title: Association of mannose-binding lectin gene polymorphisms with antiphospholipid syndrome, cardiovascular disease and chronic damage in patients with systemic lupus erythematosus.
abstract: OBJECTIVE
  To investigate the association of mannose-binding lectin (MBL)-deficient genotypes with cardiovascular disease in a large series of patients with systemic lupus erythematosus (SLE).
  
  
  METHODS
  A total of 114 patients diagnosed with SLE were included in the study. MBL polymorphisms were investigated by sequencing-based DNA typing of the promoter and exon 1 of the MBL2 gene. The genotypes 0/0, 0/XA and XA/XA were considered as MBL-low genotypes.
  
  
  RESULTS
  A higher prevalence of cardiovascular disease was observed in patients carrying MBL-low genotypes compared with those carrying MBL-high genotypes [30 vs 9%, P = 0.012, odds ratio (OR) 4.54, 95% confidence interval (CI) 1.20-16.46]. Patients with MBL-low genotypes also presented higher mean values for total cholesterol (228.6 vs 202.3 mg/dl, P = 0.017) and low-density lipoprotein (LDL) cholesterol (139.9 vs 121.9 mg/dl, P = 0.045), a higher frequency of chronic renal failure (30 vs 4%, P = 0.001), vasculitis (30 vs 11%, P = 0.043), heart valve lesions (71 vs 32%, P = 0.026), cardiac valve dysfunction (57 vs 7%, P = 0.0004) and associated APS (39 vs 12%, P = 0.005), a higher mean Systemic Lupus International Collaborating Clinics score (2.09 vs 1.26, P = 0.029) and a lower prevalence of low C4 levels (43 vs 71%, P = 0.015). Multivariate analysis of genetic, clinical and immunological variables showed that only antiphospholipid syndrome (APS) was independently associated with cardiovascular events (P = 0.001).
  
  
  CONCLUSIONS
  Although the prevalence of cardiovascular disease in our SLE patients carrying MBL-deficient genotypes was 3.3 times higher than in patients with non-deficient genotypes, only APS was independently associated with cardiovascular events. This suggests that the higher frequency of thrombotic events in SLE patients carrying MBL-deficient genotypes might be related to coexisting APS.
authors.affiliation: Department of Autoimmune Diseases, Hospital Clínic, C/Villarroel, 170 08036-Barcelona, Spain.
authors.forename: J
authors.initials: J
authors.lastname: Font
authors.forename: M
authors.initials: M
authors.lastname: Ramos-Casals
authors.forename: P
authors.initials: P
authors.lastname: Brito-Zerón
authors.forename: N
authors.initials: N
authors.lastname: Nardi
authors.forename: A
authors.initials: A
authors.lastname: Ibañez
authors.forename: B
authors.initials: B
authors.lastname: Suarez
authors.forename: S
authors.initials: S
authors.lastname: Jiménez
authors.forename: D
authors.initials: D
authors.lastname: Tàssies
authors.forename: A
authors.initials: A
authors.lastname: García-Criado
authors.forename: E
authors.initials: E
authors.lastname: Ros
authors.forename: J
authors.initials: J
authors.lastname: Sentís
authors.forename: J-C
authors.initials: JC
authors.lastname: Reverter
authors.forename: F
authors.initials: F
authors.lastname: Lozano
mesh_terms: D000293:Adolescent; D000328:Adult; D000368:Aged; D000369:Aged, 80 and over; D016736:Antiphospholipid Syndrome / Q000235:genetics*; D002318:Cardiovascular Diseases / Q000209:etiology / Q000235:genetics*; D002648:Child; D002908:Chronic Disease; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000235:genetics* / Q000276:immunology; D008297:Male; D037601:Mannose-Binding Lectin / Q000235:genetics*; D008875:Middle Aged; D011110:Polymorphism, Genetic
chemical_list: C445619:MBL2 protein, human; D037601:Mannose-Binding Lectin