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News

Genetic susceptibility influences the response to biological therapy in Crohn's disease

Genetic susceptibility to increased bacterial translocation influences the response to biological therapy in patients with Crohn's disease, reports the most recent issue of Gut.

News image

The etiology of Crohn's disease (CD) has been related to nucleotide-binding oligomerization domain containing 2 (NOD2) and ATG16L1 gene variants.

The observation of bacterial DNA translocation in patients with CD led researchers to hypothesize that this process may be facilitated in patients with NOD2/ATG16L1-variant genotypes, affecting the efficacy of anti-tumor necrosis factor (TNF) therapies.

Dr Ana Gutiérrez and colleagues evaluated 179 patients with Crohn's disease.

CD-related NOD2 and ATG16L1 variants were genotyped.

Phagocytic and bactericidal activities were evaluated in blood neutrophils.

Bacterial DNA was found in 44% of patients with active disease
Gut

Bacterial DNA, TNFα, IFNγ, IL-12p40, free serum infliximab/adalimumab levels and antidrug antibodies were measured.

The team found bacterial DNA in 44% of patients with active disease versus 23% of patients with remitting disease.

A NOD2-variant or ATG16L1-variant genotype was associated with bacterial DNA presence.

This OR was 13 for patients with a double-variant genotype.

The researchers observed bacterial DNA was associated with disease activity.

Single and double-gene variants were not associated with disease activity.

The team found that patients with a NOD2-variant genotype showed decreased phagocytic and bactericidal activities in blood neutrophils, increased TNFα levels in response to bacterial DNA and decreased trough levels of free anti-TNFα.

The proportion of patients on an intensified biological therapy was significantly higher in the NOD2-variant groups.

Dr Gutiérrez's team commented, "Our results characterize a subgroup of patients with CD who may require a more aggressive therapy to reduce the extent of inflammation and the risk of relapse."

Gut 2014; 63: 272-280 
14 January 2014

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