Pharmacogenetic variants of infliximab response in young patients with inflammatory bowel disease

Abstract

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Biomarkers for Optimization and Personalization of Anti-TNFs in Pediatric Inflammatory Bowel Disease

“…Consistent with our approach, other authors explored the association of the SNPs rs3936991 (FCGR3A) and rs1800629 (TNF) with response, serum trough levels, and ADA production in IBD patients treated with infliximab [101]. Curci et al showed that variant C rs396991 was associated with a poorer clinical response at the end of induction and at 22 and at 52 weeks of treatment with infliximab.…”

“…Curci et al showed that variant C rs396991 was associated with a poorer clinical response at the end of induction and at 22 and at 52 weeks of treatment with infliximab. In addition, patients with this variant had lower infliximab levels and were more likely to produce ADAs than patients with the wild-type genotype [101].…”

“…Of note, information on these biomarkers of response to infliximab and adalimumab in pIBD is lacking. Few studies have included children [97], and even fewer have focused only on children [98][99][100][101]. The two main strategies followed are selection of genome-wide association studies (GWAS) [97,98] and selection of SNPs [10,101].…”

“…Few studies have included children [97], and even fewer have focused only on children [98][99][100][101]. The two main strategies followed are selection of genome-wide association studies (GWAS) [97,98] and selection of SNPs [10,101]. Another approach has been to identify the genetic variants associated with parameters that correlate with a higher probability of response, such as biological drug trough level [100,101].…”

Assessing Immunogenicity of Biologic Drugs in Inflammatory Joint Diseases: Progress Towards Personalized Medicine

“…Other genetic polymorphisms, such as in the CXCL12, IL-10, and Fc gamma receptor (FCGR3A) genes, have also been proposed to be associated with a risk of ADAb formation to TNFi [67,[74][75][76]. Whilst an area of research interest, at present, there is no definitive evidence to support genetic testing to predict ADAb formation as most studies are limited by small patient numbers or a lack of replication.…”