Topical Corticosteroids

Gabros S, Nessel TA, Zito PM.

Indications
Topical corticosteroids play a major role in the treatment of many dermatologic conditions. They are FDA-approved and
indicated for the use of inflammatory and pruritic presentations of dermatologic conditions. The well-known indications are
for diseases such as psoriasis, limited areas of vitiligo, eczema, atopic dermatitis, phimosis, acute radiation dermatitis, lichen
planus, lichen simplex chronicus, discoid lupus erythematosus, and lichen sclerosis.[1] They are effective for conditions
involving hyper-proliferation, immunological, and inflammatory properties.[2]

Mechanism of Action
The mechanism of action of topical corticosteroids is vast, consisting of anti-inflammatory, anti-mitotic, and
immunosuppressive effects.[3]

The anti-inflammatory effect of topical corticosteroids consists of vasoconstriction, inhibition of the release of phospholipase
A2, and a direct inhibitory effect on DNA and inflammatory transcription factors.[3][4]Vasoconstriction of the blood vessels
within the upper dermis decreases the number of inflammatory mediators being delivered to the region applied.[3] The anti-
inflammatory effect also occurs from the synthesis of lipocortin which inhibits phospholipase A2, ultimately decreasing the
production of prostaglandins and leukotrienes.[4] Topical corticosteroids also act directly at the DNA level to increase the
expression of anti-inflammatory genes and indirectly inhibit inflammatory transcription factors, such as NFkb, to decrease the
expression of pro-inflammatory genes.[3]

The anti-mitotic effect of topical corticosteroids play a great role in the treatment of psoriasis; it is proposed that this decrease
in epidermal mitosis is secondary to an increase in lipocortin, an endogenous glucocorticoid-regulated protein. An anti-mitotic
effect is also present in the dermis which inhibits cell proliferation and collagen synthesis.[5][6]

The immunosuppressive effects of topical corticosteroids involve the inhibition of humoral factors involved in the
inflammatory response as well as suppression of the maturation, differentiation, and proliferation of all immune cells.[5]

Administration
Topical corticosteroids are administered topically; however, successful administration depends upon obtaining an accurate
diagnosis, choosing the correct drug, selecting the appropriate vehicle and potency, and the frequency of application.[1]

The vehicle is the carrier of the drug. The vehicle selection depends on the region affected and the type of lesion present. It
also functions to hydrate the skin and increase absorption. The vehicle options include the following[7]:

Ointments - administered for thick hyper-keratotic lesions; the most potent vehicle since they are the most occlusive
and should not be administered on hair-bearing regions because it may result in folliculitis[1]
Creams - less potent than ointment but cosmetically more appealing since they leave no residue; the drying, non-
occlusive nature leads to their administration for acute exudative inflammation and dermatitis within the
intertriginous areas.[1]
Lotions - less occlusive and greasy; work well in hair-bearing regions
Gels - like lotions, less occlusive and greasy; work well in hair-bearing regions; more beneficial for the scalp as they
do not cause matting of thleast occlusive and greasye hair
Foams - highly effective for steroid delivery to the scalp but are costly[8]

The potency of topical corticosteroids is the amount of drug needed to produce a desired therapeutic effect. The gold standard
for determining potency is the vasoconstrictor assay which measures the vasoconstrictive properties based upon cutaneous
vasoconstriction.[9] The United States classification consists of seven classes, with class I superpotent and class VII least
potent.[10]

Class I superpotent corticosteroids include clobetasol propionate 0.05% in any vehicle, augmented betamethasone
dipropionate 0.05% gel or ointment, diflorasone diacetate 0.05% ointment, fluocinonide 0.1% cream, and halobetasol
propionate 0.05% cream or ointment.[1]

Class II high-potency corticosteroids include amcinonide 0.1% ointment, augmented betamethasone dipropionate 0.05%
cream or lotion, betamethasone dipropionate 0.05% ointment, desoximetasone cream or gel or ointment, diflorasone diacetate
0.05% cream, fluocinonide 0.05% cream or gel or ointment, and halcinonide 0.1% cream or ointment or solution.[1]

Class III medium- to high-potency corticosteroids include amcinonide 0.1% cream, betamethasone dipropionate 0.05% cream,
fluticasone propionate 0.005% ointment, and triamcinolone acetonide 0.5% cream or ointment.[1]

Class IV and V medium-potency corticosteroids include betamethasone valerate 0.1% cream or lotion or foam,
desoximetasone 0.05% cream, Fluocinolone acetonide 0.025% cream or ointment, fluticasone propionate 0.05% cream,
hydrocortisone butyrate 0.1% ointment, hydrocortisone probutate 0.1% cream, hydrocortisone valerate 0.2% cream or
ointment, mometasone furoate 0.1% cream or lotion or ointment, triamcinolone acetonide 0.025% cream or lotion or
ointment, and triamcinolone acetonide 0.1% cream or lotion or ointment.[1]

Class VI low-potency corticosteroids include alclometasone dipropionate 0.05% cream or ointment, desonide 0.05% in any
vehicle, fluocinolone 0.01% cream, and hydrocortisone butyrate 0.1% cream.[1]

Class VII least-potent corticosteroids include hydrocortisone 1% and 2.5% cream or lotion or ointment.[1]

Corticosteroids are better absorbed and more permeable in regions of thin epidermis, such as the eyelid, compared to thicker
regions of epidermis, such as the sole. The penetration difference between the two varies by 300 fold.[11]The penetration
increases two- to ten-fold in diseased states, such as inflammation and desquamation.[1][12] High-potency steroids are used
for the palms and soles, due to the thick stratum corneum, and in nonfacial/nonintertriginous areas for severe dermatoses, such
as psoriasis and severe atopic and contact dermatitis. [1] Medium- to high-potency steroids are useful for regions of thin
epidermis and areas of occlusion, such as the eyelid and axilla, respectively.[8] Low-to-medium strength preparations should
be used for large surface areas to decrease the risk of systemic absorption. 1917[1]

The amount of steroid used plays a great part in the efficacy of treatment but also in avoiding adverse effects from overuse.
One fingertip unit (FTU) is equal to 0.5 grams. The suggested dose of FTU is dependent upon the body region being treated.
Topical corticosteroids are recommended for once to twice daily use.[13] A study regarding topical corticosteroid use for
atopic dermatitis demonstrated that there was no beneficial evidence to applying topical corticosteroid more than once per day.
Applying it more often only resulted in an increase in adverse effects.[14]

Adverse E!ects
The adverse effects of topical corticosteroids can be divided into local and systemic effects. Local adverse effects occur with
prolonged treatment and are based on the topical steroid potency, vehicle, and application site. The most common local effects
include atrophy, striae, rosacea, perioral dermatitis, acne, and purpura.[6]

Skin atrophy is the most common adverse effect and occurs due to the anti-mitotic effect of topical corticosteroids.[6] Topical
steroid causes the skin to undergo 3 phases: preatrophy, atrophy, and tachyphylaxis. Atrophy occurs when there is a persistent
use in the same region. This leads to epidermal thinning and increased resorption within the dermis ground substance. The
loss of connective tissue leads to erythema, teleangiectasias, and purpura. Atrophy presents as a burning sensation; the
vasoconstrictive effect of the topical corticosteroid relieves the burn.[4] Areas most at risk for atrophy are intertriginous due to
thinner skin and increased occlusion. Atrophy is reversible with cessation of steroid use; however, it may take months for the
skin to appear normal again.[6]

Tachyphylaxis is the result of the skin developing tolerance to the topical corticosteroid, which ultimately is a loss of
vasoconstriction at the level of the capillaries. It has been demonstrated that the capillaries regain the ability to vasoconstrict
after 4 days. For this reason, pulse therapy is recommended and the topical corticosteroid should be discontinued for 4 days if
it has lost its effectiveness.[13]

Striae develop due to injury to the dermis and mechanical stress. Inflammation and edema of the dermis results in collagen
deposition in the region of the mechanical stress. Striae appear histologically as scars and are permanent.[6]

Topical corticosteroid usage can result in acne formation due to the degradation of the follicular epithelium and an increase in
the concentration of free fatty acids on the skin surface. This fosters an environment for bacteria growth, ultimately leading to
comedogenesis.[6]

Steroid rosacea can occur when steroids are prescribed initially for erythema with or without pustules. If a low-dose potency
topical corticosteroid is prescribed, it can lead to good results until the lesions reappear and higher potency steroid use is
continuously needed.[6]

Perioral dermatitis occurs due to prolonged use of potent corticosteroids on the face. It presents as follicular pustules and
papules on an erythematous base surround the perioral region but sparing the vermillion border.[6]

Less common local adverse effects include hypertrichosis, pigment alteration, and delayed wound healing. Systemic adverse
effects are less likely to occur due to low percutaneous absorption; however, they can develop with the prolonged use of high-
potency steroids on thin epidermal regions. The systemic adverse effects include glaucoma, hypothalamic-pituitary axis
suppression, Cushing syndrome, hypertension, and hyperglycemia.[6]

Contraindications
Topical corticosteroids are contraindicated for bacterial infections as their anti-inflammatory and vasoconstrictive effect will
mask the infection, ultimately delaying diagnosis and treatment. Topical steroids should also be avoided in impetigo, furuncles
and carbuncles, cellulitis, erysipelas, lymphangitis, and erythrasma. Relative contraindications include candida and
dermatophytes.[15] The immunosuppressive effects may result in persistent fungal infections that can be identified as tinea
incognito, significant for increased spread and inflammation with pustule formation.[8]

Monitoring
Patients need to be monitored carefully as unsupervised use of these medications can result in local and systemic adverse
effects. The duration of treatment should not be greater than 2 to 4 weeks, regardless of potency. High-potency steroids should
not be administered for a longer than 2 weeks, and after this period, should be tapered to avoid adverse effects.[1]
[13] Guidelines to prevent adverse effects include the use of lower-potency steroids, morning-only applications, alternate-day
treatment, and decreasing the extent of occlusion.[16]

Enhancing Healthcare Team Outcomes

Topical corticosteroids are one of the most commonly prescribed drugs in dermatology due to the rapid effect of relieving
unwanted signs and symptoms. However, if they not properly prescribed or patients are not given adequate instructions,
topical corticosteroid abuse can occur, resulting in adverse effects.[17] Ideally, dermatologists, nurses, general practitioners,
and pharmacists should work together to enforce the way topical corticosteroids are applied. Realistically, expert advice is
quickly forgotten, and the product label is the only direction that remains. A label stating “apply thinly or use sparingly”
promotes anxiety that the product may be dangerous, resulting in poor adherence and treatment. To resolve this matter, the
fingertip unit (FTU) was designed to make it easier for practitioners to explain to patients how much medication should be
applied to different regions of the body. Taking the time to explain the FTU system can help patients feel confident that they
are using an adequate amount of steroids. It has also been recommended that labels state to "apply enough to cover
the affected area" and include an image of the fingertip unit and a chart demonstrating how many fingertip units should be
applied to each body region so patients will receive appropriate treatment. Patients should also be advised not to exceed the
prescribed treatment and to only discontinue use under medical supervision. Pharmacists are the last line of healthcare that the
patient sees before using the medication and play an important role in enforcing the correct usage and ensuring patient
understanding of the interprofessional team's treatment plan.[18]

Continuing Education / Review Questions

Earn continuing education credits (CME/CE) on this topic.
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Comment on this article.

References
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3. Ahluwalia A. Topical glucocorticoids and the skin--mechanisms of action: an update. Mediators Inflamm. 1998;7(3):183-
93. [PMC free article: PMC1781846] [PubMed: 9705606]
4. Abraham A, Roga G. Topical steroid-damaged skin. Indian J Dermatol. 2014 Sep;59(5):456-9. [PMC free article:
PMC4171912] [PubMed: 25284849]
5. Uva L, Miguel D, Pinheiro C, Antunes J, Cruz D, Ferreira J, Filipe P. Mechanisms of action of topical corticosteroids in
psoriasis. Int J Endocrinol. 2012;2012:561018. [PMC free article: PMC3508578] [PubMed: 23213332]
6. Coondoo A, Phiske M, Verma S, Lahiri K. Side-effects of topical steroids: A long overdue revisit. Indian Dermatol Online
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7. Lee NP, Arriola ER. Topical corticosteroids: back to basics. West J Med. 1999 Nov-Dec;171(5-6):351-3. [PMC free
article: PMC1308757] [PubMed: 10639873]
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Publication Details

Author Information

Authors

Sarah Gabros1; Trevor A. Nessel2; Patrick M. Zito3.

A"liations

1
Rowan University SOM
2
MSU College of Osteopathic Medicine
3
University of Miami; Miller School of Medicine

Publication History

Last Update: September 29, 2020.

Copyright
Copyright © 2020, StatPearls Publishing LLC.

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Publisher

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NLM Citation

Gabros S, Nessel TA, Zito PM. Topical Corticosteroids. [Updated 2020 Sep 29]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing;
2020 Jan-.