Abstract |
Recently, it has been shown that FCGR3A-158 gene polymorphism is associated with biological and possibly clinical response to infliximab in Crohn's disease. We further assessed this association in a subset of 344 patients from the large and well-defined cohort of 573 patients with Crohn's disease from the ACCENT I study. No association could be observed between FCGR3A-158 gene polymorphism and the clinical response to infliximab, which was primarily defined as a decrease of >or=70 points in the Crohn's disease activity index or clinical remission ( Crohn's disease activity index <150). We did, however, confirm a trend towards a greater decrease in C-reactive protein after infliximab in V/V homozygotes as compared with V/F heterozygotes and F/F homozygotes (-79.4, -76.5, and -64.3%, respectively, at week 6; P=0.085; one-tailed P=0.043). This finding has no immediate clinical impact but may enhance the understanding of the complex mechanisms of action of anti- tumor necrosis factor agents in Crohn's disease.
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Authors | Edouard J Louis, Hervé E Watier, Stefan Schreiber, Jochen Hampe, François Taillard, Allan Olson, Nicole Thorne, Hongyan Zhang, Jean-Frédéric Colombel |
Journal | Pharmacogenetics and genomics
(Pharmacogenet Genomics)
Vol. 16
Issue 12
Pg. 911-4
(Dec 2006)
ISSN: 1744-6872 [Print] United States |
PMID | 17108815
(Publication Type: Journal Article, Randomized Controlled Trial, Research Support, Non-U.S. Gov't)
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Chemical References |
- Antibodies, Monoclonal
- DNA Primers
- FCGR3A protein, human
- Receptors, IgG
- Infliximab
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Topics |
- Adolescent
- Adult
- Aged
- Antibodies, Monoclonal
(therapeutic use)
- Base Sequence
- Crohn Disease
(genetics, immunology, therapy)
- DNA Primers
(genetics)
- Female
- Genotype
- Heterozygote
- Homozygote
- Humans
- Infliximab
- Male
- Middle Aged
- Pharmacogenetics
- Polymorphism, Single Nucleotide
- Receptors, IgG
(genetics)
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