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BACKGROUND: Cardiovascular disease is an important complication in pati ents wi th systemic lupus erythematosus (SLE). Variant alleles of the mannose-binding l ectin gene are associated with SLE as well as with severe atherosclerosis. We de termined whether mannose-binding lectin variant alleles were associated with an increased risk of arterial thrombosis among patients with SLE. METHODS: Mannose -binding lectin alleles were genotyped by means of a polymerase-chain-reactio n assay in 91 Danish patients with SLE. Arterial and venous thromboses occurring after the diagnosis of SLE were assessed in a prospective study. Arterial and v enous thromboses were confirmed by appropriate diagnostic methods. RESULTS: Fift y-four patients had no mannose-binding lectin variant alleles (A/A genotype), 30 were heterozygous (A/O genotype), and 7 were homozygous (O/O genotype). Durin g a median follow-up of 9.1 years, arterial thromboses (cerebral or myocardial infarction or leg embolus) developed in 6 of the 7 patients with the O/O genotyp e, as compared with 18 of the 84 patients with the other two genotypes (hazard r atio, 5.8; 95 percent confidence interval, 2.2 to 15.2; overall incidence, 26 pe rcent). After correction for other known risk factors, the hazard ratio was 7.0 (95 percent confidence interval, 1.9 to 25.4). Venous thromboses, which occurred in 14 patients, were statistically unrelated to the mannose-binding lectin gen otype. CONCLUSIONS: Among patients with SLE, homozygosity for mannose-binding l ectin variant alleles is associated with an increased risk of arterial thrombosi s. The risk of venous thrombosis is not increased, indicating that mannose-bind ing lectin has a specific role in providing protection against arterial thrombos is.
BACKGROUND: Cardiovascular disease is an important complication in pati ents wi th systemic lupus erythematosus (SLE). Variant alleles of the mannose-binding l ectin gene are associated with SLE as well as severe atherosclerosis. We de termined whether mannose-binding lectin variant METHODS: Mannose-binding lectin alleles were genotyped by means of a polymerase-chain-reactivity assay in 91 Danish patients with SLE. Arterial and venous thromboses occurring after the diagnosis of SLE were assessed in a prospective study. Arterial and v enous thromboses were confirmed by appropriate diagnostic methods. RESULTS: Fift y-four patients had no mannose-binding lectin variant alleles (A / A genotype), 30 were heterozygous genotype), and 7 were homozygous (O / O genotype). Durin ga median follow-up of 9.1 years, arterial thromboses (cerebral or myocardial infarction or leg embolus) developed in 6 of the 7 patients with the O / O genotyp e, as compared with 18 of the 84 patients with the other two genotypes (hazard ratio 5.8; 95 percent confidence interval, 2.2 to 15.2; overall incidence, 26 pe rcent). After correction for other known risk factors, the hazard ratio was 7.0 (95 percent confidence interval, 1.9 to 25.4). Venous thromboses, which occurred in 14 patients, were statistically unrelated to the mannose-binding lectin genotype. CONCLUSIONS: Among patients with SLE , homozygosity for mannose-binding l ectin variant alleles is associated with an increased risk of arterial thrombosi s. The risk of venous thrombosis is not increased, indicating that mannose-bind ing lectin has a specific role in providing protection against arterial thrombos is.