title: Management of EGFR-inhibitor associated rash: a retrospective study in 49 patients.
abstract: BACKGROUND
  In recent years inhibitors directed against the epidermal growth factor receptor (EGFR) have evolved as effective targeting cancer drugs. Characteristic papulopustular exanthemas, often described as acneiform rashes, are the most frequent adverse effect associated with this class of novel cancer drugs and develop in > 90% of patients. Notably, the rash may significantly compromise the patients' quality of life, thereby potentially leading to incompliance as well as dose reduction or even termination of the anti-EGFR therapy. Yet, an effective dermatologic management of cutaneous adverse effects can be achieved. Whereas various case reports, case series or expert opinions on the management of EGFR-inhibitor (EGFRI) induced rashes have been published, data on systematic management studies are sparse.
  
  
  METHODS
  Here, we present a retrospective, uncontrolled, comparative study in 49 patients on three established regimens for the management of EGFRI-associated rashes.
  
  
  RESULTS
  Strikingly, patients' rash severity improved significantly over three weeks of treatment with topical mometason furoate cream, topical prednicarbate cream plus nadifloxacin cream, as well as topical prednicarbate cream plus nadifloxacin cream plus systemic isotretinoin.
  
  
  CONCLUSIONS
  In summary our results demonstrate that EGFRI-associated rashes can be effectively managed by specific dermatologic interventions. Whereas mild to moderate rashes should be treated with basic measures in combination with topical glucocorticosteroids or combined regiments using glucocorticosteroids and antiseptics/antibiotics, more severe or therapy-resistant rashes are likely to respond with the addition of systemic retinoids.
authors.affiliation: Department of Dermatology, University of Duesseldorf, Medical Faculty, Moorenstrasse 5, D-40225 Duesseldorf, Germany. peterarne.gerber@uni-duesseldorf.de
authors.forename: Peter Arne
authors.initials: PA
authors.lastname: Gerber
authors.forename: Stephan
authors.initials: S
authors.lastname: Meller
authors.forename: Tatiana
authors.initials: T
authors.lastname: Eames
authors.forename: Bettina Alexandra
authors.initials: BA
authors.lastname: Buhren
authors.forename: Holger
authors.initials: H
authors.lastname: Schrumpf
authors.forename: Sonja
authors.initials: S
authors.lastname: Hetzer
authors.forename: Laura Maximiliane
authors.initials: LM
authors.lastname: Ehmann
authors.forename: Wilfried
authors.initials: W
authors.lastname: Budach
authors.forename: Edwin
authors.initials: E
authors.lastname: Bölke
authors.forename: Christiane
authors.initials: C
authors.lastname: Matuschek
authors.forename: Andreas
authors.initials: A
authors.lastname: Wollenberg
authors.forename: Bernhard
authors.initials: B
authors.lastname: Homey
mesh_terms: D000287:Administration, Topical; D066246:ErbB Receptors / Q000037:antagonists & inhibitors; D005076:Exanthema / Q000139:chemically induced / Q000188:drug therapy / Q000473:pathology; D024841:Fluoroquinolones / Q000008:administration & dosage*; D006801:Humans; D015474:Isotretinoin / Q000008:administration & dosage; D000068656:Mometasone Furoate; D011244:Pregnadienediols / Q000008:administration & dosage*; D047428:Protein Kinase Inhibitors / Q000627:therapeutic use / Q000633:toxicity; D011807:Quinolizines / Q000008:administration & dosage*
chemical_list: D024841:Fluoroquinolones; D011244:Pregnadienediols; D047428:Protein Kinase Inhibitors; D011807:Quinolizines; D000068656:Mometasone Furoate; C062127:nadifloxacin; C512478:EGFR protein, human; D066246:ErbB Receptors; D015474:Isotretinoin