Background

Keratosis pilaris (KP) is a genetic disorder of keratinization of hair follicles of the

skin. It is an extremely common benign condition that manifests as small, rough
folliculocentric keratotic papules, often described as chicken bumps, chicken skin, or
goose bumps, in characteristic areas of the body, particularly the outer-upper arms
and thighs. Although no clear etiology has been defined, keratosis pilaris is often
described in association with other dry skin conditions such as ichthyosis vulgaris,
xerosis, and, less commonly, with atopic dermatitis, including conditions of asthma
and allergies.[1]
Keratosis pilaris affects nearly 50-80% of all adolescents and approximately 40% of
adults. It is frequently noted in otherwise asymptomatic patients visiting
dermatologists for other conditions. Most people with keratosis pilaris are unaware
the condition has a designated medical term or that it is treatable. In general, keratosis
pilaris is frequently cosmetically displeasing but medically harmless.
Overall, keratosis pilaris is described as a condition of childhood and adolescence.
Although it often becomes more exaggerated at puberty, it frequently improves with
age. However, many adults have keratosis pilaris late into senescence. Approximately
30-50% of patients have a positive family history. Autosomal dominant inheritance
with variable penetrance has been described.
Seasonal variation is sometimes described, with improvement of symptoms in
summer months. Dry skin in winter tends to worsen symptoms for some groups of
patients. Overall, keratosis pilaris is self-limited and, again, tends to improve with age
in many patients. Some patients have lifelong keratosis pilaris with periods of
remissions and exacerbations. More widespread atypical cases may be cosmetically
disfiguring and psychologically distressing.

Pathophysiology
Keratosis pilaris (KP) is a genetically based disorder of hyperkeratinization of the
skin. An excess formation and/or buildup of keratin is thought to cause the abrasive
goose-bump texture of the skin. In these patients, the process of keratinization (the
formation of epidermal skin) is faulty. One theory is that surplus skin cells build up
around individual hair follicles. The individual follicular bumps are often caused by a
hair that is unable to reach the surface and becomes trapped beneath the keratin
debris. Often, patients develop mild erythema around the hair follicles, which is
indicative of the inflammatory condition. Often, a small, coiled hair can be seen

beneath the papule. Not all the bumps have associated hairs underneath. Papules are
thought to arise from excessive accumulation of keratin at the follicular orifice.

Epidemiology
Frequency
International
Keratosis pilaris (KP) is overall a very common condition and is present worldwide.
Keratosis pilaris affects 50-80% of adolescents and approximately 40% of adults
worldwide.
In India and other countries, a specific condition called erythromelanosis follicularis
faciei et colli is described. This is an unusual condition with a possible genetic or
other relationship to keratosis pilaris. Erythromelanosis follicularis faciei et colli is
characterized by the triad of hyperpigmentation, follicular plugging, and erythema of
the face and neck.[2, 3]

Mortality/Morbidity
Keratosis pilaris (KP) is not associated with increased mortality or morbidity. Often,
patients are bothered by the cosmetic appearance of their skin and its rough,
gooseflesh texture. Obesity has been implicated in a wide spectrum of dermatologic
diseases, including keratosis pilaris.[4] Keratosis pilaris is commonly present in
otherwise healthy individuals and does not have any known, long-term health
implications.

Race
Keratosis pilaris (KP) has no widely described racial predilection or predominance. It
is commonly noted worldwide in persons of all races.

Sex
Both sexes are affected by keratosis pilaris (KP), but females may be affected more
frequently than males.[5]

Age

Age of onset of keratosis pilaris (KP) is often within the first decade of life;
symptoms particularly intensify during puberty. However, keratosis pilaris may
manifest in persons of any age and is common in young children. Some authorities
believe individuals can outgrow the disorder by early adulthood, but often this is not
the case.

History
Keratosis pilaris (KP) patients often report a rough texture (gooseflesh appearance)
and overall poor cosmetic appearance of their skin. Eruptions are usually
asymptomatic, except for occasional pruritus. Many people with keratosis pilaris are
unaware the skin condition has a designated medical term or that it is treatable. In
general, keratosis pilaris is often cosmetically displeasing but, medically, is
completely harmless. Keratosis pilaris is frequently noted in otherwise healthy,
asymptomatic patients visiting dermatologists and other physicians for unrelated skin
conditions.

Physical
Physical findings of keratosis pilaris (KP) are limited to the skin. Upon gross
examination, the skin of the outer-upper arms and thighs is frequently affected. The
skin is described as chicken skin or goose bumps. Often, 10-100 very small, slightly
rough bumps are scattered in an area. Palpation may reveal a fine, sandpaper like
texture to the area. Some of the bumps may be slightly red or have an accompanying
light-red halo, indicating inflammation. In some instances, scratching away the
surface of some bumps may reveal a small, coiled hair.
Small (up to 1-2 mm) folliculocentric keratotic papules are noted (see the image
below). These are small bumps centered on small hair follicles. Some associated
inflammation (erythema) may be present, and lesions may be the color of the skin.
Often, a small, coiled hair can be seen beneath the papule. In other instances, a
keratin plug or pimple like material may be expressed from each bump. Pustules and
cysts are fairly rare.

Close-up view of keratosis pilaris. Keratotic follicularbased erythematous papules are noted on upper arm.
Commonly involved areas include posterolateral upper arms (see the image below),
anterior thighs, buttocks, and facial cheeks. The single most characteristic area in
keratosis pilaris is the upper-outer arms.

Keratosis pilaris in characteristic location on outer

upper arm of a 30-year-old woman.
Ulerythema ophryogenes (keratosis pilaris atrophicans faciei) is described as an
uncommon variant of keratosis pilaris characterized by follicular-based, small horny,
red papules of the eyebrows and cheeks. This may be complicated and followed by a
gradual loss of hair in the affected facial areas.[6]
Note the additional images below

Classic skin-colored bumps on upper arm of young

white female twin. Image courtesy of The Skin Center of Laguna.

Keratosis pilaris on the upper arm of a twin female. Image

courtesy of The Skin Center of Laguna.

Keratosis pilaris bumps
on arm of a white female twin. Image courtesy of The Skin Center of Laguna.

Keratosis pilaris on upper arm. Image courtesy of The Skin

Center of Laguna.
Keratosis pilaris on upper arm of
twin. Image courtesy of The Skin Center of Laguna.

Causes
The etiology of keratosis pilaris (KP) is not fully known. The definite association of
hyperkeratinization has been established. Of persons affected, 50-70% have a genetic
predisposition. Dry skin conditions seem to exacerbate the disease. Symptoms
generally tend to worsen in winter and improve in summer. Common associations
include several ichthyoses, especially ichthyosis vulgaris and atopic dermatitis.[7]
Keratosis pilaris is more common in siblings and in twins
Diagnostic Considerations

Keratosis pilaris (KP) may be associated with phrynoderma (vitamin A deficiency).

Interestingly, a significant association has also been found between acquired
ichthyosis and keratosis pilaris as common cutaneous manifestations in persons with
type 1 diabetes.
Keratosis pilaris may resemble the following uncommon skin conditions:

Lichen spinulosus

Pityriasis rubra pilaris

Ulerythema ophryogenes (ulerythema)

Ichthyosis vulgaris

Eruptive vellus hair cysts

Erythromelanosis follicularis faciei et colli

Keratosis follicularis (Darier disease)

Kyrle disease

Lichen nitidus

Perforating folliculitis

Trichostasis spinulosa

Keratosis pilaris rubra

Differential Diagnoses

Acne Vulgaris

Atopic Dermatitis

Eruptive Vellus Hair Cysts

Erythromelanosis follicularis faciei et colli

Folliculitis

Keratosis Follicularis (Darier Disease)

Keratosis pilaris atrophicans faciei

Keratosis pilaris rubra

Kyrle Disease

Lichen Nitidus

Lichen Spinulosus

Milia

Perforating Folliculitis

Pityriasis Rubra Pilaris

Trichostasis Spinulosa

Ulerythema ophryogenes

Xerosis

Laboratory Studies

No specific laboratory tests aid in the diagnosis of keratosis pilaris (KP). The
diagnosis of keratosis pilaris is very straightforward and is based on a typical skin
appearance in areas such as the upper arms. A family history of keratosis pilaris is
also very helpful because keratosis pilaris has a strong genetic component. The
diagnosis is confirmed on the basis of the physicians clinical examination findings. A
few other medical conditions look similar to keratosis pilaris, and these must be
excluded.
Imaging Studies

Imaging studies are not indicated.

Procedures

Skin biopsy with histopathological examination may be useful in atypical cases.

Histologic Findings

Microscopic examination (histopathology) of keratosis pilaris (KP) lesions shows the

triad of epidermal hyperkeratosis, hypergranulosis, and plugging of individual hair
follicles. The upper dermis may have mild superficial perivascular lymphocytic
inflammatory changes.
The individual papules in keratosis pilaris are thought to arise from excessive
accumulation of keratin at the follicular orifice. The overlying epidermis shows mild
thickening and plugging of the small follicular orifice.

Medical Care
In view of the described genetic predisposition and possible genetic etiology of
keratosis pilaris (KP), no cure or universally effective treatment is available.
Inconsistent remissions and variations with seasons and hormonal states (eg,
pregnancy[8] ) are described. Although symptoms usually remit with increasing age,
this is not always the case. Some cases clear spontaneously without treatment.

Many treatment options and skin care recipes are available for treating keratosis
pilaris. Many patients have very good temporary improvement following a regular
skin care program. As a general rule, treatment needs to be continuous. Because no
single therapy is effective, the list of potential lotions and creams is long. Importantly,
keep in mind that as with any condition, no therapy is uniformly effective in all
people. Complete clearing may not be possible.

General measures to prevent excessive skin dryness, such as using mild soapless cleansers (eg, Dove, Cetaphil), are recommended, and lubrication is the
mainstay of treatment for nearly all cases.

Best results may be achieved with combination therapy.

Mild cases of keratosis pilaris may be improved with basic lubrication using
over-the-counter moisturizer lotions such as Cetaphil, Purpose, or Lubriderm.

Additional available therapeutic options for more involved cases of keratosis

pilaris include lactic acid lotions (AmLactin, Lac-Hydrin), alpha hydroxy acid
lotions (Glytone, glycolic body lotions, urea cream (Carmol 10, Carmol 20,
Carmol 40, Urix 40), salicylic acid (Salex lotion), and topical steroid creams
(triamcinolone 0.1%, Locoid Lipocream), retinoic acid products such as
tretinoin (Retin-A), tazarotene (Tazorac), and adapalene (Differin). Specially
mixed designer compound creams with multiple different combined
ingredients can also be prescribed by physicians.

The affected area may be washed once or twice a day with a gentle cleanser
such as Dove. Acne-prone skin may benefit from more therapeutic cleansers
such as GlySal, Proactiv, salicylic acid, or benzoyl peroxide.

Lotions should be gently massaged into the affected area 2-3 times a day.
Irritated or abraded skin should be treated only with bland moisturizers until
the inflammation resolves.

Occasionally, physicians may prescribe a 7- to 10-day course of a medium

potency, emollient-based topical steroid cream (eg, Locoid Lipocream,
Cloderm) to be applied once or twice a day for inflamed, red rash areas. Once
the inflammation has remitted, the residual dry rough bumps may be treated
with a routine of twice-daily application of a compounded preparation of 23% salicylic acid in 20% urea cream.

Intermittent dosing of topical retinoids (eg, weekly or biweekly) seems to be

quite effective and well tolerated, but usually the response is only partial.
After initial clearing with stronger medications, patients may then be placed
on a milder maintenance regimen.

Persistent skin discoloration, termed hyperpigmentation, may be treated with

fading creams such as hydroquinone 4%, kojic acid, and azelaic acid 15-20%.
Special compounded creams for particularly resistant skin discoloration using
higher concentrations of hydroquinone 6%, 8%, and 10% may also be
formulated by compounding pharmacists. Higher concentrations of
hydroquinone may be irritating and carry an increased risk of adverse effects,
including ochronosis.

Keratosis pilaris may be treated with topical immunomodulators such as

pimecrolimus (Elidel) or tacrolimus (Protopic). Although these products are
approved for atopic dermatitis and eczema, their use would be considered off
label for keratosis pilaris. These may be used in more resistant cases or when
the patient has considerable skin redness or inflammation.

Photodynamic therapy (PDT) using a 2-step combination of a topical

photosensitizer and a light source may be used in off-label fashion for the
temporary treatment of keratosis pilaris. Available photosensitizers include
aminolevulinic acid (Levulan) or methyl levulinate (Metvixia). Light sources
include sunlight, blue light (417 nm), red light (630 nm), and multiple laser
devices. PDT has been anecdotally reported as effective, but this successful
use of off-label photodynamic therapy requires confirmation.

Laser hair removal (LHR) has been used in keratosis pilaris to decrease hair
growth in affected areas. Theoretically, LHR may help decrease the portion of
bumps in keratosis pilaris caused by small, coiled, ingrown hairs. There are no
studies showing a cure of keratosis pilaris with LHR.

Laser therapies including more aggressive resurfacing lasers, carbon dioxide,

fractional lasers, and other aggressive laser therapies have been used in
limited cases for keratosis pilaris. There are no studies showing a cure of
keratosis pilaris with these types of lasers.

Severe cases of keratosis pilaris have been treated orally with isotretinoin pills
for several months. Isotretinoin is generally a very potent oral medication
reserved for severe, resistant, or scarring cases of acne. Its use in keratosis

pilaris would be considered off label and not routine. There are no studies
showing a permanent cure of keratosis pilaris using isotretinoin.

Vitamin D (calcipotriol) is not effective for keratosis pilaris, but clinical trials
have found it moderately effective for ichthyosis.[9]

As with most treatments for keratosis pilaris, data exist only in the form of
small group observations and anecdotal reports. Because keratosis pilaris is
generally a chronic condition that requires long-term maintenance, most
therapies would require repeated or long-term use to maintain results.

Surgical Care
Minor surgical procedures such as gentle acne extractions may be useful in resistant
keratosis pilaris (KP). Extractions of keratotic papules and milia are performed using
a small 30-gauge needle, larger 18-gauge needle, or a small diabetic lancet to pierce
the overlying skin. A comedone extractor or 2 cotton-tipped applicators can be used
to extract the keratin plugs or trapped coiled hairs. Best results may be achieved with
combination therapy using topical emollients and physical treatments, such as manual
extraction of white heads (termed acne surgery), microdermabrasion, and chemical
peels.
In-office, physician-performed treatments such as chemical peels; dermabrasion;
microdermabrasion; photodynamic therapy; and blue-light, laser, and intense pulsed
light devices may be helpful as adjunctive treatment. Because keratosis pilaris has no
cure and no universally effective treatment is available, proceed with caution using a
combination of in-office treatments and a physician-directed home maintenance skin
care routine.
In-office treatments include the following:

Chemical peels

Extraction of keratin plugs or trapped coiled hairs

Vacubrasion (uses vacuum suction and synthetic diamond abrasion)

Microdermabrasion

Photodynamic therapy

Blue-light

Laser

Intense pulsed light

Case reports in the literature have described effective keratosis pilaris treatment with
modalities such as the 595-nm pulsed dye laser, intense pulsed light devices, and
various other laser devices, including hair removal lasers.[10, 11] More expansive and
larger-scale studies are required to assess the efficacy of potential laser therapies for
this chronic, relapsing skin condition.[12]
Microdermabrasion is a safe, minimally invasive, in-office procedure used to gently
exfoliate skin. Using vacuum-assisted suction, the skin is rubbed with an abrasive
particle such as fine, powdery aluminum crystals or small diamond tips.
Microdermabrasion assists in removing the excess keratin and outer layers of the
epidermis in a controlled manner. As with other treatments for keratosis pilaris, the
reports on this procedure are anecdotal and from small group observations. Instead of
in-office microdermabrasion, another option is in-home personal exfoliation with a
loofah sponge or a commercially available pad such as Buf-Puff. Newer available
home therapies include gentle exfoliation with vacubrasion (fine diamond abrasives)
home microdermabrasion systems. Often, vacubrasion and other skin vacuuming
procedures combined with retinoid creams over the counter and lactic acid lotions are
very effective in controlling keratosis pilaris.
Home therapies may include the following:

Exfoliation pads like Buf-Puf

Retinol creams

Gentle suction exfoliation including Vacubrasion

Topical emollients

Glycolic acid peels 10-20%

Consultations
Consultation with a dermatologist is appropriate for refractory or widespread cases.[13]

Diet
Keratosis pilaris has no dietary associations.

Activity
Keratosis pilaris does not limit any patient activities

Medication Summary

The goals of pharmacotherapy for keratosis pilaris (KP) are to reduce morbidity and
to prevent complications.
Retinoid-like Agents
Class Summary

Retinoic acid decreases cohesiveness of follicular epithelial cells, stimulates mitotic

activity, and increases turnover of follicular epithelial cells.
View full drug information
Tretinoin topical (Retin-A, Avita, Retin A Micro)

Inhibits microcomedo formation and eliminates lesions present. Makes keratinocytes

in sebaceous follicles less adherent and easier to remove. Available as 0.025%,
0.05%, and 0.1% creams. Available also as 0.01%, 0.025%, 0.04%, and 0.1% gels.
View full drug information
Tazarotene (Tazorac)

Receptor-selective retinoid is a synthetic retinoid prodrug that is rapidly converted

into tazarotenic acid. Because use of tretinoin often is hampered by its irritancy, this
product may be advantageous. Available as 0.05% and 0.1% cream or gel.

Retinoid prodrug whose active metabolite modulates differentiation and proliferation

of epithelial tissue; may also have anti-inflammatory and immunomodulatory
properties.
View full drug information
Adapalene (Differin)

Modulates cellular differentiation, inflammation, and keratinization. May be tolerated

by individuals who cannot tolerate tretinoin creams. A therapeutic response can be
expected following 8-12 wk of therapy. Available as 0.1% gel or solution or 0.3% gel.
Topical Skin Products
Class Summary

Alpha hydroxy acid is a normal constituent of tissues and blood. Alpha hydroxy acids
act as humectants when applied topically and may decrease corneocyte cohesion.
Topically applied urea has a hygroscopic effect by increasing the water retention in
skin and it decreases pruritus.
View full drug information
Urea (Carmol, Aluvea, Keralac, Kerol, Remeven)

Promotes hydration and removal of excess keratin in conditions of hyperkeratosis.

Available in 10-40% concentrations.
View full drug information
Ammonium lactate lotion (AmLactin, Lac-Hydrin, Geri-Hydrolac)

Indicated for treatment of ichthyosis vulgaris and xerosis. Contains lactic acid, an
alpha-hydroxy acid that has keratolytic action, thus facilitating release of comedones.
Causes disadhesion of corneocytes. Use 12% cream or lotion.

Corticosteroids
Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied

metabolic effects. In addition, these agents modify the body's immune response to
diverse stimuli.
View full drug information
Fluticasone (Cutivate)

Extremely potent vasoconstrictive and anti-inflammatory activities. Has weak

inhibitory affect on HPA axis when applied topically.
Deterrence/Prevention

In patients with keratosis pilaris (KP), measures should be taken to prevent excessive
skin dryness. Mild soaps and cleansers should be used. Frequent application of
emollients is very beneficial.
Complications

Complications from keratosis pilaris (KP) are infrequent. However, post

inflammatory hypopigmentation or hyperpigmentation and scarring may occur.
A gradual loss of hair in affected facial areas, especially the lateral eyebrows, may be
seen in ulerythema ophryogenes (keratosis pilaris atrophicans faciei).
Prognosis

Overall prognosis is good. Many cases resolve with increasing age. However, others
may persist into late adulthood with intermittent exacerbations and remissions.
Patient Education

Patient education should focus on the tendency for chronicity of the condition and the
need for ongoing maintenance therapy. Patients should also be advised that the
condition is not contagious and is not a threat to their overall health. For patient
education resources, see the Skin, Hair, and Nails Center.