CYP2C19 polymorphism has no correlation with the efficacy and safety of thalidomide in the treatment of immune‐related bowel disease

Abstract

Objective To explore the relationship between hepatic cytochrome P450 2C19 (CYP2C19) gene polymorphisms and the effectiveness and safety of thalidomide in the treatment of patients with immune‐related bowel disease (IRBD). Methods CYP2C19 variants in 79 patients treated with thalidomide were analyzed using a polymerase chain reaction‐restriction fragment length polymorphism (PCR‐RFLP). The clinical response and adverse events of the thalidomide treatment were recorded. The potential influences of the CYP2C19 genotype polymorphisms on the clinical efficacy and adverse events of thalidomide were then investigated. Results Altogether 79 patients with IRBD (70 with Crohn's disease, three with ulcerative colitis and six with Behcet's disease) receiving thalidomide therapy were recruited from January 2013 to February 2015 in a tertiary IBD center in China. Overall, 21.5% (17/79) of these patients had CYP2C19 poor metabolizers genotype (PM). The overall response rate and the incidence of adverse events of CYP2C19 extensive metabolizers genotype were not significantly different from that of the PM when IRBD patients were treated with thalidomide (P = 0.517 and 0.816, respectively). Conclusion CYP2C19 polymorphisms do not seem to be associated with efficacy of thalidomide and the incidence of adverse events in treating IRBD.

Identification of hub genes and key pathways in pediatric Crohn’s disease using next generation sequencing and bioinformatics analysis

“…CLEC12A [604], CBS (cystathionine beta-synthase) [605], PEPD (peptidase D) [606], ABCG2 [607], CYP3A4 [608], CYP2J2 [609], SLC23A1 [610], UGT1A1 [611], GUCA2A [612], CYP2D6 [613], APOC3 [614], CYP2C18 [615], DGAT1 [616], SULT1A2 [617], CYP2C19 [618], CNR1 [521], ABCB1 [619], ACE2 [620], SLC6A4 [621], SLC22A4 [622], MGAT3 [623], SLC22A5 [624], DPP4 [625], TMIGD1 [626], ACE (angiotensin I converting enzyme) [525], SLC15A1 [627], CCR9 [628], GP2 [629], CLDN8 [630], SI (sucrase-isomaltase) [631], TF (transferrin) [632], MEP1A [633], LCT (lactase) [634], BTNL2 [635], VIPR1 [636], F11 [637], ALPI (alkaline phosphatase, intestinal) [638], FCRL3 [639], BCHE (butyrylcholinesterase) [640] and SLC26A3 [641] plays a substantial role in CD. S100A8 [642], OSM (oncostatin M) [643], LCN2 [644], S100A9 [642], HGF (hepatocyte growth factor) [645], GDF15 [646], STAT1 [647], MMP1 [648], TLR8 [649], CD55 [650], SOD2 [651], DYSF (dysferlin) [652], FOXP3 [653], TLR2 [654], VWF (von Willebrand factor) [655], COL4A1 [656], IFNG (interferon gamma) [657], APOE (apolipoprotein E) [658], IL6 [659], CCL4 [421], IL11 [660], MMP2 [661], CSF2 [662], PLAU (plasminogen activator, urokinase) [663], CTLA4 [664], MPO (myeloperoxidase) [665], LEFTY1 [666], HP (haptoglobin) [667], CUBN (cubilin) [668], ABCG2 [669], CYP3A4 [67...…”