Two edged role of mannose binding lectin in rheumatoid arthritis: a cross sectional study

Citation
P. Garred et al., Two edged role of mannose binding lectin in rheumatoid arthritis: a cross sectional study, J RHEUMATOL, 27(1), 2000, pp. 26-34
Citations number
50
Categorie Soggetti
Rheumatology,"da verificare
Journal title
JOURNAL OF RHEUMATOLOGY
ISSN journal
0315162X → ACNP
Volume
27
Issue
1
Year of publication
2000
Pages
26 - 34
Database
ISI
SICI code
0315-162X(200001)27:1<26:TEROMB>2.0.ZU;2-W
Abstract
Objective. We investigated whether polymorphisms in the gene of mannose bin ding lectin (MBL) may be associated with onset of rheumatoid arthritis (RA) , and whether MBL in conjunction with aggregated agalactosyl IgG (IgG-GO) m ay be associated with clinical and paraclinical variables. Methods. MBL genotypes and serum concentrations were measured by polymerase ch:lin reaction and ELISA in 189 patients with established RA. Binding of purified MBL to IgG-G0 in serum was assessed and clinical and paraclinical variables were recorded. Results. The median age at onset of RA in the 3 genotypes (normal: A/A, het ero: A/0, and homozygous: 0/0 for variant alleles) was 54.1 (n = 108), 47.0 (n = 68), and 38.4 years (n = 13), respectively (D = 0.01). The frequency of variant alleles in patients with onset below the median age (50.8 yrs) w as 0.32, but was 0.17 in patients with onset above 50.8 years (p = 0.003) a nd 0.20 in 250 controls (p = 0.001). Stratification according to erosion sc ore (no, small, large) revealed an increasing tendency among the different groups in binding of MBL to IgG-G0, increased Health Assessment Questionnai re score, and acute phase reactants in A/A individuals, while no difference was seen among carriers of variant alleles. This effect was most pronounce d in those with late onset RA. Conclusion. Presence of MBL variant alleles was associated with early onset of RA. MBL deficiency may, therefore, accelerate the disease. However, in patients with late onset and advanced disease our results indicate that the A/A type may be associated with additional inflammation different from tha t seen in carriers of variant alleles.