Key Points

• Keratosis pilaris (KP) is a common, often autosomal dominantly inherited benign disorder
that presents with hyperkeratotic papules with a central spicule on facial cheeks, upper
posterior arms, lateral thighs, and buttocks.
• KP often presents in association with atopic dermatitis.
• Facial and upper arm involvement may present a cosmetic problem for patients. Frictional
folliculitis arising from areas of KP may result in increased erythema or pustules in the
affected area.
• Long-term management to reduce hyperkeratosis is the mainstay of the therapeutic strategy
and sometimes improves cosmetic appearance. Several treatments reduce inflammation of
KP lesions.
Introduction
Keratosis pilaris (KP) is an extremely common, often autosomal dominantly inherited disorder that
usually does not require treatment. Keratosis pilaris is most frequently seen in association with
atopic dermatitis. The classic skin lesions are small, monomorphous, hyperkeratotic papules with a
central spicule, often with an erythematous base or overlying an erythematous patch. On biopsy,
these lesions are characterized by keratinous follicular plugging with orthohyperkeratosis to create a
follicular spicule. Typical sites of involvement include facial cheeks, upper posterior arms, lateral
thighs, and buttocks, and involvement is almost always bilateral and symmetric. Involvement of the
face and upper arms may be a significant cosmetic problem for patients, and frictional folliculitis
can complicate KP on the buttocks and thighs. Folliculitis may present as development of increased
erythema or pustules in the affected area. Since KP is a benign and non-curable skin condition,
long-term management is the mainstay of the therapeutic strategy; cosmetic improvement and
reduction of inflammation are the primary therapeutic goals.
KP may be seen in association with other cutaneous features suggestive of a genetic syndrome with
either cutaneous-only or systemic involvement (such as cardiofaciocutaneous syndrome). Keratosis
pilaris rubra is a relatively common variant of KP with highly inflammatory KP lesions that
primarily involves the cheeks, sometimes with extension of lesions onto the forehead and chin. A
rarer variant is keratosis pilaris atrophicans faciei, a form that presents in infancy and is marked by
atrophic lesions of the lateral eyebrows, sometimes with scarring alopecia. The latter variant is
notable because it may present as an idiopathic form or in association with genetic syndromes, such
as Noonan syndrome, Cornelia de Lange syndrome, Rubenstein-Taybi syndrome, as well as others.
Initial Evaluation
Keratosis pilaris

Lichen spinulosus
Lichen spinulosus, a condition often seen in children, likely represents a clinical variant of KP in
which typical lesions seen in KP (e.g., monomorphous hyperkeratotic papules with a central
spicule) are arranged in nummular patches at sites not typically affected by KP. Hyperpigmentation
of the papules or hyperkeratotic plug is common.

Differential diagnosis
Atopic dermatitis
Treatment
First-line therapy: Educate patients so that they understand that KP is not curable and that any
therapeutic option only minimizes but does not eradicate the clinical lesions. Long-term
management improves and maintains the cosmetic appearance of skin lesions, and interventions to
reduce inflammation are outlined below.
Initial therapy
• A mild soap (e.g., Dove) or a soapless cleanser (e.g., Cetaphil, Cerave) should be used with
a mild exfoliating scrub pad or washcloth. This treatment will gradually remove follicular
plugs (over several weeks) and prevent new ones from emerging.
• Salicylic acid 6% lotion (e.g., Keralyt gel) should be applied q.h.s. or after bathing. This
therapy is particularly effective when used in conjunction with mechanical exfoliation (see
above).
• Urea creams or lotions in concentrations of 10 to 20% (e.g., Carmol) may be effective, and
can be tolerated by many patients with atopic dermatitis.
• Ammonium lactate 12% lotion (e.g., LacHydrin or Amlactin) applied once daily after
bathing is also effective for KP. It may be combined with urea.
• Individuals with atopic disease tend to tolerate high concentrations of lactic acid (>5%)
without some adjunctive therapy to control their atopic condition. Alternatively, lower
concentrations of lactic acid or combinations of lactic acid and urea may be considered.
• There is evidence that ointment-based emollients (such as petrolatum or Aquaphor ointment)
may be sufficient to improve the cosmetic appearance of KP.
• Topical medium strength corticosteroids (e.g., triamcinolone 0.1% lotion, cream, or
ointment) or tacrolimus 0.1% ointment (e.g., Protopic) may be effective in KP associated
with atopic dermatitis, but are best utilized for flares of inflammatory KP and not for chronic
use.
• If highly inflammatory lesions are present, an empiric trial of erythromycin or dicloxacillin
250 mg q.i.d. for 10 days may reduce erythema and pustule formation.
Alternative therapy
• Tretinoin 0.025% cream q.h.s., increasing to 0.05% and 0.1%, as tolerated, may be helpful,
but may be prohibitively expensive for the treatment of widespread disease.
• There is emerging evidence that use of pulsed-dye laser (585 or 595 nm) may improve the
cosmetic appearance of KP, especially in reducing erythema associated with KP.

Subsequent therapy
• After the keratinous plugs have been removed, use of an emollient cream containing 20%
urea (Carmol) may prevent reappearance of lesions.
• Use of the abrasive scrub pad should be resumed at the first sign of reappearance of crops of
new lesions.
• Patient education on gentle skin care, including discussion of bathing, mild soaps, and
lubrication also should be taught; KP is almost invariably associated with xerosis, and
xerosis may, in fact, predispose to exacerbations of KP. (See handout Skin Care in Atopic
Dermatitis.)