Things You Need To Know About Treatments for Folliculitis Decalvans
Folliculitis decalvans on the scalp comes under the category of neutrophilic cicatricial alopecias. This is a commonly found primary scarring alopecia, with an incidence rate of 1.9-11.2% in those diagnosed with any form of scarring alopecia. The condition is typified by a destructive, suppurative folliculitis, meaning inflammation of the hair follicle with the presence of pus. The said infection has been described as a cicatrical alopecia characterized by erythematous scalp with pustules around the hair follicles, commonly called Folliculitis. Each crop of pustules results in progression of hair loss. Follicle destruction and scarring with permanent hair loss is the end-result of the condition.
The term cicatricial alopecia encompasses a diverse group of disorders characterized by permanent destruction of the hair follicle and irreversible hair loss. The onset of folliculitis decalvans can occur at any time after adolescence. Although the role of the bacteria as a cause of the disease is unproven, an abnormal host response to S. Aureus has been implicated by many authors. A genetically determined immune deficiency with increased risk of follicular infection is another possibility supported by case studies. Both acquired and inherited immune disturbances are associated with folliculitis decalvans.
One school of thought considers this as a subset of Central Centrifugal Cicatricial Alopecia (CCCA). These authors purport that the pustules seen in it are a manifestation of either bacterial superinfectio or an intense immune response to degenerating follicular components. According to their studies, if inflamed but non-pustular areas of affected individuals are sent for biopsy, the histological findings are similar to those seen in Follicular Degeneration syndrome or pseudopelade. As it broadly overlaps with pseudopelade and Follicular Degeneration syndrome, these authors believe that folliculitis decalvans represents the same basic pathological process.
Until quite recently, folliculitis decalvans was a difficult condition to treat, and prognosis of patients afflicted with this form of alopecia was also rather bleak. As a rule, intact pustules should be cultured, and sensitivity to various antibiotics should be determined. The condition can be controlled temporarily to some degree by administering anti-staphylococcal antibiotics such as erythromycin, cephalosporins, trimethroprim/ sulfamethoxozole, clindamycin, or a fluoroquinalone with or without rifampin. Additionally, anti-nuetrophilic and broad-spectrum antibiotics have been found to be variably and temporarily effective.
In addition with Folliculitis decalvans, Rifampin, a bacteriocidal drug, with the combined use of fusidic acid and zinc has led to successful remission lasting from months to years in some patients under study. It is important to remember that Rifampin should never be used alone. The exact scientific base of the use of zinc is not established, but in all probability, it has an anti-inflammatory effect and can modulate the immune response. Rifampin and fusidic acid are probably effective because of their excellent intracellular penetration and pathogen eradication potential.
Folliculitis decalvans can mimic classic folliculitis, acne necrotica, lichen planopilaris, discoid lupus erythematosus, and dissecting cellulitis (also called perifolliculitis capitis abscedens et suffodiens). Other than that, all forms of treatment have their own side effects, and benefits of treatment must be evaluated against the consequences of the drugs. Rifampin causes red staining of bodily secretions including tears. Zinc at high dosage levels competes with copper metabolism and can result in severe refractory anemia and neutropenia, a hematological disorder.
Diagnosis of the condition is based on clinical, microbiological, histo-pathological and laboratory features. Grouped follicular pustules as seen in folliculitis decalvans are not seen in ordinary folliculitis or acne necrotica. Dissecting cellulitis can be distinguished easily as early pustules and papule formation develop immediately into dermal nodules. In addition, folliculitis decalvans does not display the sinus tract formation in histological skin biopsies, a characteristic typical of dissecting folliculitis.
The term cicatricial alopecia encompasses a diverse group of disorders characterized by permanent destruction of the hair follicle and irreversible hair loss. The onset of folliculitis decalvans can occur at any time after adolescence. Although the role of the bacteria as a cause of the disease is unproven, an abnormal host response to S. Aureus has been implicated by many authors. A genetically determined immune deficiency with increased risk of follicular infection is another possibility supported by case studies. Both acquired and inherited immune disturbances are associated with folliculitis decalvans.
One school of thought considers this as a subset of Central Centrifugal Cicatricial Alopecia (CCCA). These authors purport that the pustules seen in it are a manifestation of either bacterial superinfectio or an intense immune response to degenerating follicular components. According to their studies, if inflamed but non-pustular areas of affected individuals are sent for biopsy, the histological findings are similar to those seen in Follicular Degeneration syndrome or pseudopelade. As it broadly overlaps with pseudopelade and Follicular Degeneration syndrome, these authors believe that folliculitis decalvans represents the same basic pathological process.
Until quite recently, folliculitis decalvans was a difficult condition to treat, and prognosis of patients afflicted with this form of alopecia was also rather bleak. As a rule, intact pustules should be cultured, and sensitivity to various antibiotics should be determined. The condition can be controlled temporarily to some degree by administering anti-staphylococcal antibiotics such as erythromycin, cephalosporins, trimethroprim/ sulfamethoxozole, clindamycin, or a fluoroquinalone with or without rifampin. Additionally, anti-nuetrophilic and broad-spectrum antibiotics have been found to be variably and temporarily effective.
In addition with Folliculitis decalvans, Rifampin, a bacteriocidal drug, with the combined use of fusidic acid and zinc has led to successful remission lasting from months to years in some patients under study. It is important to remember that Rifampin should never be used alone. The exact scientific base of the use of zinc is not established, but in all probability, it has an anti-inflammatory effect and can modulate the immune response. Rifampin and fusidic acid are probably effective because of their excellent intracellular penetration and pathogen eradication potential.
Folliculitis decalvans can mimic classic folliculitis, acne necrotica, lichen planopilaris, discoid lupus erythematosus, and dissecting cellulitis (also called perifolliculitis capitis abscedens et suffodiens). Other than that, all forms of treatment have their own side effects, and benefits of treatment must be evaluated against the consequences of the drugs. Rifampin causes red staining of bodily secretions including tears. Zinc at high dosage levels competes with copper metabolism and can result in severe refractory anemia and neutropenia, a hematological disorder.
Diagnosis of the condition is based on clinical, microbiological, histo-pathological and laboratory features. Grouped follicular pustules as seen in folliculitis decalvans are not seen in ordinary folliculitis or acne necrotica. Dissecting cellulitis can be distinguished easily as early pustules and papule formation develop immediately into dermal nodules. In addition, folliculitis decalvans does not display the sinus tract formation in histological skin biopsies, a characteristic typical of dissecting folliculitis.
Steven Jan Clark is a writer for almost a year and usually he used to write about interesting topics like travel, adventures, internet facts, hair
