CAN YOU IDENTIFY THIS CONDITION?
A 37-year-old woman presented with multiple atrophic patches on both legs. The patches, which were asymptomatic, had a “cigarette paper” appearance. They had appeared gradually over a number of years. She had a history of pyoderma gangrenosum that had been treated for several years with topical corticosteroids.
The most likely diagnosis is:
Mycosis fungoides
Anetoderma
Corticosteroid-induced atrophy
Localized lipodystrophy
Cutis laxa
3. Corticosteroid-induced atrophy
Topical corticosteroids are used widely for a variety of inflammatory (eg, atopic dermatitis, contact dermatitis) and hyperproliferative (eg, psoriasis) skin conditions (Table 1).1-4 Triamcinolone acetonide, the most commonly used injectable glucocorticoid, can be introduced directly into isolated lesions or lesions that involve the subcutaneous layers of the skin (eg, discoid lupus erythematosus, keloids, alopecia areata, acne nodules, plaques of psoriasis).2
Table 1.
Conditions commonly treated with topical corticosteroids
Topical hydrocortisone, one of the least potent topical corticosteroids, came into use in the early 1950s for treating inflammatory dermatoses. Over the years, more potent concentrations, formulations (eg, optimized ointments and creams), and compounds with greater anti-inflammatory properties were developed. In Canada and the United States, topical corticosteroids are classified according to their strength from very low to very high potency; very high–potency compounds are approximately 1000 times more potent than hydrocortisone. Table 2 lists topical corticosteroids commonly prescribed in Canada by their potency.1,2 In general, as we move from lotion to cream to ointment, the potency of corticosteroids increases.
Table 2.
Potency of commonly prescribed corticosteroids
Although high-potency topical corticosteroids generate greater anti-inflammatory activity, they are also associated with an increased incidence of adverse cutaneous reactions (Table 3).1,2 General skin atrophy consists of a reduction in epidermal and dermal thickness, regression of the sebaceous glands, subcutaneous fat loss, and muscle-layer atrophy. These changes are typically observed following 2 to 3 weeks of moderate- to high-potency topical corticosteroid use.1,5 A single application of a very potent topical steroid can cause an ultrasonographically detectable decrease in skin thickness that lasts up to 3 days.6 Even low-potency topical steroids can cause slight skin atrophy that often reverses upon discontinuation of the drugs.7 Atrophy and striae are of concern on areas of the skin with high permeability, such as the face and intertriginous areas, but these adverse events can occur anywhere, especially after long-term use of moderate- or high-potency topical corticosteroids. While mild atrophy and telangiectasia might be reversible upon discontinuation of corticosteroids,8 overtly visible changes in skin texture and striae are considered permanent manifestations of corticosteroid-induced atrophy and are resistant to treatment.
Table 3.
Prevalence of adverse cutaneous reactions to topical corticosteroids
The therapeutic effects of topical steroids can be negated by the resulting thinning of the stratum corneum. Such thinning impairs its barrier function and allows transepidermal water loss that can lead to skin irritation.9 Sometimes, the visible and textural changes to the skin are described as looking like “cigarette paper.” The skin thins because of decreased production of fibroblasts and abnormal deposition of collagen and elastin. Loss of hyaluronic acid leads to decreased retention of dermal moisture.10
With the introduction of potent and very potent steroids, systemic absorption has become a concern. Infants and children who have larger surface-to-body ratios and adults with liver failure who might not be able to metabolize steroid molecules effectively are most at risk. Systemic side effects include reversible suppression of the hypothalamic-pituitary axis, Cushing syndrome, growth suppression, and glaucoma.1,2 Unless otherwise indicated, only low-potency topical corticosteroids should be used on infants. Potent and very potent topical corticosteroids should not be used on children younger than 12 years. Exceptions to this general rule can be made for acute inflammatory conditions, when more potent topical steroids can be used for short periods (less than 2 weeks) and on less atrophy-prone areas of the body (eg, scalp, palmoplantar areas).
In recent years, 2 novel anti-inflammatory agents have been released: tacrolimus and pimecrolimus. Both are noncorticosteroid immune-response modifiers and are safe for long-term application on the face and intertriginous areas. Studies comparing tacrolimus and pimecrolimus with midpotency corticosteroids have reported comparable anti-inflammatory properties and clinical efficacy for maintenance treatment.11 Pimecrolimus is safe to use on infants as young as 3 months, and tacrolimus is approved for children older than 2 years. Although topical corticosteroids still have an important role in short-term management of exacerbations, these new agents are increasingly being used as first-line treatment for traditionally corticosteroid-responsive dermatoses (especially eczema) based on their safety profile, potential for long-term use, and minimal adverse reactions. Despite the effectiveness of these novel immunomodulators, they are not accessible to everyone because they are expensive and sometimes are not covered by third-party health insurance.
Biographies
Dr Ting is a recent graduate of the University of Calgary Medical School in Alberta.
Dr Barankin is a dermatologist in Toronto, Ont.
References
- 1.Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF. Dermatology in general medicine. 4th ed. New York, NY: McGraw-Hill Inc; 1999. [Google Scholar]
- 2.Arndt KA, Bowers KE. Manual of dermatologic therapeutics. 6th ed. Philadelphia, Pa: Lippincott Williams & Wilkins; 2002. [Google Scholar]
- 3.Goa KL. Clinical pharmacology and pharmacokinetic properties of topically applied corticosteroids. A review. Drugs. 1988;36(Suppl 5):51–61. doi: 10.2165/00003495-198800365-00011. [DOI] [PubMed] [Google Scholar]
- 4.Sams WM, Lynch PJ. Principles and practice of dermatology. 2nd ed. New York, NY: Churchill Livingstone Inc; 1996. [Google Scholar]
- 5.Woodbury R, Kligman AM. The hairless mouse model for assaying the atrophogenicity of topical corticosteroids. Acta Derm Venereol. 1992;72(6):403–406. [PubMed] [Google Scholar]
- 6.Lubach D, Rath J, Kietzmann M. Skin atrophy induced by initial continuous topical application of clobetasol followed by intermittent application. Dermatology. 1995;190(1):51–55. doi: 10.1159/000246635. [DOI] [PubMed] [Google Scholar]
- 7.Black MM, Platt NE, Mugglestone CJ. A study of potential skin atrophy following topical application of weak corticosteroids. Curr Med Res Opin. 1981;7(7):463–470. doi: 10.1185/03007998109114285. [DOI] [PubMed] [Google Scholar]
- 8.Zheng PS, Lavker RM, Lehmann P, Kligman AM. Morphologic investigations on the rebound phenomenon after corticosteroid-induced atrophy in human skin. J Invest Dermatol. 1984;82(4):345–352. doi: 10.1111/1523-1747.ep12260665. [DOI] [PubMed] [Google Scholar]
- 9.Kolbe L, Kligman AM, Schreiner V, Stoudemayer T. Corticosteroid-induced atrophy and barrier impairment measured by non-invasive methods in human skin. Skin Res Technol. 2001;7(2):73–77. doi: 10.1034/j.1600-0846.2001.70203.x. [DOI] [PubMed] [Google Scholar]
- 10.Sarnstrand B, Brattsand R, Malmstrom A. Effect of glucocorticoids on glycosaminoglycan metabolism in cultured human skin fibroblasts. J Invest Dermatol. 1982;79(6):412–417. doi: 10.1111/1523-1747.ep12530360. [DOI] [PubMed] [Google Scholar]
- 11.Paul C, Graeber M, Stuetz A. Ascomycins: promising agents for the treatment of inflammatory skin diseases. Expert Opin Invest Drugs. 2000;9(1):69–77. doi: 10.1517/13543784.9.1.69. [DOI] [PubMed] [Google Scholar]