononuclear phagocyte function. [ABSTRACT FROM AUTHOR] |
| Databáze: |
Complementary Index |
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