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Acne Vulgaris

Acne Vulgaris EDITORIAL State of the Science N THIS ISSUE of the ARCHIVES, Thiboutot et al re- bances similar to those seen in essential fatty acid– port new findings on the hormonal aspects of deficient mice and that calcium gradients may be acne, a multifactorial disease whose understand- disturbed. A different explanation was proposed by Guy ing has progressed in bursts over the past few et al, who studied pilosebaceous units in culture. They I decades. The 1960s and 1970s were the de- found that follicular hypercomification could be in- cades when the central role of Propionibacterium acnes duced by interleukin 1a and exacerbated by epidermal was discovered. In those decades, the interaction of P ac- growth factor or transforming growth factor. Isotreti- nes with neutrophils and complement was elucidated, and noin inhibited the process. A connection between these the roles of immunity and hypersensitivity in determin- findings and secondary comedones in severely inflam- 2,3 ing acne severity were appreciated. Current thinking matory acne is apparent, but it is difficult to understand holds that the microcomedo is the initial lesion of acne. how these facts relate to the natural induction of micro- Microcomedones form, at least in part, before puberty comedones http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png JAMA Dermatology American Medical Association

Acne Vulgaris

JAMA Dermatology , Volume 135 (9) – Sep 1, 1999

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Publisher
American Medical Association
Copyright
Copyright 1999 American Medical Association. All Rights Reserved. Applicable FARS/DFARS Restrictions Apply to Government Use.
ISSN
2168-6068
eISSN
2168-6084
DOI
10.1001/archderm.135.9.1101
Publisher site
See Article on Publisher Site

Abstract

EDITORIAL State of the Science N THIS ISSUE of the ARCHIVES, Thiboutot et al re- bances similar to those seen in essential fatty acid– port new findings on the hormonal aspects of deficient mice and that calcium gradients may be acne, a multifactorial disease whose understand- disturbed. A different explanation was proposed by Guy ing has progressed in bursts over the past few et al, who studied pilosebaceous units in culture. They I decades. The 1960s and 1970s were the de- found that follicular hypercomification could be in- cades when the central role of Propionibacterium acnes duced by interleukin 1a and exacerbated by epidermal was discovered. In those decades, the interaction of P ac- growth factor or transforming growth factor. Isotreti- nes with neutrophils and complement was elucidated, and noin inhibited the process. A connection between these the roles of immunity and hypersensitivity in determin- findings and secondary comedones in severely inflam- 2,3 ing acne severity were appreciated. Current thinking matory acne is apparent, but it is difficult to understand holds that the microcomedo is the initial lesion of acne. how these facts relate to the natural induction of micro- Microcomedones form, at least in part, before puberty comedones

Journal

JAMA DermatologyAmerican Medical Association

Published: Sep 1, 1999

References