Evidence map›Paper›PMID 20693349›Full record

ArticleDiabetes care2010

Mannose-binding lectin genotype and phenotype in patients with type 2 diabetes and myocardial infarction: a report from the DIGAMI 2 trial.

L G Mellbin, A Hamsten, K Malmberg, R Steffensen, L Rydén, J Ohrvik, T K Hansen

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Article in Diabetes care, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

14 citing papers in PubMed.

  1. Trial
  2. Article
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  5. Article
  6. Article
  7. Article
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  9. Article
  10. Mannan-binding lectin in cardiovascular disease.BioMed research international · 2014
    Review
  11. Article
  12. Article
  13. Article
  14. Article
4 · The record

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5 · Who and what money

Authors and funding

7 authors.

L G MellbinDepartment of Medicine, Karolinska Institutet, Stockholm, Sweden. linda.mellbin@karolinska.se
A Hamsten
K Malmberg
R Steffensen
L Rydén
J Ohrvik
T K Hansen

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

objectiveThe present study characterizes mannose-binding lectin (MBL), an activator of the complement system and thereby important for inflammatory activation, in patients with diabetes and myocardial infarction. RESEARCH DESIGN AND

methodsSerum (S)-MBL was determined at hospital admission in 387 patients with type 2 diabetes (median age 70 years; 68% male) with myocardial infarction, and genotyping was performed in 287 patients. Cardiovascular events (cardiovascular mortality and nonfatal myocardial infarction or stroke) were recorded during 2.5 years.

resultsMedian S-MBL was 1,212 μg/l (interquartile range [IQR] 346-2,681 μg/l). Of the subjects, 54% in the geno- and phenotype subgroup had a high-coding MBL genotype (median S-MBL=2,658 μg/l [IQR 1,715-3,829]) and 46% a low-coding MBL genotype (373 μg/l [100-765]). S-MBL did not correlate with age, BMI, creatinine clearance, glucose, or A1C. Cardiovascular events occurred in 136 (35%) patients. S-MBL did not predict events in univariable analyses (hazard ratio 0.93 [95% CI 0.85-1.01]; P=0.09). In unadjusted analyses, the risk of events was lower in patients with a high genotype and S-MBL above the median for their genotype (0.49 [0.26-0.92]; P=0.026) than for patients with a low genotype and S-MBL below the median for their genotype. The prediction capacity of the geno- and phenotype model was of borderline significance in adjusted Cox regression.

conclusionsPatients with type 2 diabetes and myocardial infarction have MBL genotypes that are similar to those known in the general population. The combination of a low-coding MBL genotype with a low S-MBL appears to be prognostically unfavorable, but the association is blunted by traditional risk markers.

Indexed as

AgedDiabetes Mellitus, Type 2FemaleGenotypeHumansKaplan-Meier EstimateMaleMannose-Binding LectinMiddle AgedMyocardial InfarctionPhenotypeProportional Hazards ModelsMannose-Binding Lectin

Identifiers

PMID20693349
PMCPMC2963511

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