Mannose-binding lectin serum levels in patients with systemic lupus erythematosus: association with thrombocytopaenia and seizure

• Published in: Lupus Vol. 27; no. 3; pp. 372 - 379
• Main Authors: Cieslinski, J Z, Skare, T L, Nisihara, R, De Messias-Reason, I J, Utiyama, S R R
• Format: Journal Article
• Language: English
• Published: London, England SAGE Publications 01.03.2018; Sage Publications Ltd
• Subjects: Adult; Brazil; Case-Control Studies; Complement C3 - metabolism; Complement C4 - metabolism; Complement system; Female; Humans; Lectins; Logistic Models; Lupus; Lupus Erythematosus, Systemic - blood; Lupus Erythematosus, Systemic - complications; Male; Mannose; Mannose-binding lectin; Mannose-Binding Lectin - blood; Mannose-Binding Lectin - genetics; Middle Aged; Seizures; Seizures - blood; Seizures - etiology; Serum levels; Severity of Illness Index; Systemic lupus erythematosus; Thrombocytopenia; Thrombocytopenia - blood; Thrombocytopenia - etiology; Systemic lupus erythematosus; seizure; thrombocytopaenia; mannose-binding lectin
• ISSN: 0961-2033; 1477-0962
• DOI: 10.1177/0961203317722846

The complement system contributes to the pathogenesis of systemic lupus erythematosus (SLE). Mannose-binding lectin (MBL) is a key molecule of the lectin pathway of complement and seems to be related to the clinical manifestations of this disease. We evaluated the serum levels of MBL and its relationship with disease onset and clinical findings in SLE patients. Serum samples were analysed in 195 patients and 145 healthy controls from southern Brazil. Patients with high MBL levels (above 2000 ng/ml) showed a significant increase in the frequency of thrombocytopaenia (p = 0.007; OR = 2.71; 95% CI = 1.32–5.55); and seizures (p = 0.034; OR = 2.61; 95% CI = 1.07–6.37). A positive correlation between disease activity and MBL levels (>2000 ng/ml; p = 0.031, rho = 0.279) as well as of MBL concentration with accumulated organ damage (p = 0.021; rho = 0.232) was observed. Our results suggest a role for MBL in the development of clinical manifestations such as thrombocytopaenia and seizures in SLE patients. These findings corroborate the participation of the lectin pathway of complement in the pathophysiologic mechanisms underlying clinical manifestations of SLE.