Folliculitis decalvans

Classification according to ICD-10
L66.2	Folliculitis decalvans
ICD-10 online (WHO version 2019)

The folliculitis decalvans is an inflammation of the hair follicles , which is rare and chronic runs. Due to the inflammation, hair is lost and replaced by scar tissue (= scarring alopecia ).

Other names for this skin disease are: Quinquaud's disease , folliculitis depilans , acne décalvante .

Introduction and Epidemiology

This disease was first described by Quinquaud in 1888. This isolated bacteria from the hair follicles of affected patients and brought them to rats, mice and rabbits, but without success. In 1905, Quinquaud's disease was discovered by Brocq et al. differentiated from other scarring alopecia and the name of folliculitis decalvans, which still exists today, was introduced. Approximately 11% of the primary scarring alopecia are attributable to folliculitis decalvans. Men are more likely to be affected than women and the occurrence is concentrated in early to middle adulthood. According to studies in the United States of America, African Americans are more likely to be affected than fair-skinned Americans.

root cause

There is no conclusive clarity about the cause of the disease, but it is certain that the Gram-positive bacterium Staphylococcus aureus plays a central role. This bacterium can be found in the lesions of most patients with the disease . It is still unclear whether there is a primarily sterile infection with secondary colonization by Staphylococcus aureus or whether this bacterium primarily leads to a strong immune reaction. Even by the bacterium toxins formed could be used as superantigens which the T cells via the variable domain of the T cell receptor to activate the full act. In any case, Staphylococcus aureus can be detected in almost all patients with this disease, which is otherwise only the case in 20–30% of the “normal population” on the skin.

However, since not all people colonized with Staphylococcus aureus also have folliculitis decalvans, there must be other factors. Investigations in families have shown that there is a familial accumulation and so one has come to the conclusion of a genetic predisposition , B. can express in the fact that patients with folliculitis decalvans have a congenital different hair follicle opening, which could facilitate the establishment of the bacteria. From an immunological point of view, the particularly strongly expressed intercellular anchoring protein ICAM-1, with its enhanced effect of attracting neutrophils and lymphocytes (white blood cells), can contribute to increased inflammation.

Clinical picture

At the beginning of the disease, follicular papules and later pustules appear. The lesions stride, if not treated, peripheral back away and leave a scar center, accompanied by the (irretrievable) with irreversible hair loss. Hemorrhagic crusts , erosions , spontaneous bleeding, itching, pain, and burning sensations can also occur. Hair loss is unpredictable. Even if folliculitis decalvans can occur in all hairy areas (e.g. have been described in the beard, neck, armpit hair or pubic region), the head is by far the most common place of manifestation.

Diagnosis

The diagnostics are based on the following essential pillars:

• A smear, usually from the scalp or correspondingly affected areas of the body, at best with the preparation of an antibiogram and possibly also a nasal smear to identify occult colonization sites.
• Production of a culture (for pathogen detection) from an intact pustule.
• Sample biopsy with histological work-up. In short, chronic purulent folliculitis and perifolliculitis can be identified. Initially, perifolliculitis with destruction of the hair follicles occurs, which is characterized in the further course by the additional appearance of small abscesses and an accumulation of neutrophil granulocytes (= white blood cells) in particular. With persistent disease activity, granulation tissue forms over the course of the disease and, when burned out, the picture of fibrosis becomes visible.
• Incident light microscopy can be helpful in detecting follicular ostia, perifollicular erythema, and follicular hyperkeratosis.

therapy

Eradication of Staphylococcus aureus can be formulated as the main goal of therapy . The therapy of choice is anti-inflammatory therapy and antibiotic therapy. Both options can be applied externally to the skin or administered internally.

External: External products should only be used as individual therapy in mild cases of folliculitis decalvans, as a rule they represent an accompanying therapy. The antimicrobial therapy of the agents to be applied to the skin can be treated with solutions containing 2% erythromycin , 2% mupirocin, 1% Clindamycin or 1.5% fusidic acid . Also Glukokortikoidcremes Class 1-2 are used and can be applied twice daily. However, the period of application is limited.

Internal: The main medication in internal therapy are antibiotics. Rifampicin 300 mg twice a day for 10–12 weeks is said to have the best effect against Staphylococcus aureus and the best long-term effect. However, due to the development of resistance, this antibiotic should be combined with clindamycin or ciprofloxacin . The most common therapy is the antibiotic tetracycline , which should initially be dosed at 1 g / day orally and with a subsequent dose reduction to 500 mg / day. The discontinuation of antibiotic therapy can lead to a relapse in disease activity, which could make it possible to extend the therapy for up to years. A systemic attempt at therapy with isotretinoin can also be tried. If the inflammation is severe, i.e. the disease is more active, glucocorticoids can be used in a medium dose of 60–80 mg / day (e.g. Decortin H) in decreasing doses. In a therapy-resistant individual case, the combination of isotretinoin, clindamycin and prednisolone was successful. (PDF; 113 kB)

Other approaches in therapy are the oral administration of zinc sulfate or fusidic acid, or internal therapy with dapsone . Since hair loss is irreversible and unpredictable, therapy should start as early as possible. In addition, it is advisable to apply 2% or 5% minoxidil locally twice a day to areas that are not yet scarred.

literature

• Alexander Meves: 5.2.3 Folliculitis Decalvans. In: Dermatology intensive course. Urban & Fischer at Elsevier, Munich / Jena 2006, ISBN 3-437-41162-4 , pp. 103-104. Full text
• Peter Fritsch: Dermatology and Venereology. Springer, Berlin a. a. 2004, ISBN 3-540-00332-0 .
• Peter Altmeyer, Martina Bacharach-Buhles: Folliculitis decalvans. In: Springer Enzyklopädie Dermatologie, Allergologie, Umweltmedizin. Springer, Berlin a. a. 2002, ISBN 3-540-41361-8 , pp. 548-549. Full text online version
• Torchia Chiarini et al. a .: Immunopathogenesis of folliculitis decalvans: clues in early lesions. In: American Journal of Clinical Pathology . VOL: 130 (4); Pp. 526-534 PMID 18794044 . Full text (PDF; 1.38 MB)
• Kang Otberg u. a .: Folliculitis decalvans. In: Dermatologic therapy. VOL: 21 (4); Pp. 238-244 / 2008 PMID 18715292 .
• Electricity Abeck u. a .: Pyoderma - an interdisciplinary problem. In: Deutsches Ärzteblatt. Volume 98 issue 45, November 2001. Full text (PDF; 330 kB)
• Wollina Gemmeke: Folliculitis decalvans of the scalp: Response to triple therapy with isotretinoin, clindamycin and prednisolone. In: Acta Dermatoven APA. Vol. 15, 2006, No.4 PMID 17982613 . Full text (PDF; 113 kB)

Web links

• Images of folliculitis decalvans

Individual evidence

1. ^ ^{A b c} Peter Altmeyer, Martina Bacharach-Buhles: Folliculitis decalvans. In: Springer Enzyklopädie Dermatologie, Allergologie, Umweltmedizin. Springer, Berlin a. a. 2002, ISBN 3-540-41361-8 , pp. 548-549. Full text online version .
2. ↑ Kang Otberg et al. a .: Folliculitis decalvans. In: Dermatologic therapy. VOL: 21 (4); Pp. 238-244 / 2008 PMID 18715292 .
3. ↑ Wollina Gemmeke: Folliculitis decalvans of the scalp: Response to triple therapy with isotretinoin, clindamycin and prednisolone. In: Acta Dermatoven APA Vol. 15, 2006, No.4 PMID 17982613 . Full text

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