AUTHOR AND EDITOR INFORMATION

Section 1 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

INTRODUCTION

Section 2 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

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, KP 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. See Ichthyosis Vulgaris, Hereditary and Acquired and Atopic Dermatitis for more information.

KP 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 KP are unaware the condition has a designated medical term  or that it is treatable. In general, KP is frequently cosmetically displeasing but medically harmless.

Overall, KP 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 KP 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, KP is self-limited and, again, tends to improve with age in many patients. Some patients have lifelong KP with periods of remissions and exacerbations. More widespread atypical cases may be cosmetically disfiguring and psychologically distressing.

Pathophysiology

KP is a genetically based disorder of hyperkeratinization of the skin. The excess formation and/or buildup of keratin is thought to cause the abrasive goose-bump texture of the skin. 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

KP is overall a very common condition and is present worldwide. KP 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 KP. 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

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. KP is present in otherwise healthy individuals and does not have any long-term health implications.

Race

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 KP, but females may be affected more frequently than males.

Age

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

CLINICAL

Section 3 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

History

Patients often report a rough texture (gooseflesh appearance) and overall poor cosmetic appearance of their skin. Eruption is usually asymptomatic, except for occasional pruritus.

Physical

Physical findings 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, sandpaperlike 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 pimplelike material may be expressed from each bump. Pustules and cysts are fairly rare. 

Commonly involved areas include posterolateral upper arms (see Media File 2), anterior thighs, buttocks, and facial cheeks. The single most characteristic area in KP is the upper outer arms.

Causes

The etiology of KP is not fully known. The definite association of hyperkeratinization has been established. Of those 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 KP, ichthyosis, or atopic dermatitis.³

DIFFERENTIALS

Section 4 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Other Problems to be Considered

KP may be associated with phrynoderma (vitamin A deficiency). Interestingly, a significant association was also found between acquired ichthyosis and KP as common cutaneous manifestations in persons with type 1 diabetes.

WORKUP

Section 5 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Lab Studies

No specific laboratory tests aid in diagnosis.

Imaging Studies

Imaging studies are not indicated.

Procedures

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

Histologic Findings

Papules are thought to arise from excessive accumulation of keratin at the follicular orifice. The epidermis shows mild hyperkeratosis, hypergranulosis, and follicular plugging. The upper dermis may have some mild superficial perivascular lymphocytic inflammatory changes.

TREATMENT

Section 6 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Medical Care

In view of the described genetic predisposition and genetic etiology, no cure or universally effective treatment is available. Inconsistent remissions and variations with seasons and hormonal states (eg, pregnancy⁴) are described. Although symptoms usually remit with increasing age, this is not always the case.

• General measures to prevent excessive skin dryness and use of mild cleansers (eg, Dove, Cetaphil) are recommended.
• Some available therapeutic options include emollients, lactic acid, tretinoin cream, tazarotene, alpha-hydroxy acid lotions and peels, urea cream, salicylic acid, topical steroids, and topical immunomodulators. Pulse weekly topical retinoids are generally the most effective, but the response usually is not complete. Vitamin D (calcipotriol) is not effective for KP, but clinical trials have found it moderately effective for ichthyoses.⁵
• Aminolevulinic acid (Levulan) photodynamic therapy has been anecdotally reported as effective,  but this successful use of off-label photodynamic therapy requires confirmation.
• Microdermabrasion is described as machine-assisted fine abrasion of the skin using vacuum suction and debris removal. An abrasive particle such as fine powdery crystals or diamond tip is used to remove the keratin and outer layers of the epidermis in a controlled manner. As with other treatments for KP, data exists only in the form of small group observations and anecdotal reports. Because KP is generally a chronic condition that requires long-term maintenance, most therapies would require repeated or long-term use to maintain results. An additional option to in-office microdermabrasion is manual gentle exfoliation using a loofah sponge or a commercially available Buf-Puff sponge.

Surgical Care

Surgery is not indicated.

Consultations

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

Diet

KP has no dietary associations.

Activity

KP does not limit any patient activities.

MEDICATION

Section 7 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

The goals of pharmacotherapy are to reduce morbidity and to prevent complications.

Drug Category: Retinoids

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

Drug Category: Alpha-hydroxy acids

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

Drug Category: Topical Skin Product

Drug Category: Keratolytic Agent

Drug Category: Acne Products

FOLLOW-UP

Section 8 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Deterrence/Prevention

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 are infrequent. However, postinflammatory hypopigmentation or hyperpigmentation and scarring may occur.

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

Section 9 of 10  

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

Media file 1:  Close-up view of keratosis pilaris. Keratotic follicular-based erythematous papules are noted on upper arm.
	View Full Size Image
Media type:  Photo

Media file 2:  Keratosis pilaris in characteristic location on outer upper arm of a 30-year-old woman.
	View Full Size Image
Media type:  Photo

REFERENCES

Section 10 of 10

• Authors and Editors
• Introduction
• Clinical
• Differentials
• Workup
• Treatment
• Medication
• Follow-up
• Multimedia
• References

1. Sardana K, Relhan V, Garg V, Khurana N. An observational analysis of erythromelanosis follicularis faciei et colli. Clin Exp Dermatol. Jan 11 2008;[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. 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].
4. 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].
5. Kragballe K, Steijlen PM, Ibsen HH, van de Kerkhof PC, Esmann J, Sorensen LH, 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].
6. Bielan B. What's your assessment? Keratosis pilaris. Dermatol Nurs. Aug 2004;16(4):357-8. [Medline].
7. Lateef A, Schwartz RA. Keratosis pilaris. Cutis. Apr 1999;63(4):205-7. [Medline].
8. Novick NL. Practical management of widespread, atypical keratosis pilaris. J Am Acad Dermatol. Aug 1984;11(2 Pt 1):305-6. [Medline].
9. Poskitt L, Wilkinson JD. Natural history of keratosis pilaris. Br J Dermatol. Jun 1994;130(6):711-3. [Medline].

Article Last Updated: Mar 7, 2008