eMedicine Specialties > Dermatology > Diseases of the Adnexa

Keratosis Pilaris

Nili N Alai, MD, FAAD, Assistant Clinical Professor, Department of Dermatology, Clinical Faculty and Preceptor, Department of Family Practice, University of California, Irvine; Clinical Faculty and Preceptor, Department of Family Practice Residency Training, Downey Medical Center; Medical Director, The Skin Center at Laguna; Expert Medical Reviewer, Medical Board of California
Dena Thompson, MS, Boston University School of Medicine; Arash Michael Saemi, MD, Department of Internal Medicine, Naval Medical Center San Diego; Raul Del Rosario, MD, Consulting Staff, Surgical Pathology and Dermatopathology, South Coast Medical

Updated: Oct 16, 2009

Introduction

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.

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.

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.^1,2

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.³ 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.⁴

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.

Clinical

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 Media File 1). 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 follicular-based erythematous papules are noted on upper arm.

Keratosis pilaris in characteristic location on outer upper arm of a 30-year-old woman.

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 a family history of keratosis pilaris, ichthyosis, or atopic dermatitis.⁶ Keratosis pilaris is more common in siblings and in twins.

Differential Diagnoses

Other Problems to Be Considered

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 (u lerythema)
• 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

Workup

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 physician’s 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.

Treatment

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, pregnancy⁷ ) 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 soap-less 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 2-3% 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 using aminolevulinic acid (Levulan) and blue light (417 nm) has been anecdotally reported as effective, but this successful use of off-label photodynamic therapy requires confirmation.
• Severe cases of keratosis pilaris have been treated orally with isotretinoin (Accutane) 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.
• Vitamin D (calcipotriol) is not effective for keratosis pilaris, but clinical trials have found it moderately effective for ichthyosis.⁸
• 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.

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.

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.

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. More expansive and larger-scale studies are required to assess the efficacy of potential laser therapies for this chronic, relapsing skin condition.^9,10

Consultations

Consultation with a dermatologist is appropriate for refractory or widespread cases.¹¹

Diet

Keratosis pilaris has no dietary associations.

Activity

Keratosis pilaris does not limit any patient activities.

Medication

The goals of pharmacotherapy for keratosis pilaris (KP) are to reduce morbidity and to prevent complications.

Retinoids

Retinoic acid decreases cohesiveness of follicular epithelial cells, stimulates mitotic activity, and increases turnover of follicular epithelial cells.

Tretinoin (Retin-A, Avita)

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.

Dosing

Adult

Begin with lowest tretinoin formulation and increase as tolerated; apply hs or qod; decrease frequency of application if irritation develops

Pediatric

<12 years: Not established
>12 years: Administer as in adults

Interactions

Toxicity increases with coadministration of benzoyl peroxide, salicylic acid, and resorcinol; avoid topical sulfur, resorcinol, salicylic acid, other keratolytics, abrasives, astringents, spices, and lime

Contraindications

Documented hypersensitivity to tretinoin or parabens

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Photosensitivity may occur with excessive sunlight exposure; caution in eczema; do not apply to mucous membranes, mouth, and angles of nose

Alpha-hydroxy acids

Normal constituent of tissues and blood. Act as humectants when applied topically and may decrease corneocyte cohesion.

Ammonium lactate lotion (AmLactin, Lac-Hydrin)

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.

Dosing

Adult

Apply bid to affected skin

Pediatric

<12 years: Not established
>12 years: Apply as in adults

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

B - Fetal risk not confirmed in studies in humans but has been shown in some studies in animals

Precautions

May sting or cause pain if applied to broken skin; may cause irritation with erythema, burning, and peeling if applied to face at 12% concentration; avoid contact with eyes, mucous membranes, and lips; minimize sun exposure because of possibility of heightened photosensitivity

Topical skin products

Urea

Promotes hydration and removal of excess keratin in conditions of hyperkeratosis.
Available in 10-40% concentrations.

Dosing

Adult

Apply prn to affected areas

Pediatric

10-20% concentrations acceptable in adolescents; caution with 30-40% concentrations in pediatric patients
Apply bid

Interactions

May decrease effects of lithium

Contraindications

Documented hypersensitivity; severely impaired renal function, active intracranial bleeding, marked dehydration, frank liver failure; infusion into veins of lower extremities in elderly persons may cause phlebitis and thrombosis

Precautions

Pregnancy

D - Fetal risk shown in humans; use only if benefits outweigh risk to fetus

Precautions

Do not use if intracranial bleeding present, unless prior to surgical intervention to control hemorrhage (reduction of brain edema by urea may result in reactivation of intracranial bleeding); may increase risk of venous thrombosis and hemoglobinuria in hypothermic patients; caution in renal impairment

Hydroquinone and tretinoin (Solage)

Mequinol (hydroquinone) is a depigmenting agent theorized to cause cytotoxic products in melanocytes or inhibit melanin formation. Tretinoin is a retinoid, which also elicits depigmenting effect. Available as a topical solution combination product containing mequinol 2% and tretinoin 0.01%.

Dosing

Adult

Once or twice a day to affected areas

Pediatric

£ 12 years: Not established
<12 years: Administer as in adults

Interactions

Avoid concurrent use with other topical agents causing skin irritation; tretinoin toxicity increases with coadministration of benzoyl peroxide, salicylic acid, and resorcinol; avoid topical sulfur, resorcinol, salicylic acid, other keratolytics, abrasives, astringents, spices, and lime

Contraindications

Documented hypersensitivity to tretinoin or parabens; pregnancy

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

Avoid bathing or showering for at least 6 h following application; wait 30 min following application to apply cosmetics; avoid sun exposure; avoid application to skin surrounding lesions and mucous membranes; may cause burning; erythema, desquamation, pruritus, phototoxicity, or hypopigmentation
Hydroquinone: Avoid contact with eyes; blue-black darkening of skin can occur rarely with emulsion formulation (discontinue use); limit sun exposure during and after treatment; wear sun-protective clothing to prevent repigmentation of treated areas; perform a 24-h skin sensitivity test; do not use if itching, vesicle formation, or excessive inflammatory response occurs; sulfite hypersensitivity; contains sodium metabisulfite
Tretinoin: Photosensitivity may occur with excessive sunlight exposure; caution in eczema; do not apply to mucous membranes, mouth, and angles of nose

Keratolytic agents

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.

Dosing

Adult

Apply 0.05% gel every other night for 2 wk initially, then may increase to nightly as tolerated

Pediatric

Not established

Interactions

Do not use concomitantly with dermatologic drugs or cosmetics that have a strong drying effect on the skin (eg, salicylic acid, benzoyl peroxide, astringents)

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

X - Contraindicated; benefit does not outweigh risk

Precautions

May cause burning or stinging sensations; discontinue if excessive irritation; rinse thoroughly if contact with eyes, eyelids, or mouth; may cause severe irritation in eczematous skin; photosensitivity may occur

Acne products

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.

Dosing

Adult

Apply hs; some patients may tolerate bid dosing

Pediatric

Not established

Interactions

None reported

Contraindications

Documented hypersensitivity

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

Avoid contact with mucous membranes, eyes, mouth, and nostrils; avoid exposure to sunlight and sunlamps; dryness of skin, scaling, erythema, burning, and pruritus may occur

Corticosteroids, topical (medium potency)

Fluticasone (Cutivate)

Extremely potent vasoconstrictive and anti-inflammatory activities. Has weak inhibitory affect on HPA axis when applied topically.

Dosing

Adult

Apply sparingly to affected area bid; not to exceed 50 g/wk

Pediatric

Apply as in adults

Interactions

None reported for topical use

Contraindications

Documented hypersensitivity; fungal, viral, and bacterial skin infections

Precautions

Pregnancy

C - Fetal risk revealed in studies in animals but not established or not studied in humans; may use if benefits outweigh risk to fetus

Precautions

May cause suppression of HPA axis, especially when used over large areas of the body, denuded areas, for prolonged periods, with occlusive dressings, and/or on infants or small children

Follow-up

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 excellent patient education resources, visit eMedicine's Skin, Hair, and Nails Center.

Multimedia

Media file 1: Close-up view of keratosis pilaris. Keratotic follicular-based erythematous papules are noted on upper arm.

Media file 2: Keratosis pilaris in characteristic location on outer upper arm of a 30-year-old woman.

Media file 3: Classic skin-colored bumps on upper arm of young white female twin. Image courtesy of The Skin Center of Laguna.

Media file 4: Keratosis pilaris on the upper arm of a twin female. Image courtesy of The Skin Center of Laguna.

Media file 5: Keratosis pilaris bumps on arm of a white female twin. Image courtesy of The Skin Center of Laguna.

Media file 6: Keratosis pilaris on upper arm. Image courtesy of The Skin Center of Laguna.

Media file 7: Keratosis pilaris on upper arm of twin. Image courtesy of The Skin Center of Laguna.

References

1. Sardana K, Relhan V, Garg V, Khurana N. An observational analysis of erythromelanosis follicularis faciei et colli. Clin Exp Dermatol. May 2008;33(3):333-6. [Medline].

2. Augustine M, Jayaseelan E. Erythromelanosis follicularis faciei et colli: relationship with keratosis pilaris. Indian J Dermatol Venereol Leprol. Jan-Feb 2008;74(1):47-9. [Medline].

3. Yosipovitch G, DeVore A, Dawn A. Obesity and the skin: skin physiology and skin manifestations of obesity. J Am Acad Dermatol. Jun 2007;56(6):901-16; quiz 917-20. [Medline].

4. Poskitt L, Wilkinson JD. Natural history of keratosis pilaris. Br J Dermatol. Jun 1994;130(6):711-3. [Medline].

5. Arnold AW, Buechner SA. [Keratosis pilaris and keratosis pilaris atrophicans faciei]. J Dtsch Dermatol Ges. Apr 2006;4(4):319-23. [Medline].

6. Mevorah B, Marazzi A, Frenk E. The prevalence of accentuated palmoplantar markings and keratosis pilaris in atopic dermatitis, autosomal dominant ichthyosis and control dermatological patients. Br J Dermatol. Jun 1985;112(6):679-85. [Medline].

7. Jackson JB, Touma SC, Norton AB. Keratosis pilaris in pregnancy: an unrecognized dematosis of pregnancy?. W V Med J. Jan-Feb 2004;100(1):26-8. [Medline].

8. Kragballe K, Steijlen PM, Ibsen HH, et al. Efficacy, tolerability, and safety of calcipotriol ointment in disorders of keratinization. Results of a randomized, double-blind, vehicle-controlled, right/left comparative study. Arch Dermatol. May 1995;131(5):556-60. [Medline].

9. Kaune KM, Haas E, Emmert S, Schon MP, Zutt M. Successful treatment of severe keratosis pilaris rubra with a 595-nm pulsed dye laser. Dermatol Surg. Oct 2009;35(10):1592-5. [Medline].

10. Clark SM, Mills CM, Lanigan SW. Treatment of keratosis pilaris atrophicans with the pulsed tunable dye laser. J Cutan Laser Ther. Sep 2000;2(3):151-6. [Medline].

11. Novick NL. Practical management of widespread, atypical keratosis pilaris. J Am Acad Dermatol. Aug 1984;11(2 Pt 1):305-6. [Medline].

12. Lateef A, Schwartz RA. Keratosis pilaris. Cutis. Apr 1999;63(4):205-7. [Medline].

Keywords

keratosis pilaris, keratosis pilaris treatment, KP, hyperkeratosis, folliculocentric keratotic papules, follicular keratotic papules, atopic dermatitis, ichthyosis vulgaris, excessive accumulation of keratin, benign skin lesion, Ulerythema ophryogenes, keratosis pilaris atrophicans faciei, gooseflesh appearance, erythema, chickenskin bumps, chicken skin, goosebumps.

Contributor Information and Disclosures

Author

Nili N Alai, MD, FAAD, Assistant Clinical Professor, Department of Dermatology, Clinical Faculty and Preceptor, Department of Family Practice, University of California, Irvine; Clinical Faculty and Preceptor, Department of Family Practice Residency Training, Downey Medical Center; Medical Director, The Skin Center at Laguna; Expert Medical Reviewer, Medical Board of California
Nili N Alai, MD, FAAD is a member of the following medical societies: American Academy of Dermatology and American Society for MOHS Surgery
Disclosure: Nothing to disclose.

Coauthor(s)

Dena Thompson, MS, Boston University School of Medicine
Disclosure: Nothing to disclose.

Arash Michael Saemi, MD, Department of Internal Medicine, Naval Medical Center San Diego
Arash Michael Saemi, MD is a member of the following medical societies: American College of Physicians, Radiological Society of North America, Sigma Xi, and Society of Interventional Radiology
Disclosure: Nothing to disclose.

Raul Del Rosario, MD, Consulting Staff, Surgical Pathology and Dermatopathology, South Coast Medical
Raul Del Rosario, MD is a member of the following medical societies: American Society for Clinical Pathology
Disclosure: Nothing to disclose.

Medical Editor

Günter Burg, MD, Professor and Chairman Emeritus, Department of Dermatology, University of Zürich School of Medicine; Delegate of The Foundation for Modern Teaching and Learning in Medicine Faculty of Medicine, University of Zürich, Switzerland
Günter Burg, MD is a member of the following medical societies: American Academy of Dermatology, American Dermatological Association, International Society for Dermatologic Surgery, North American Clinical Dermatologic Society, and Pacific Dermatologic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Michael J Wells, MD, Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center
Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association
Disclosure: Nothing to disclose.

Managing Editor

Rosalie Elenitsas, MD, Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System
Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology
Disclosure: Nothing to disclose.

CME Editor

Joel M Gelfand, MD, MSCE, Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania
Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology
Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds None; Genentech Consulting fee Consulting; Centocor Consulting fee Consulting; Centocor Grant/research funds None; Covance Consulting fee Consulting; Shire  Consulting

Chief Editor

Dirk M Elston, MD, Director, Department of Dermatology, Geisinger Medical Center
Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology
Disclosure: Nothing to disclose.

We authors appreciate the clinical photos supplied as a courtesy of The Skin Center at Laguna.

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