Pediatric Keratosis Pilaris Medication

  • Author: Mark A Crowe, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Mar 30, 2012
 

Alpha hydroxy acids

Class Summary

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

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Ammonium lactate (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.

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Emollients containing urea

Class Summary

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

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

 

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

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Gels containing salicylic acid

Class Summary

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

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Salicylic acid topical (Keralyt gel)

 

Removes excess keratin.

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Retinoids

Class Summary

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

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

 

Reduces cohesion among keratinized cells.

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Topical corticosteroids

Class Summary

These agents elicit anti-inflammatory and immunosuppressive properties.

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Triamcinolone topical (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.

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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  Staff, 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, and Society of Critical Care Medicine

Disclosure: Nothing to disclose.

Specialty Editor Board

Kevin P Connelly, DO  Clinical Assistant Professor, Department of Pediatrics, Division of General Pediatrics and Emergency Care, Virginia Commonwealth University School of Medicine; 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.

Mary L Windle, PharmD  Adjunct Associate Professor, University of Nebraska Medical Center College of Pharmacy; Editor-in-Chief, Medscape Drug Reference

Disclosure: Nothing to disclose.

Robert A Schwartz, MD, MPH  Professor and Head, Dermatology, Professor of Pathology, Pediatrics, Medicine, and Preventive Medicine and Community Health, University of Medicine and Dentistry of New Jersey-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.

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 Pediatric Endocrine Society

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

References

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  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].

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  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].

 
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Although other sites may be involved, keratosis pilaris is most common on the lateral upper arms and upper thighs.
Upon closer examination of keratosis pilaris, the lesions are very evenly spaced. This even distribution is consistent with the follicular origin of this disorder.
Close examination of keratosis pilaris shows keratotic papules associated with hair follicles. Keratinocytes normally shed from the surrounding skin become dust on the floor. Keratinocytes at the follicular orifice are retained, producing these papules.
Bacteria associated with the follicular papules of keratosis pilaris may cause some lesions to become erythematous or pustular.
This patient has lichen nitidus. Lichen nitidus is a differential diagnosis for keratosis pilaris. The papules of lichen nitidus tend to be flatter, and lesions develop in crops. Etiology of lichen nitidus is unknown.
Lichen nitidus also shows the property of koebnerization. Keratosis pilaris does not koebnerize.
Disseminate and recurrent infundibulofolliculitis is an uncommon slightly pruritic papular follicular eruption that affects the neck, face, trunk, and proximal extremities. It is a differential diagnosis for keratosis pilaris and occurs almost exclusively in blacks. The cause is unknown, and treatment has been totally unsuccessful. Disseminate and recurrent infundibulofolliculitis differs from keratosis pilaris in distribution and is less keratotic.
 
 
 
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