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Details

Autor(en) / Beteiligte
Titel
Gene Signatures of Early Response to Anti-TNF Drugs in Pediatric Inflammatory Bowel Disease
Ist Teil von
  • International journal of molecular sciences, 2020-05, Vol.21 (9), p.3364
Ort / Verlag
Switzerland: MDPI AG
Erscheinungsjahr
2020
Link zum Volltext
Quelle
MEDLINE
Beschreibungen/Notizen
  • Around a 20-30% of inflammatory bowel disease (IBD) patients are diagnosed before they are 18 years old. Anti-TNF drugs can induce and maintain remission in IBD, however, up to 30% of patients do not respond. The aim of the work was to identify markers that would predict an early response to anti-TNF drugs in pediatric patients with IBD. The study population included 43 patients aged <18 years with IBD who started treatment with infliximab or adalimumab. Patients were classified into primary responders ( = 27) and non-responders to anti-TNF therapy ( = 6). Response to treatment could not be analyzed in 10 patients. Response was defined as a decrease in over 15 points in the disease activity indexes from week 0 to week 10 of infliximab treatment or from week 0 to week 26 of adalimumab treatment. The expression profiles of nine genes in total RNA isolated from the whole-blood of pediatric IBD patients taken before biologic administration and after 2 weeks were analyzed using qPCR and the 2 method. Before initiation and after 2 weeks of treatment the expression of was decreased in patients who were considered as non-responders ( value < 0.05). Changes in expression were also observed for at T0 and T2, although that did not reach the level of statistical significance. In addition, the expression of decreased 1.75-fold during the first 2 weeks of anti-TNF treatment in responders, whereas no changes were observed in non-responders. Expression of the gene is a pharmacogenomic biomarker of early response to anti-TNF agents in pediatric IBD. and need to be validated in larger studies.
Sprache
Englisch
Identifikatoren
ISSN: 1422-0067, 1661-6596
eISSN: 1422-0067
DOI: 10.3390/ijms21093364
Titel-ID: cdi_doaj_primary_oai_doaj_org_article_bc5201994a9846f6992dcaa116427813
Format
Schlagworte
adalimumab, Adalimumab - pharmacology, Adalimumab - therapeutic use, Adolescent, Adults, alpha-Defensins - biosynthesis, alpha-Defensins - genetics, Anti-Inflammatory Agents - pharmacology, Anti-Inflammatory Agents - therapeutic use, Antirheumatic Agents - pharmacology, Antirheumatic Agents - therapeutic use, Biological products, biomarker, Biomarkers, Child, Child, Preschool, Clinical medicine, Crohn’s disease, Drugs, Female, Gene expression, Gene Expression Regulation - drug effects, Humans, Immunotherapy, Infant, Inflammatory bowel disease, Inflammatory bowel diseases, Inflammatory Bowel Diseases - blood, Inflammatory Bowel Diseases - drug therapy, Inflammatory Bowel Diseases - genetics, Infliximab, Infliximab - pharmacology, Infliximab - therapeutic use, Intestine, Male, Monoclonal antibodies, Patients, Pediatrics, Pharmacogenomics, Population studies, Receptors, Tumor Necrosis Factor, Type II - biosynthesis, Receptors, Tumor Necrosis Factor, Type II - genetics, Remission, RNA, Messenger - biosynthesis, RNA, Messenger - blood, RNA, Messenger - genetics, Smad7 protein, Smad7 Protein - biosynthesis, Smad7 Protein - genetics, Studies, TLR2 protein, TNF inhibitors, Toll-Like Receptor 2 - biosynthesis, Toll-Like Receptor 2 - genetics, Toll-like receptors, Transcriptome - drug effects, Treatment Outcome, Triggering Receptor Expressed on Myeloid Cells-1 - biosynthesis, Triggering Receptor Expressed on Myeloid Cells-1 - genetics, Tumor Necrosis Factor-alpha - antagonists & inhibitors, Tumor Necrosis Factor-alpha - biosynthesis, Tumor Necrosis Factor-alpha - genetics, Tumor necrosis factor-α, ulcerative colitis

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