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Mannan‐binding lectin is a determinant of survival in infective endocarditis
Author(s) -
Tran C. T.,
Kjeldsen K.,
Haunsø S.,
Høiby N.,
Johansen H. K.,
Christiansen M.
Publication year - 2007
Publication title -
clinical & experimental immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.329
H-Index - 135
eISSN - 1365-2249
pISSN - 0009-9104
DOI - 10.1111/j.1365-2249.2007.03324.x
Subject(s) - mannan binding lectin , infective endocarditis , immunology , lectin pathway , complement system , collectin , endocarditis , medicine , disease , lectin , biology , alternative complement pathway , innate immune system , immune system
Summary Mannan‐binding lectin (MBL) is a collectin plasma protein activating the lectin pathway of the complement system, enhancing opsonophagocytosis and modulating the cytokine response to inflammation. Deficiency of MBL, caused by structural mutations or promoter polymorphisms in the MBL2 gene, has been associated with increased susceptibility to infection and autoimmune disease. Thus, as infective endocarditis remains a severe disease requiring intensive and long‐term treatment with antibiotics, we examined whether there was an association between MBL and clinical outcome in 39 well‐characterized patients with infective endocarditis. Five patients (13%) had MBL concentrations < 100 µg/l and were considered MBL‐deficient. This proportion was similar to that in a healthy control group of blood donors. Mortality 3 months after diagnosis was 20% in patients with MBL‐deficiency and 9% in patients with normal MBL. The 5‐year mortality was 80% and 25%, respectively. MBL‐deficiency was on univariate survival statistics associated with significantly higher mortality on follow‐up ( P  = 0·03). In conclusion, this is the first report of an association between MBL‐deficiency and survival in infective endocarditis. The present observation is important, as replacement therapy in MBL‐deficient patients is possible. For certain high‐risk subgroups, it opens new perspectives for improvement of treatment and outcome in infective endocarditis.

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