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Mannose Binding Lectin Polymorphisms as a Disease-Modulating Factor in Women with Systemic Lupus Erythematosus from Canary Islands, Spain

M. ISABEL GARCÍA-LAORDEN, IÑIGO RÚA-FIGUEROA, PALOMA PÉREZ-ACIEGO, J. CARLOS RODRÍGUEZ-PÉREZ, M. JESÚS CITORES, FAYNA ÁLAMO, CELIA ERAUSQUIN, and CARLOS RODRÍGUEZ-GALLEGO

ABSTRACT.

Objective.
To determine whether mannose binding lectin (MBL) polymorphisms are associated with clinical characteristics and with susceptibility to systemic lupus erythematosus (SLE) in women from the Canary Islands, Spain.

Methods. MBL alleles and genotypes were determined by polymerase chain reaction in 89 female patients and 188 female controls.

Results. No differences in the allelic or genotypic frequencies were observed between patients and controls. Anti-U1RNP autoantibodies were less frequent in association with mutated alleles (p = 0.037), and in association with MBL deficient genotypes, although this association was not statistically significant. The patients with low or nonproducer genotypes exhibited a decreased frequency of anti-Sm antibodies (p = 0.059). A nonsignificant trend toward lower prevalence of anti-Sm and anticardiolipin antibodies in association with both mutated alleles and low or nonproducer genotypes was also observed. The prevalence of more than one autoantibody was lower in association with mutated alelles (p = 0.022) and with low or nonproducer genotypes (p = 0.052). Homozygous or heterozygous patients with mutated alleles were significantly older at disease onset and at SLE diagnosis (p = 0.005, p = 0.014, respectively). An increase in the mean age at disease onset and at SLE diagnosis was observed with regard to the number of nonproducer alleles present (p = 0.021, p = 0.038, respectively).

Conclusion. MBL deficiency is not a risk factor for SLE in women from the Canary Islands, but it is associated with lower prevalence of autoantibodies and with later age at disease onset and at SLE diagnosis. (J Rheumatol 2003;30:740-6)

Key Indexing Terms:

SYSTEMIC LUPUS ERYTHEMATOSUS
AUTOANTIBODIES
MANNOSE BINDING LECTIN
COMPLEMENT
POLYMORPHISM


From the Department of Immunology, Department of Rheumatology and Research Unit, Hospital de Gran Canaria Dr. Negrín, Las Palmas de Gran Canaria, Spain, and Fundación LAIR, Madrid, Spain.

Supported in part by Fondo de Investigaciones Sanitarias (Ministerio de Sanidad) grant FIS 98/1513.

M.I. García-Laorden, BSc, Department of Immunology; I. Rúa-Figueroa, MD, Department of Rheumatology; J.C. Rodríguez-Pérez, PhD; F. Álamo, BS, Research Unit; C. Erausquin, PhD, Department of Rheumatology; C. Rodríguez-Gallego, PhD, Department of Immunology, Hospital de Gran Canaria Dr. Negrín; P. Pérez-Aciego, PhD; M.J. Citores, PhD, Fundación LAIR.

Address reprint requests to Dr. C. Rodríguez-Gallego, Department of Immunology, Hospital de Gran Canaria Dr. Negrín, Barranco de la Ballena s/n 35020, Las Palmas de Gran Canaria, Spain. E-mail: jrodgal@gobiernodecanarias.org

Submitted May 1, 2002; revision accepted September 18, 2002.




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