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The association of mannose-binding lectin 2 polymorphisms with outcome in very low birth weight infants
The association of mannose-binding lectin 2 polymorphisms with outcome in very low birth weight infants
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The association of mannose-binding lectin 2 polymorphisms with outcome in very low birth weight infants
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The association of mannose-binding lectin 2 polymorphisms with outcome in very low birth weight infants
The association of mannose-binding lectin 2 polymorphisms with outcome in very low birth weight infants

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The association of mannose-binding lectin 2 polymorphisms with outcome in very low birth weight infants
The association of mannose-binding lectin 2 polymorphisms with outcome in very low birth weight infants
Journal Article

The association of mannose-binding lectin 2 polymorphisms with outcome in very low birth weight infants

2017
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Overview
Studies on the influence of mannose-binding lectin (MBL) deficiency on infection susceptibility in preterm infants have yielded controversial results. We investigated the association of genotype-based MBL levels with outcome in very-low-birth weight infants (VLBWI). We genotyped 3 genetic variants of MBL2 (rs1800450, rs1800451, rs5030737) in 6878 VLBWI. MBL plasma levels were categorized as normal (wild type, A/A), low (heterozygotes, A/O) or undetectable (homozygotes, O/O). Primary outcome was the effect of genotype-based MBL2 levels on blood-culture proven and clinical sepsis during primary stay in hospital. We also evaluated burden of infection within 24 months after discharge. We found no association between MBL levels and sepsis risk in the whole cohort. Infants without measurable MBL levels born between 32 0/7 to 36 6/7 weeks of gestation, however, had a higher rate of Gram-negative sepsis than infants with normal or reduced MBL levels. In a follow-up investigation at 24 months (n = 1070 infants), infants without measurable MBL levels suffered more frequently from stomatitis and urinary tract infection. In a large cohort of VLBWI MBL2 deficiency had no major impact on infection risk unless children were born between 32 0/7 and 36 6/7 weeks of gestation.