title: Mannose-binding lectin expression genotype in pediatric-onset systemic lupus erythematosus: associations with susceptibility to renal disease and protection against infections.
abstract: OBJECTIVE
  To study possible associations between extended mannose-binding lectin (MBL) expression genotypes and clinical manifestations and infections in children with systemic lupus erythematosus (SLE).
  
  
  METHODS
  Clinical and laboratory variables for a cohort of 125 patients with pediatric-onset SLE were obtained by clinical examinations and chart reviews. Controls were 137 age-matched and sex-matched healthy children and adolescents. MBL gene polymorphisms were genotyped by polymerase chain reaction. Serum MBL concentrations were measured by ELISA.
  
  
  RESULTS
  The frequencies of extended MBL expression genotypes did not differ between patients and controls. There were 82 patients with SLE who had high MBL expression genotypes and 43 who had medium and low MBL expression genotypes. Patients with the high MBL expression genotype had renal disorders more frequently than patients in the group with medium and low MBL expression genotypes [54/82 (65.9%) vs 18/43 (41.9%), respectively; p = 0.013] and fewer serious bacterial infections [22/82 (26.8%) vs 20/43 (46.5%); p = 0.030]. Using logistic regression for patients with SLE, a high MBL expression genotype was independently associated with renal disorders (OR 2.49, 95% CI 1.15-5.39, p = 0.021) and had a protective effect against serious bacterial infections (OR 0.29, 95% CI 0.12-0.71, p = 0.007). MBL levels decreased significantly when patients with active SLE reached an inactive stage (1.56 ± 0.55 μg/ml vs 1.08 ± 0.65 μg/ml; p = 0.001), but these levels were still higher than those in controls.
  
  
  CONCLUSIONS
  Our findings suggest that a high MBL expression genotype is a risk factor for renal disorder, while it has a protective effect against infections. Serum MBL levels reflect SLE activity.
authors.affiliation: Department of Pediatrics, Chang Gung Memorial Hospital, Chia-Yi, Taiwan.
authors.forename: Yi-Chan
authors.initials: YC
authors.lastname: Tsai
authors.forename: Kou-Wei
authors.initials: KW
authors.lastname: Yeh
authors.forename: Tsung-Chieh
authors.initials: TC
authors.lastname: Yao
authors.forename: Yu-Lin
authors.initials: YL
authors.lastname: Huang
authors.forename: Ming-Ling
authors.initials: ML
authors.lastname: Kuo
authors.forename: Jing-Long
authors.initials: JL
authors.lastname: Huang
mesh_terms: D017668:Age of Onset; D001424:Bacterial Infections / Q000453:epidemiology / Q000517:prevention & control*; D015415:Biomarkers / Q000097:blood; D016022:Case-Control Studies; D002681:China; D020022:Genetic Predisposition to Disease / Q000235:genetics*; D005838:Genotype; D006801:Humans; D007674:Kidney Diseases / Q000453:epidemiology / Q000235:genetics*; D016015:Logistic Models; D008137:Longitudinal Studies; D008180:Lupus Erythematosus, Systemic / Q000097:blood* / Q000453:epidemiology; D037601:Mannose-Binding Lectin / Q000097:blood* / Q000235:genetics*; D012307:Risk Factors; D012720:Severity of Illness Index
chemical_list: D015415:Biomarkers; D037601:Mannose-Binding Lectin