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  1. J Wehkamp1,
  2. C L Bevins2,
  3. E F Stange3
  1. 1
    Dr Margarete Fischer-Bosch-Institute of Clinical Pharmacology, Stuttgart, Germany
  2. 2
    Department of Microbiology and Immunology, School of Medicine, University of California, Davis, California, USA
  3. 3
    Department of Internal Medicine I, Robert Bosch Hospital, Stuttgart, Germany
  1. Dr J Wehkamp, Dr Margarete Fischer-Bosch-Institute of Clinical Pharmacology, D-70376 Stuttgart, Germany; Jan.wehkamp{at}ikp-stuttgart.de

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We read with interest the reply from Simms, Doecke and Radford-Smith. We welcome the opportunity to clarify questions about our previous studies,13 because the details serve to emphasise the validity of our conclusions that differ from those of Simms et al (Gut 2008;57:903–10). First, our data from independent sample sets support that NOD2 SNP13 is associated with a decrease in HD5 mRNA levels. In the first study,1 the genotypes were mixed, but the majority (5/8, fig 1A) within the ileal Crohn’s disease (CD) group were SNP13 frameshift mutations; in the second study,2 larger sample sizes from US patients allowed the conclusion that only SNP13 samples were further decreased (as compared with wild-type NOD2) with ileal CD. Perhaps a sampling error resulting from their small sample size will explain the data …

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