Steroid Atrophy

Steroid atrophy was first described by Epstein et al. in 1963 [1] and is known to occur following the use of topical as well as systemic corticosteroids [2]. Risk factors for the condition include the strength of the steroid formulation prescribed, duration and the frequency of use [2] [3]. Skin areas with a less depth of the dermal layer e.g. on the face and other areas e.g. groin, axilla, and vulva are more susceptible [4] [5] [6] while the palmar and plantar surfaces are less prone [7] to steroid atrophy.

Three stages in steroid atrophy have been reported: the first stage of pre-atrophy, followed by atrophy and the terminal stage of tachyphylaxis [8]. Patients present initially with a burning sensation in the area where the topical steroid is being applied. Continued use of the medication leads to vasoconstriction with a resolution of symptoms [8]. Atrophic thinning of the skin with telangiectasia is more common on the face while striae are more frequently seen in the axilla, groin, and vulva. The disorder is characterized by a transparent, fragile appearance of the skin, dryness, laxity with telangiectasia [9] [10] and an increased tendency for bruising, which has been described as steroid purpura [11].

The condition may improve if the medication is discontinued as soon as the patient presents with symptoms. Otherwise, long-term steroid use leads to irreversible striae and more prominent telangiectasias. Dermatological features of steroid atrophy resemble those of the skin in the elderly. However, steroid atrophy is usually not associated with malignant change while striae are not observed in aging skin.

The diagnosis of steroid atrophy is based on the typical clinical appearance of the skin: increased skin transparency, consistency resembling that of a cigarette paper, and increased fragility with a tendency to bruise easily [2]. History will reveal either a short or long-term use of steroids, with symptoms related to the area in which the medication was applied.

As the condition in chronic stage is irreversible and as there is a potential for complications following an invasive procedure, surgical skin biopsies are not routinely performed. But if they are performed then, the following features are noted on histology: flattening of the epidermal-dermal areas [11], diminished epidermal width [10], reduced keratinocyte size [12], decreased number of fibroblasts [12] [13] and narrowing of the lipid lamella of the stratum corneum [14].

Several non-invasive techniques and assays to diagnose the condition have been devised both for clinical and experimental use. Evaporimeter assesses water loss from the transepidermal layer while the loss of cholesterol and fatty acids can be detected with stratum corneum lipid measurement [12]. Skin thinning can be measured using a screw gauge, laser microscope and ultrasound [12] [15]. However, these tests are cumbersome and patients have to use the medication for up to six weeks before results can be obtained [16].

1. Epstein NN, Epstein WL, Epstein JH. Atrophic striae in patients with inguinal intertrigo. Arch Dermatol. 1963;87: 450–457.
2. Schoepe S, Schacke H, May E, Asadullah K. Glucocorticoid therapy-induced skin atrophy. Exp Dermatol. 2006;15(6):406–420.
3. Garbe C, Wolf G. Topische Therapie. In: Braun-FalcoO, PlewigG, WolffH H, BurgdorfW, LandthalerM, eds. Dermatologie und Venerologie. Berlin: Springer, 2005: 1431–1461.
4. Cornell RC, Stoughton RB. The use of topical steroids in psoriasis. Dermatol Clin 1984;2: 397–408.
5. Schacke H, Docke WD, Asadullah K. Mechanisms involved in the side effects of glucocorticoids. Pharmacol Ther. 2002;96(1):23–43.
6. Johnson E, Groben P, Eanes A, et al. Vulvar skin atrophy induced by topical glucocorticoids. J Midwifery Womens Health. 2012 May -Jun; 57(3):296-299
7. Luger T, Loske KD, Elsner P, et al. Topische Dermatotherapie mit Glukokortikoiden Therapeutischer Index. J Dtsch Dermatol Ges 2004; 2: 629–634.
8. Abraham A, Roga G. Topical steroid damaged skin. Indian J Dermatol. 2014 Sept-Oct; 59(5):456-459
9. Booth BA, Tan EM, Oikarinen A, Uitto J. Steroid-induced dermal atrophy: effects of glucocorticosteroids on collagen metabolism in human skin fibroblast cultures. Int J Dermatol 1982; 21: 333–337.
10. Mills CM, Marks R. Side effects of topical glucocorticoids. Curr Probl Dermatol 1993; 21: 122–131.
11. Kimura T, Doi K. Dorsal skin reactions of hairless dogs to topical treatment with corticosteroids. Toxicol Pathol 1999; 27: 528–535.
12. 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: 73–77.
13. Saarni H, Hopsu-Havu VK. The decrease of hyaluronate synthesis by anti-inflammatory steroids in vitro. Br J Dermatol 1978; 98: 445–449.
14. Sheu HM, Lee JY, Chai CY, Kuo KW. Depletion of stratum corneum intercellular lipid lamellae and barrier function abnormalities after long-term topical corticosteroids. Br J Dermatol 1997; 136: 884–890.
15. Newton JA, Whitaker J, Sohail S, et al. A comparison of pulsed ultrasound, radiography and micrometer screw gauge in the measurement of skin thickness. Curr Med Res Opin 1984; 9: 113–118.
16. Lehmann P, Zheng P, Lavker RM, Kligman AM. Corticosteroid atrophy in human skin. A study by light, scanning, and transmission electron microscopy. J Invest Dermatol 1983; 81: 169–176.

• Steroid Atrophy
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