ACNE KELOIDALIS
NUCHAE
Acne keloidalis nuchae is a fairly common form of
inflammatory, scarring alopecia that typically occurs on the posterior
occipital scalp. There is a variable spectrum of disease, ranging from very
mild cases to severe scarring alopecia. The condition has psychosocial
implications and is difficult to treat effectively. It is diagnosed clinically,
and biopsies are rarely needed.
Clinical Findings: Acne keloidalis nuchae begins on the posterior
scalp or nape of the neck as tiny, follicular, flesh-colored to red papules.
The papules enlarge to form plaques, which coalesce into larger plaques.
Ultimately in severe cases, the entire posterior scalp is involved. Early in
the disease, no hair loss is appreciated. As the disease progresses, the hair
follicles become scarred down and crowded out by the encroaching fibrosis,
resulting in a variable amount of scarring alopecia.
This condition is far more common in
young adult men, with a predilection for African Americans. It was originally
believed to be caused by close shaving of the hair and the subsequent
inflammation caused by the newly regrowing hair as it pierces the epidermis.
The curly nature of the hair follicle was believed to be one of the most
important factors. This theory of the pathophysiology of the disease has been
questioned, and the cause of the condition is not as simple as once theorized.
The plaques, if left untreated,
eventually form thickened scar tissue resembling the appearance of a keloid
scar. The scarring alopecia is permanent, and the patient is left with a
considerable cosmetic issue. Severe cases of this condition can cause
psychological issues, as can almost any form of severe alopecia.
Pathogenesis: Originally, acne keloidalis was believed to be
caused by the close haircut in African American men, which caused the hairs to
penetrate the epidermis on regrowth, setting off an inflammatory reaction. It
has now been determined that this is an oversimplification of the disease
state. Other factors are likely to play more important roles in the
pathogenesis.
Histology: Early disease often appears as a dense, mixed
inflammatory infiltrate around the hair follicle and adnexal structures with
plasma cells present. This appears similar to folliculitis. As the hair
follicles rupture, the contents spill into the dermis and set off a dermal
inflammatory reaction. There is overlying epidermal hyperplasia and acanthosis.
Occasional pustule formation is seen and is composed of pools of neutrophils.
Late disease is very similar to the
pathology of a keloid. There is a lack of adnexal structures and fibrosis
throughout the dermis.
Treatment: Therapy for mild disease requires a multifaceted
approach. If only a few papules are present with minimal hair loss, a
combination of a topical and an oral antibiotic can be used for their
antiinflammatory effects. The most commonly used oral antibiotics are in the
tetracycline class. The topical antibiotic most often prescribed is
clindamycin. Strict hair care regimens are required to help decrease the trauma
to the skin. Shaving of the scalp should be avoided, and haircuts with shears
should also be minimized, because the shears can cause microtrauma to the skin
and potentially induce the process and scarring formation.
Cutting the hair to a length of 3 to 5
mm is a reasonable approach that minimizes trauma to the skin. Topical
retinoids such as tretinoin and tazarotene have been used with varying results.
The theory is that they help the follicular epithelium mature and help correct
the abnormal keratinization of the epidermis. Intralesional triamcinolone
injections into the papules and plaques can also be an effective method of
treating mild disease.
Severe disease is rarely responsive to
medical therapy. Surgical options remain the best therapeutic choice. The goal
is to remove the abnormal skin and close the wound under as little tension as
possible. If the tension is too great, it is best to leave the wound open to
granulate and heal by secondary intention. The scar that results is often
better appear ng than the thick, plaque-like scar that it is replacing.
