Hidradenitis suppurativa: a review of cause and treatment.

Curr Opin Infect Dis

Department of Dermatology, Roskilde Hospital, Health Sciences Faculty, University of Copenhagen, Copenhagen, Denmark.

Published: April 2011

Purpose Of Review: Hidradenitis suppurativa is a chronic or relapsing inflammatory cutaneous disorder manifested by recurrent formation of abscesses, fistulating sinus and scarring in the apocrine-gland-bearing skin. This review discusses the different aetiological theories and management opportunities.

Recent Findings: Current understanding of the pathogenesis suggests that hyperkeratosis of the infundibulum, leading to follicular occlusion of the pilosebaceous unit plays a role. Bacterial infection with staphylococci, Escherichia coli and streptococcus is considered as a secondary event in the pathogenesis. Smoking and obesity are both known as risk factors and are associated with more severe disease course. Recently, more attention has been put into the understanding of the immunopathology of the skin and the results indicate that hidradenitis suppurativa may be considered as an inflammatory disease of unknown cause based on a defect in the hair follicle immunity. The treatments are most appropriately chosen on the basis of disease severity and the existence of any associated risk factors or comorbidities. There are three levels in the management of hidradenitis suppurativa: topical options, systemic options and surgical methods including laser therapy. At each level several treatment principles have shown themselves to be efficient, and may therefore be used either alone or in combination. Therapies are generally effective against microorganisms, inflammation or infundibular hyperkeratosis. Where an antimicrobial therapy is used, the drugs used often have significant additional immunomodulatory effects.

Summary: The recent studies give us a better insight into the pathogenesis of hidradenitis suppurativa and should translate into improved therapies.

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Source
http://dx.doi.org/10.1097/QCO.0b013e3283428d07DOI Listing

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