eMedicine Specialties > Pediatrics: General Medicine > Dermatology

Keratosis Pilaris: Treatment & Medication

Author: Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Coauthor(s): Steven J Escobar, MD, Fellow, Division of Pulmonary and Critical Care Medicine, Naval Medical Center, San Diego
Contributor Information and Disclosures

Updated: Oct 12, 2009

Treatment

Medical Care

  • Education and reassurance are the cornerstones of therapy for keratosis pilaris.5
  • The noninflamed horny papules usually remit with age and increasing time, but they are resistant to most forms of short-term therapy.
  • Encourage tepid showers instead of hot baths, along with the use of mild soaps and a home humidifier.
  • An emollient cream may help alleviate rough surfaces in mild cases. A topical keratolytic agent such as lactic acid, salicylic acid, or urea preparations may be beneficial in more extensive cases. Several recent reports claim good results with 2-3% salicylic acid in 20% urea cream. Topical tretinoin therapy has also been used with varying degrees of success.
  • Lesions with significant inflammation may improve with the use of medium-potency emollient-based topical steroid preparations. Inflammation is usually reduced markedly by 7 days, at which point the steroid should be discontinued.

Medication

Alpha hydroxy acids

Alpha hydroxy acid is a normal constituent of tissues and blood. Acids act as humectants when applied topically and may decrease corneocyte cohesion.


Ammonium lactate cream (Lac-Hydrin cream 12%)

Emollient available in 225-g and 400-g bottles and promotes hydration and removal of excess keratin. Contains lactic acid, an alpha hydroxy acid that has keratolytic action, thus facilitating release of comedones.

Adult

Apply to affected area bid/tid
Application to the skin while moist after washing or bathing enhances the moisturizing effect

Pediatric

Apply as in adults

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

Apply hydration, moisturizers, and possibly topical corticosteroids until fissures and inflammation are reduced; transient stinging, burning, erythema, and peeling have been noted after application of ammonium lactate lotion, especially when applied to abraded, inflamed, or irritated skin

Emollients containing urea

Topically applied urea has a hygroscopic effect by increasing the water retention in skin and it decreases pruritus.


Urea cream 20% (Carmol 20, Ureacin, Lanaphilic)

Application of 20% urea promotes hydration and removal of excess keratin.

Adult

Apply to affected area bid/tid
Application to the skin while moist after washing or bathing enhances the moisturizing effect

Pediatric

Apply as in adults

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

Apply hydration, moisturizers, and possibly topical corticosteroids until fissures and inflammation are reduced; transient stinging, burning, erythema, and peeling have been noted after application of 20% urea, especially when applied to abraded, inflamed, or irritated skin

Gels containing salicylic acid

These agents produce desquamation of the skin's horny layer. They are keratolytic at concentrations of 2-6%.


Salicylic acid 6% (Keralyt gel)

Removes excess keratin.

Adult

Apply a thin layer to affected area qd/bid

Pediatric

Apply as in adults

Documented hypersensitivity; prolonged use in infants, patients with diabetes mellitus, and patients with impaired circulation (not recommended); use on moles, birthmarks or warts with hair growing from them, genital or facial warts or warts on mucous membranes, irritated skin, or any area infected or reddened

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

Burning and irritation at site of exposure may occur; avoid contact with mucous membranes and eyes; prolonged use over large areas, especially in children, may result in salicylate toxicity

Retinoids

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


Tretinoin (Retin-A 0.025% - 0.1% cream)

Reduces cohesion among keratinized cells.

Adult

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

Pediatric

Apply as in adults

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

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

Photosensitivity may occur with excessive sunlight exposure, wear sunscreen over exposed areas; during the first few wk, the patient may experience redness, burning, or peeling; most patients adapt to treatment; switch those who become excessively irritated to qod or q3d therapy; do not apply to mucous membranes, mouth, and angles of nose

Topical corticosteroids

These agents elicit anti-inflammatory and immunosuppressive properties.


Triamcinolone acetonide 0.1% cream (Aristocort, Kenalog)

A moderate-potency steroid with anti-inflammatory properties. It treats inflammatory dermatosis that is responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes and reversing capillary permeability.

Adult

Apply sparingly to affected areas qd/bid until inflammatory component begins to resolve (typically 7 d)

Pediatric

Apply as in adults with caution

Documented hypersensitivity; fungal, viral, and bacterial skin infections

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

As with all topical corticosteroids, skin atrophy with telangiectasia, stria, purpura, and acne may occur; limit the use of topical steroids to the initial inflammatory treatment phase; long-term use of topical corticosteroids has no role in keratosis pilaris; limit tube size to reflect area and duration of treatment; do not use in decreased skin circulation; prolonged use, applications over large areas, and use of potent steroids and occlusive dressings may result in systemic absorption; systemic absorption may cause Cushing syndrome, reversible HPA axis suppression, hyperglycemia, and glycosuria

More on Keratosis Pilaris

Overview: Keratosis Pilaris
Differential Diagnoses & Workup: Keratosis Pilaris
Treatment & Medication: Keratosis Pilaris
Follow-up: Keratosis Pilaris
Multimedia: Keratosis Pilaris
References

References

  1. Hwang S, Schwartz RA. Keratosis pilaris: a common follicular hyperkeratosis. Cutis. Sep 2008;82(3):177-80. [Medline].

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

  3. Marqueling AL, Gilliam AE, Prendiville J, Zvulunov A, Antaya RJ, Sugarman J. Keratosis pilaris rubra: a common but underrecognized condition. Arch Dermatol. Dec 2006;142(12):1611-6. [Medline].

  4. Sallakachart P, Nakjang Y. Keratosis pilaris: a clinico-histopathologic study. J Med Assoc Thai. Jul 1987;70(7):386-9. [Medline].

  5. Novick NL. Practical management of widespread, atypical keratosis pilaris. J Am Acad Dermatol. Aug 1984;11(2 Pt 1):305-6. [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. Barth JH, Wojnarowska F, Dawber RP. Is keratosis pilaris another androgen-dependent dermatosis?. Clin Exp Dermatol. Jul 1988;13(4):240-1. [Medline].

  8. Callaway SR, Lesher JL. Keratosis pilaris atrophicans: case series and review. Pediatr Dermatol. Jan-Feb 2004;21(1):14-7. [Medline].

  9. 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].

  10. Di Lernia V, Ricci C. Folliculitis spinulosa decalvans: an uncommon entity within the keratosis pilaris atrophicans spectrum. Pediatr Dermatol. May-Jun 2006;23(3):255-8. [Medline].

  11. Dogra S, Kumar B. Epidemiology of skin diseases in school children: a study from northern India. Pediatr Dermatol. Nov-Dec 2003;20(6):470-3. [Medline].

  12. Ehsani A, Namazi MR, Barikbin B, Nazemi MJ. Unilaterally generalized keratosis pilaris. J Eur Acad Dermatol Venereol. May 2003;17(3):361-2. [Medline].

  13. Gerbig AW. Treating keratosis pilaris. J Am Acad Dermatol. Sep 2002;47(3):457. [Medline].

  14. 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].

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

  16. Owen WR, Wood C. Disseminate and recurrent infundibulofolliculitis. Arch Dermatol. Feb 1979;115(2):174-5. [Medline].

  17. Ravikumar BC, Balachandran C, Shenoi SD, et al. Disseminate and recurrent infundibulofolliculitis: response to psoralen plus UVA therapy. Int J Dermatol. Jan 1999;38(1):75-6. [Medline].

  18. Rook A, Wilkinson DS, Ebling FJG, et al. Disorders of keratinization. In: Textbook of Dermatology. Oxford, England: Blackwell Publishers; 1986:1435-6.

  19. Zouboulis CC, Stratakis CA, Gollnick HP, Orfanos CE. Keratosis pilaris/ulerythema ophryogenes and 18p deletion: is it possiblethat the LAMA1 gene is involved?. J Med Genet. Feb 2001;38(2):127-8. [Medline][Full Text].

Further Reading

Keywords

keratosis pilaris alba, keratosis pilaris rubra, goose bumps, hair follicle, keratinized hair follicles, keratotic papule, perifollicular erythema, ichthyosis vulgaris, atopic dermatitis, hyperandrogenism, erythematous papules, corneocyte adhesion, hyperkeratosis, hypogranulosis

Contributor Information and Disclosures

Author

Mark A Crowe, MD, Assistant Clinical Instructor, Department of Medicine, Division of Dermatology, University of Washington School of Medicine
Mark A Crowe, MD is a member of the following medical societies: American Academy of Dermatology and North American Clinical Dermatologic Society
Disclosure: Nothing to disclose.

Coauthor(s)

Steven J Escobar, MD, Fellow, Division of Pulmonary and Critical Care Medicine, Naval Medical Center, San Diego
Steven J Escobar, MD is a member of the following medical societies: American College of Chest Physicians, American College of Physicians, Society of Critical Care Medicine, and Undersea and Hyperbaric Medical Society
Disclosure: Nothing to disclose.

Medical Editor

Kevin P Connelly, DO, Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University; Medical Director, Paws for Health Pet Visitation Program of the Richmond SPCA; Pediatric Emergency Physician, Emergency Consultants Inc, Chippenham Medical Center
Kevin P Connelly, DO is a member of the following medical societies: American Academy of Pediatrics, American College of Osteopathic Pediatricians, and American Osteopathic Association
Disclosure: Nothing to disclose.

Pharmacy Editor

Mary L Windle, PharmD, Adjunct Assistant Professor, University of Nebraska Medical Center College of Pharmacy, Pharmacy Editor, eMedicine
Disclosure: Pfizer Inc Stock Investment from financial planner; Avanir Pharma Stock Investment from financial planner ; WebMD Salary and stock Employment and investment from financial planner

Managing Editor

Robert A Schwartz, MD, MPH, Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, UMDNJ-New Jersey Medical School
Robert A Schwartz, MD, MPH is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, and Sigma Xi
Disclosure: Nothing to disclose.

CME Editor

Merrily P M Poth, MD, Professor, Department of Pediatrics and Neuroscience, Uniformed Services University of the Health Sciences
Merrily P M Poth, MD is a member of the following medical societies: American Academy of Pediatrics, Endocrine Society, and Lawson-Wilkins Pediatric Endocrine Society
Disclosure: Nothing to disclose.

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.

 
 
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