kiny
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http://www.ncbi.nlm.nih.gov/pubmed/23274341
Infliximab-Induced Psoriasis And Psoriasiform Skin Lesions In Pediatric Crohn's Disease And A Potential Association With IL-23 Receptor Polymorphisms.
Sherlock ME, Walters T, Tabbers MM, Frost K, Zachos M, Muise A, Pope E, Griffiths AM.
Division of Gastroenterology, and Nutrition, McMaster Children's Hospital, Hamilton, Canada
2012 Dec 27
BACKGROUND: Infliximab, an established therapy for pediatric Crohn disease (CD), is also efficacious in treating psoriasis, a skin disorder, in which TNF-α is implicated pathogenically. Paradoxically, there have been numerous reports of new-onset psoriasis following TNF-α antagonist therapy in adult inflammatory bowel disease (IBD) patients, but pediatric data are sparse.
METHODS: A retrospective review of all infliximab treated CD patients, who subsequently developed psoriasis, at a single pediatric IBD center, was performed. A subset of affected patients (10 of 18) and CD controls (147 of 172), treated with infliximab but without the development of psoriasis were genotyped for polymorphisms in the Il-23 receptor (IL-23R) gene, which has been identified as conferring susceptibility to both CD and psoriasis.
RESULTS: Eighteen (10.5%) of 172 infliximab treated CD patients developed new-onset psoriasis (n = 17) or worsening of existing psoriasis (n = 1). The duration of infliximab exposure was variable, ranging from 1 to 25 infusions. Three patients discontinued infliximab due to this complication. Most patients responded well to topical steroid therapy. In comparison to disease-matched controls, CD patients developing psoriasis following infliximab therapy were more likely to be homozygous for specific polymorphisms in the Il-23R gene (rs10489628, rs10789229 and rs1343151).
CONCLUSION:As in adults, the development of psoriasis or psoriasiform skin lesions occurs in pediatric CD patients treated with infliximab. Adequately powered studies are required to further explore the preliminary findings reported here to determine if polymorphisms in the Il-23 receptor gene have a role in the pathogenesis of this paradoxical process, which currently remains unexplained.
Infliximab-Induced Psoriasis And Psoriasiform Skin Lesions In Pediatric Crohn's Disease And A Potential Association With IL-23 Receptor Polymorphisms.
Sherlock ME, Walters T, Tabbers MM, Frost K, Zachos M, Muise A, Pope E, Griffiths AM.
Division of Gastroenterology, and Nutrition, McMaster Children's Hospital, Hamilton, Canada
2012 Dec 27
BACKGROUND: Infliximab, an established therapy for pediatric Crohn disease (CD), is also efficacious in treating psoriasis, a skin disorder, in which TNF-α is implicated pathogenically. Paradoxically, there have been numerous reports of new-onset psoriasis following TNF-α antagonist therapy in adult inflammatory bowel disease (IBD) patients, but pediatric data are sparse.
METHODS: A retrospective review of all infliximab treated CD patients, who subsequently developed psoriasis, at a single pediatric IBD center, was performed. A subset of affected patients (10 of 18) and CD controls (147 of 172), treated with infliximab but without the development of psoriasis were genotyped for polymorphisms in the Il-23 receptor (IL-23R) gene, which has been identified as conferring susceptibility to both CD and psoriasis.
RESULTS: Eighteen (10.5%) of 172 infliximab treated CD patients developed new-onset psoriasis (n = 17) or worsening of existing psoriasis (n = 1). The duration of infliximab exposure was variable, ranging from 1 to 25 infusions. Three patients discontinued infliximab due to this complication. Most patients responded well to topical steroid therapy. In comparison to disease-matched controls, CD patients developing psoriasis following infliximab therapy were more likely to be homozygous for specific polymorphisms in the Il-23R gene (rs10489628, rs10789229 and rs1343151).
CONCLUSION:As in adults, the development of psoriasis or psoriasiform skin lesions occurs in pediatric CD patients treated with infliximab. Adequately powered studies are required to further explore the preliminary findings reported here to determine if polymorphisms in the Il-23 receptor gene have a role in the pathogenesis of this paradoxical process, which currently remains unexplained.
