Mannose-binding lectin serum levels in patients with systemic lupus erythematosus: association with thrombocytopaenia and seizure
| Autor: | Thelma L. Skare, I. J. T. De Messias-Reason, Renato Nisihara, Shirley Ramos da Rosa Utiyama, Juliana Z Cieslinski |
|---|---|
| Rok vydání: | 2017 |
| Předmět: |
Adult
Male 0301 basic medicine Disease Mannose-Binding Lectin Severity of Illness Index Pathogenesis 03 medical and health sciences 0302 clinical medicine Rheumatology Seizures Severity of illness Humans Lupus Erythematosus Systemic Medicine Mannan-binding lectin 030203 arthritis & rheumatology business.industry Case-control study Complement C4 Complement C3 Middle Aged Thrombocytopenia Pathophysiology Complement system Logistic Models 030104 developmental biology Case-Control Studies Lectin pathway Immunology Female business Brazil |
| Zdroj: | Lupus. 27:372-379 |
| ISSN: | 1477-0962 0961-2033 |
| DOI: | 10.1177/0961203317722846 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
| Externí odkaz: |
|