Genetically determined mannan-binding lectin deficiency is of minor importance in determining susceptibility to severe infections and vascular organ damage in systemic lupus erythematosus

Author:

Jönsen A.1,Gullstrand B.2,Güner N.3,Bengtsson A.A.4,Nived O.4,Truedsson L.2,Sturfelt G.4

Affiliation:

1. Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden,

2. Department of Laboratory Medicine, Section of Microbiology, Immunology and Glycobiology, Lund University, Lund, Sweden

3. Competence Centre for Clinical Research, Lund University Hospital, Lund, Sweden

4. Department of Clinical Sciences, Section of Rheumatology, Lund University, Lund, Sweden

Abstract

Deficiency of mannan-binding lectin (MBL) has been reported to impact susceptibility to severe infections and atherosclerosis in systemic lupus erythematosus (SLE). In this study, MBL gene polymorphisms were analysed in 143 SLE patients and the frequency of severe infections and organ damage according to SLICC/ACR Damage Index regarding cerebrovascular accidents, angina pectoris, coronary by-pass surgery, myocardial infarction and peripheral arterial disease leading to significant tissue loss, were recorded during a mean follow-up time of 15 years from diagnosis. In a multiple logistic regression model, smoking ( P = 0.001), hypertension ( P = 0.030), alcohol intake ( P = 0.027) and higher triglyceride concentration ( P = 0.026) were associated with cerebrovascular, cardiovascular and peripheral arterial organ damage (CPAD), while the association with MBL deficiency did not reach significance ( P = 0.098). Alcohol intake (>15 g/month) was inversely correlated with CPAD (OR = 0.29, 95%CI 0.096—0.87). MBL deficiency was not significantly more common in SLE patients with severe infections in a multivariate analysis ( P > 0.3). In conclusion, classical risk factors such as smoking, hypertension, low alcohol intake and elevated triglyceride concentration were relatively more important for development of CPAD than MBL deficiency in SLE. Furthermore, MBL deficiency did not contribute to development of major infections in SLE. Lupus (2007) 16, 245—253.

Publisher

SAGE Publications

Subject

Rheumatology

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