title: Infliximab-induced psoriasis and psoriasiform skin lesions in pediatric Crohn disease and a potential association with IL-23 receptor polymorphisms.
abstract: BACKGROUND
  Infliximab (IFX), an established therapy for pediatric Crohn disease (CD), is also efficacious in treating psoriasis, a skin disorder, in which tumor necrosis factor-α is implicated pathogenically. Paradoxically, there have been numerous reports of new-onset psoriasis following tumor necrosis factor-α antagonist therapy in adult patients with inflammatory bowel disease, but pediatric data are sparse.
  
  
  METHODS
  A retrospective review of all IFX-treated patients with CD, who subsequently developed psoriasis, at a single pediatric inflammatory bowel disease center, was performed. A subset of affected patients (10/18) and CD controls (147 of 172) treated with IFX but without the development of psoriasis were genotyped for polymorphisms in the interleukin-23 receptor (IL-23R) gene, which has been identified as conferring susceptibility to both CD and psoriasis.
  
  
  RESULTS
  Eighteen (10.5%) of 172 IFX-treated patients with CD developed new-onset psoriasis (n = 17) or worsening of existing psoriasis (n = 1). The duration of IFX exposure was variable, ranging from 1 to 25 infusions. Three patients discontinued IFX because of this complication. Most patients responded well to topical steroid therapy. In comparison to disease-matched controls, patients with CD developing psoriasis following IFX therapy were more likely to be homozygous for specific polymorphisms in the IL-23R gene (rs10489628, rs10789229, and rs1343151).
  
  
  CONCLUSIONS
  As in adults, the development of psoriasis or psoriasiform skin lesions occurs in pediatric patients with CD treated with IFX. Adequately powered studies are required to further explore the preliminary findings reported here to determine whether polymorphisms in the IL-23R gene have a role in the pathogenesis of this paradoxical process, which presently remains unexplained.
authors.affiliation: Division of Gastroenterology, and Nutrition, McMaster Children's Hospital, Hamilton, Ontario, Canada. sherlom@mcmaster.ca
authors.forename: Mary E
authors.initials: ME
authors.lastname: Sherlock
authors.forename: Thomas
authors.initials: T
authors.lastname: Walters
authors.forename: Merit M
authors.initials: MM
authors.lastname: Tabbers
authors.forename: Karen
authors.initials: K
authors.lastname: Frost
authors.forename: Mary
authors.initials: M
authors.lastname: Zachos
authors.forename: Aleixo
authors.initials: A
authors.lastname: Muise
authors.forename: Elena
authors.initials: E
authors.lastname: Pope
authors.forename: Anne M
authors.initials: AM
authors.lastname: Griffiths
mesh_terms: D000293:Adolescent; D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000009:adverse effects* / Q000627:therapeutic use; D000911:Antibodies, Monoclonal / Q000009:adverse effects* / Q000627:therapeutic use; D016022:Case-Control Studies; D002648:Child; D003424:Crohn Disease / Q000150:complications* / Q000188:drug therapy / Q000235:genetics; D005838:Genotype; D006720:Homozygote; D006801:Humans; D000069285:Infliximab; D011110:Polymorphism, Genetic; D011565:Psoriasis / Q000139:chemically induced / Q000235:genetics* / Q000473:pathology; D018123:Receptors, Interleukin / Q000235:genetics*; D012867:Skin / Q000187:drug effects* / Q000473:pathology; D013256:Steroids / Q000627:therapeutic use
chemical_list: D000894:Anti-Inflammatory Agents, Non-Steroidal; D000911:Antibodies, Monoclonal; C515500:IL23R protein, human; D018123:Receptors, Interleukin; D013256:Steroids; D000069285:Infliximab