79. Acne

  1. Alan D. Irvine MD, FRCPI, FRCP2,3,
  2. Peter H. Hoeger MD4,5 and
  3. Albert C. Yan MD, FAAP, FAAD6,7
  1. Bodo C. Melnik MD

Published Online: 24 MAY 2011

DOI: 10.1002/9781444345384.ch79

Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition

Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition

How to Cite

Melnik, B. C. (2011) Acne, in Harper's Textbook of Pediatric Dermatology, Volume 1, 2, Third Edition (eds A. D. Irvine, P. H. Hoeger and A. C. Yan), Wiley-Blackwell, Oxford, UK. doi: 10.1002/9781444345384.ch79

Editor Information

  1. 2

    Trinity College, Dublin, Ireland

  2. 3

    Our Lady's Children's Hospital, Dublin, Ireland

  3. 4

    University of Hamburg, Hamburg, Germany

  4. 5

    Catholic Children's Hospital Wilhelmstift, Hamburg, Germany

  5. 6

    University of Pennsylvania School of Medicine, Philadelphia, PA, USA

  6. 7

    The Children's Hospital of Philadelphia, Philadelphia, PA, USA

Author Information

  1. Department of Dermatology, Environmental Medicine and Health Theory, University of Osnabrück, Osnabrück, Germany

Publication History

  1. Published Online: 24 MAY 2011
  2. Published Print: 3 JUN 2011

ISBN Information

Print ISBN: 9781405176958

Online ISBN: 9781444345384

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Keywords:

  • acne;
  • Apert syndrome;
  • androgen receptor polymorphism;
  • comedogenesis;
  • insulin resistance;
  • fibroblast growth factor receptor-2;
  • metformin;
  • milk;
  • risk factors;
  • sebaceous lipogenesis

Summary

Acne vulgaris is a multifactorial androgen-dependent disorder of the pilosebaceous unit. The clinical picture varies significantly, from mild and comedonal, to more inflammatory acne, as well as less common acne conglobata and fulminant systemic disease. Acne vulgaris usually starts in puberty when secretion of growth hormone, transient insulin resistance, insulin-like growth factor-1 and plasma androgens levels are physiologically elevated. The manifestation of acne is dependent on genetic and environmental factors. Milk consumption, carbohydrates with high glycaemic index, and smoking increase serum insulin and insulin-like growth factor-1 levels and may aggravate acne. Increased signal transduction by insulin, insulin-like growth factor-1 and androgen-dependent fibroblast growth factor receptor-2b have been detected as major pathways in acne pathogenesis. Genetic polymorphisms of the androgen receptor gene with shorter CAG repeats increase androgen-mediated signal transduction and impair insulin resistance. In as many as 50% of individuals, acne is a chronic disease and persists into adulthood and might be associated with ongoing insulin resistance and insulin resistance-related risk constellations.