A new study suggests that in patients with systemic lupus erythematosus (SLE), mannose-binding lectin of the complement system may contribute to the development of clinical manifestations including seizures and thrombocytopenia.1
The study, published in Lupus, sought to examine the impact of mannose-binding lectin (MBL) on SLE. To conduct the investigation, researchers examined MBL serum levels and the molecule’s involvement in disease onset and clinical findings from 195 patients with SLE and 145 healthy controls from southern Brazil.
Patients with high MBL levels (>2000 ng/ml) showed a significant increase in thrombocytopaenia frequency (P =.007; odds ratio [OR],2.71; 95% CI, 1.32-5.55) and seizures (P =.034; OR, 2.61; 95% CI, 1.07-6.37).
“Thrombocytopaenia in SLE may be due to several factors including bone marrow failure, increased peripheral platelet destruction, and presence of autoantibodies against platelets and thrombopoietin, such as TPO [thrombopoietin] receptor c-MpL and CD40L,” the researchers wrote. They noted a positive correlation between accumulated organ damage and MBL concentration (P =.021; P =.232).
“Although polymorphism of MBL2 gene has been largely studied in the pathogenesis of SLE, one must consider the evaluation of MBL protein levels in relation to clinical profile may also provide useful information in the disease process,” the researchers added. “These findings corroborate the participation of the lectin pathway of complement in the pathophysiologic mechanisms underlying clinical manifestations of SLE,” they concluded.