Published on 19/03/2015 by admin
Filed under Dermatology
Last modified 19/03/2015
This article have been viewed 3852 times
Andrew J.G. McDonagh
Evidence Levels: A Double-blind study B Clinical trial ≥ 20 subjects C Clinical trial < 20 subjects D Series ≥ 5 subjects E Anecdotal case reports
Folliculitis decalvans is a rare progressive purulent folliculitis of the scalp resulting in follicular atrophy and subsequent scarring alopecia. ‘Tufted folliculitis’ is a characteristic of the disorder in evolution, with multiple hair tufts emerging from inflamed and crusted follicular orifices.
The etiology is unknown. Impaired immune responses, Staphylococcus aureus infection, nevoid lesions, and seborrheic states have been suggested as playing a role in its pathogenesis, though much controversy surrounds the role of each factor. Gram-positive organisms are usually present during active disease phases.
Folliculitis ‘decalvans’ may affect any hair-bearing region, i.e., scalp, face, axillae, pubes, and inner thighs. Scalp disease affects both sexes. In other sites it is confined to adult males. It occurs predominantly in men from adolescence onwards, and in women between the third and sixth decades.
Treatment of this chronic and progressive disease is notoriously difficult. Underlying diseases such as immunodeficiency or fungal infection should be sought. Staphylococcus aureus or other Gram-positive organisms are present in follicular pustules and sometimes also in the anterior nares. Bacteriology swabs should be taken for culture and to determine sensitivity.
Topical and systemic antibiotics are the mainstay of treatment. Systemic antibiotics such as tetracycline, minocycline, flucloxacillin, and third-generation cephalosporins may inhibit the extension of disease, but only for as long as they are administered. Rifampin has been proposed as the most beneficial therapeutic option in recalcitrant cases, but should not be used as monotherapy because of the rapid emergence of resistance. A regimen of systemic rifampin 300 mg twice daily and clindamycin 300 mg twice daily for 10 weeks has produced marked improvement, with infrequent relapse after one or more treatment courses. Prolonged courses of dapsone can also be beneficial.
Systemic corticosteroids suppress the inflammatory response and may provide moderate temporary improvement. There have been anecdotal reports of success using oral zinc sulfate (in combination with fusidic acid). Treatments that destroy hair follicles and prevent hair regrowth may be considered; these include X-ray epilation, laser epilation, cryosurgery, and surgical excision. Improvement has also been reported with shaving the scalp. Keratolytics and tar shampoos may reduce the scaling and erythema that herald extension of the disease. There is a single published report of response to anti-TNF therapy with infliximab.
Swabs for bacteriology of follicular pustules and carrier sites
Fungal microscopy and culture
Scalp biopsy
Immunodeficiency screen
Sullivan JR, Kossard S. Australas J Dermatol 1999; 40: 61–72.
An individual with HIV developed severe folliculitis decalvans after commencing triple antiviral therapy.
Shitara A, Igareshi R, Morohashi M. Jpn J Dermatol 1974; 28: 133.
Severe folliculitis decalvans in two siblings who also had chronic oral candidiasis; defective cell-mediated immunity was demonstrated.
Treatment of Skin Disease Comprehensive Therapeutic Strategies 4e
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