title: Characteristics of Skin Lesions Associated With Anti-Tumor Necrosis Factor Therapy in Patients With Inflammatory Bowel Disease: A Cohort Study.
abstract: BACKGROUND
  A subgroup of patients with inflammatory bowel disease (IBD) treated with anti-tumor necrosis factor (TNF) antibodies develop skin lesions, but the lesions and their clinical course are not well-characterized.
  
  
  OBJECTIVE
  To describe patients treated with anti-TNF antibodies who did and did not develop skin lesions.
  
  
  METHODS
  Retrospective cohort.
  
  
  METHODS
  Single IBD tertiary referral center.
  
  
  METHODS
  917 consecutive patients with IBD who initiated anti-TNF therapy.
  
  
  METHODS
  Skin lesions, patient demographic characteristics, treatments, clinical course, and serologic and genetic markers.
  
  
  RESULTS
  During a median follow-up of 3.5 years (interquartile range [IQR], 0.5 to 7.4 years), skin lesions associated with the use of anti-TNF therapy developed in 264 of 917 (29%) patients (psoriasiform eczema, 30.6%; eczema, 23.5%; xerosis cutis, 10.6%; palmoplantar pustulosis, 5.3%; psoriasis, 3.8%; other, 26.1%). Lesions typically developed at flexural regions, genitalia, and the scalp, especially the psoriasiform lesions. Thirty-one percent of women and 26% of men developed lesions. Median cumulative doses (2864 mg/y [IQR, 2203 to 3819 mg/y] and 2927 mg/y [IQR, 2377 to 3667 mg/y]) and trough levels (4.2 µg/mL [IQR, 2.6 to 5.8 µg/mL] and 4.0 µg/mL [IQR, 1.6 to 5.9 µg/mL]) of infliximab were similar in patients with and without lesions. All but 28 patients (11%) were successfully managed without needing to stop therapy because of lesions.
  
  
  CONCLUSIONS
  Retrospective nature and no matched control group of patients not receiving anti-TNF therapy.
  
  
  CONCLUSIONS
  Skin lesions occur frequently in association with anti-TNF therapy but rarely require discontinuation of therapy. Close surveillance and early referral to a dedicated dermatologist are recommended.
  
  
  BACKGROUND
  Research Foundation Flanders (FWO), Belgium; Geconcerteerde Onderzoekacties of KU Leuven; and Janssen Biologics.
authors.forename: Isabelle
authors.initials: I
authors.lastname: Cleynen
authors.forename: Wouter
authors.initials: W
authors.lastname: Van Moerkercke
authors.forename: Thomas
authors.initials: T
authors.lastname: Billiet
authors.forename: Pieter
authors.initials: P
authors.lastname: Vandecandelaere
authors.forename: Niels
authors.initials: N
authors.lastname: Vande Casteele
authors.forename: Christine
authors.initials: C
authors.lastname: Breynaert
authors.forename: Vera
authors.initials: V
authors.lastname: Ballet
authors.forename: Marc
authors.initials: M
authors.lastname: Ferrante
authors.forename: Maja
authors.initials: M
authors.lastname: Noman
authors.forename: Gert Van
authors.initials: GV
authors.lastname: Assche
authors.forename: Paul
authors.initials: P
authors.lastname: Rutgeerts
authors.forename: Joost J
authors.initials: JJ
authors.lastname: van den Oord
authors.forename: Ann
authors.initials: A
authors.lastname: Gils
authors.forename: Siegfried
authors.initials: S
authors.lastname: Segaert
authors.forename: Séverine
authors.initials: S
authors.lastname: Vermeire
mesh_terms: D000328:Adult; D003875:Drug Eruptions / Q000209:etiology* / Q000235:genetics; D004485:Eczema / Q000139:chemically induced; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D015212:Inflammatory Bowel Diseases / Q000188:drug therapy*; D008297:Male; D011565:Psoriasis / Q000139:chemically induced; D012189:Retrospective Studies; D014409:Tumor Necrosis Factor-alpha / Q000037:antagonists & inhibitors*
chemical_list: D014409:Tumor Necrosis Factor-alpha