Chapter 216. Topical Corticosteroids
Chapter 216. Topical Corticosteroids
Chapter 216. Topical Corticosteroids
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Fitzpatrick's Dermatology in General Medicine, 8e
Chapter 216. Topical Corticosteroids
Isabel C. Valencia; Francisco A. Kerdel
Topical Corticosteroids: Introduction
Topical Corticosteroids at a Glance
Most frequently prescribed of all dermatologic drug products.
Are effective at reducing the symptoms of inflammation, but do not address the underlying cause of the disease.
Topical glucocorticoid research has focused on strategies to optimize potency while minimizing side effects.
The new molecules have an overall higher antiinflammatory effect, good compliance (only once daily application), rarely induce crosssensitivity
reactions and have weak atrophogenic properties.
Mechanism of Action
Corticosteroids have specific and nonspecific effects that are related to different mechanisms of action, including antiinflammatory,
immunosuppressive, antiproliferative, and vasoconstrictive effects. Most of their actions are mediated by an intracellular receptor called the
glucocorticoid receptor. The glucocorticoid receptor αisoform is located in the cytosol, binds glucocorticoids, and translocates to a region of the
nuclear DNA known as the corticosteroid responsive element, where it is then able to stimulate or inhibit transcription of the adjacent genes, thus
regulating the inflammatory process.1 The glucocorticoid receptor βisoform does not bind glucocorticoids, but is able to bind the
antiglucocorticoid/antiprogestin compound RU486 to regulate gene expression.2 The glucocorticoid receptor β can attenuate the ligandmediated
transactivation of hormonesensitive genes by the αisoform and may be an important marker of steroid insensitivity.3
AntiInflammatory Effects
Corticosteroids are thought to exert their potent antiinflammatory effects by inhibiting the release of phospholipase A2, an enzyme responsible for
the formation of prostaglandins, leukotrienes, and other derivatives of the arachidonic acid pathway. Corticosteroids also inhibit transcription factors,
such as activator protein 1 and nuclear factor κβ, which are involved in the activation of proinflammatory genes. Genes known to be upregulated by
corticosteroids and that play a role in the resolution of inflammation include lipocortin and p11/calpactinbinding proteins, both involved in the
release of arachidonic acid.1,4,5 Lipocortin I inhibits phospholipase A2, reducing the release of arachidonic acid from phospholipids.1,6,7
Corticosteroids also decrease the release of interleukin1α (IL1α), an important proinflammatory cytokine, from keratinocytes.1,8 Other proposed
mechanisms for the antiinflammatory effects of corticosteroids include inhibition of phagocytosis and stabilization of lysosomal membranes of
phagocytizing cells.9
Immunosuppressive Effects
The effectiveness of corticosteroids is, in part, also due to their immunosuppressive properties. Corticosteroids suppress the production and effects
of humoral factors involved in the inflammatory response, inhibit leukocyte migration to sites of inflammation, and interfere with the function of
endothelial cells, granulocytes, mast cells, and fibroblasts.1,10–12 Several studies have shown that corticosteroids can cause mast cell depletion in the
skin.13 Experiments have also shown that topical corticosteroids cause local inhibition of chemotaxis of neutrophils in vitro, and decrease the number
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Chapter 216. Topical Corticosteroids, Isabel C. Valencia; Francisco A. Kerdel Page 1 / 14
14,15 Corticosteroids reduce eosinophilia in patients with asthma. They also reduce Tcell proliferation and induce T
of Ia+ Langerhans cells in vivo.
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cell apoptosis, in part from inhibition of the Tcell growth factor IL2.1,16 In addition, several cytokines are directly affected by corticosteroids,
including IL1, tumor necrosis factorα, granulocytemacrophage colonystimulating factor, and IL8. These effects may also be a result of the steroid
Immunosuppressive Effects
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The effectiveness of corticosteroids is, in part, also due to their immunosuppressive properties. Corticosteroids suppress the production and effects
of humoral factors involved in the inflammatory response, inhibit leukocyte migration to sites of inflammation, and interfere with the function of
endothelial cells, granulocytes, mast cells, and fibroblasts.1,10–12 Several studies have shown that corticosteroids can cause mast cell depletion in the
skin.13 Experiments have also shown that topical corticosteroids cause local inhibition of chemotaxis of neutrophils in vitro, and decrease the number
of Ia+ Langerhans cells in vivo.14,15 Corticosteroids reduce eosinophilia in patients with asthma. They also reduce Tcell proliferation and induce T
cell apoptosis, in part from inhibition of the Tcell growth factor IL2.1,16 In addition, several cytokines are directly affected by corticosteroids,
including IL1, tumor necrosis factorα, granulocytemacrophage colonystimulating factor, and IL8. These effects may also be a result of the steroid
action on antigen presenting cells.17
Antiproliferative Effects
The antiproliferative effect of topical corticosteroids is mediated by inhibition of DNA synthesis and mitosis, partly explaining the therapeutic action of
these drugs in scaling dermatoses.18 They are known to reduce the keratinocyte size and proliferation. Fibroblast activity and collagen formation are
also inhibited by topical corticosteroids.19
Vasoconstriction
The mechanism by which corticosteroids induce vasoconstriction is not yet completely clear. It is thought to be related to inhibition of natural
vasodilators such as histamine, bradykinins, and prostaglandins.1,20,21 Topical steroids cause capillaries in the superficial dermis to constrict, thus
reducing erythema. The ability of a given corticosteroid agent to cause vasoconstriction usually correlates with its antiinflammatory potency, and
thus, vasoconstriction assays are often used to predict the clinical activity of an agent. These assays, in combination with doubleblind clinical trials,
have been used to separate the topical corticosteroids into seven classes based on potency. Class 1 includes the most potent, while class 7 contains the
least potent. eTable 2160.1 lists many of the available topical corticosteroids according to this classification. Notice that the same drug can be found in
different potency classifications depending on the delivery vehicle used.
eTable 2160.1 Potency Ranking of Selected Topical Corticosteroid Preparations
Generic Name
Class 1—Superpotent
Betamethasone dipropionate 0.05% optimized vehicle
Clobetasol propionate 0.05%
Diflorasone diacetate 0.05%
Fluocinonide 0.1% optimized vehicle
Flurandrenolide 4 mcg/cm2
Halobetasol propionate 0.05%
Class 2—Potent
Amcinonide 0.1%
Betamethasone dipropionate 0.05%
Desoximetasone 0.25%
Desoximetasone 0.05%
Diflorasone diacetate 0.05%
Fluocinonide 0.05%
Halcinonide 0.1%
Mometasone furoate 0.1%
Class 3—Potent, upper midstrength
Amcinonide 0.1%
Betamethasone dipropionate 0.05%
Betamethasone valerate 0.1%
Diflorasone diacetate 0.05%
Fluocinonide 0.05%
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Fluticasone propionate 0.005%
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Triamcinolone acetonide 0.5%
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Class 4—Midstrength
Class 3—Potent, upper midstrength
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Amcinonide 0.1%
Betamethasone dipropionate 0.05%
Betamethasone valerate 0.1%
Diflorasone diacetate 0.05%
Fluocinonide 0.05%
Fluticasone propionate 0.005%
Triamcinolone acetonide 0.5%
Class 4—Midstrength
Betamethasone valerate 0.12%
Clocortolone pivalate 0.1%
Desoximetasone 0.05%
Fluocinolone acetonide 0.025%
Flurandrenolide 0.05%
Hydrocortisone probutate 0.1%
Hydrocortisone valerate 0.2%
Mometasone furoate 0.1%
Prednicarbate 0.1%
Triamcinolone acetonide 0.1%
Class 5—Lower midstrength
Betamethasone dipropionate 0.05%
Betamethasone valerate 0.1%
Fluocinolone acetonide 0.025%
Fluocinolone acetonide 0.01%
Flurandrenolide 0.05%
Fluticasone propionate 0.05%
Hydrocortisone butyrate 0.1%
Hydrocortisone valerate 0.2%
Prednicarbate 0.1%
Triamcinolone acetonide 0.1%
Triamcinolone acetonide 0.025%
Class 6—Mild strength
Alclometasone dipropionate 0.05%
Desonide 0.05%
Fluocinolone acetonide 0.01%
Triamcinolone acetonide 0.025%
Class 7—Least potent
Topicals with dexamethasone, flumethasone, hydrocortisone, methylprednisolone, prednisolone
Pharmacokinetics
Corticosteroids have a basic skeletal structure comprising 17 carbon atoms arranged in three sixmembered rings and one fivemembered ring.
Modifications of cortisol (Fig. 2161), by addition or alteration of functional groups at certain positions, have led to compounds with variable anti
inflammatory potency, glucocorticosteroid versus mineralocorticoid activity, and adverse effects.22
Figure 2161
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Modifications of cortisol (Fig. 2161), by addition or alteration of functional groups at certain positions, have led to compounds with variable anti
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inflammatory potency, glucocorticosteroid versus mineralocorticoid activity, and adverse effects.22
Figure 2161
Basic steroid molecule.
Topical corticosteroid research has focused on strategies to optimize potency while minimizing side effects. One strategy is to develop compounds
with enhanced antiinflammatory effects and minimal unwanted atrophogenic and adrenal suppressive effects. In this sense, progress has been made
with the development of glucocorticoid molecules that, while retaining high activity in the skin following topical application, are quickly broken down
into inactive metabolites, thereby mitigating systemic and possibly some local toxic effects (“soft” glucocorticoids). Some of these compounds include
the diesters 17,21hydrocortisone aceponate and hydrocortisone 17butyrate21propionate, prednicarbate, mometasone furoate,
methylprednisolone aceponate, alclometasone dipropionate, and carbothioates such as fluticasone propionate.1,23 This last agent is classified as a
potent corticosteroid with lower potential to cause skin atrophy and adrenal suppression due to its high lipophilicity, high glucocorticoid receptor
binding and activation and rapid metabolism in the skin.24 It offers the advantage of once daily application and infrequent local allergic reactions.
Mometasone furoate also has highly antiinflammatory effects with low incidence of adrenal suppression.1 Hydrocortisone aceponate, prednicarbate,
and methylprednisolone aceponate have significant antiinflammatory effects, but the least capacity to induce skin atrophy; therefore, they can be
used to treat areas such as the face, the scrotum, and large body surface areas in children, with minimal adverse effects.1,25
Before choosing a topical glucocorticoid preparation, one must consider the patientrelated and drugrelated factors that can affect its systemic
absorption. The age of the patient, the extent and location of the body surface area to be treated and the presence or absence of skin inflammation,
greatly affect the activity of the topical agent. Penetration of the glucocorticoid varies according to the skin site, which, in turn, is related to the
thickness of the stratum corneum and the vascular supply to the area. For example, penetration of topical steroids through the eyelids and scrotum is
four times greater than for the forehead and 36 times greater than for the palms and soles. Inflamed, moist, and denuded skin also shows increased
penetration. Areas of the body where the skin is inherently thin not only allow for increased penetration of the drug but also are more susceptible to
develop side effects than other areas where the skin is thick. Potent topical steroids (classes 1 and 2) should rarely, if ever, be used in the areas with the
highest level of penetration, such as the eyelids. The concentration of the therapeutic agent used, the duration of the application, the use of occlusive
dressings, the elected vehicle, and the intrinsic characteristics of the chosen molecule, can also affect the absorption and the degree of adverse
effects.26,27 The target site for topical corticosteroids is the viable epidermis or dermis, and clinical response to a formulation is directly proportional
to the concentration of corticosteroid achieved at the target site. A comparison study of skin concentrations after topical versus oral corticosteroid
treatment found that most topical corticosteroids have the potential to achieve greater effective drug levels in the superficial layers of the skin than
those achieved with standard doses of oral prednisone. Therefore, the apparently greater efficacy of oral corticosteroid therapy may be due in part to
poor patient compliance with topical therapy.28
Topical corticosteroids are compounded in several formulations and with varying strengths. Recent research has emphasized the importance of
treatment adherence in the management of skin conditions. As such, newer formulations including spray, foam, lotion, hydrogel, and shampoo
formulations have been developed to improve patient convenience and acceptance, without sacrificing the efficacy, safety and tolerability of the
traditional ointment and cream formulations. A recent systematic review of the literature found that while there are few direct comparison studies
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between clobetasol propionate, a class 1 steroid, in different vehicles, the efficacy rates for more recent formulations is roughly comparable to that of
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clobetasol ointment in the treatment of psoriasis. The most common adverse effect was mild and transient stinging/burning at the lesion site, which
may be due to the alcohol content found in these formulations.29 None of the clinical trials directly compared these formulations with one
poor patient compliance with topical therapy.28 Access Provided by:
Topical corticosteroids are compounded in several formulations and with varying strengths. Recent research has emphasized the importance of
treatment adherence in the management of skin conditions. As such, newer formulations including spray, foam, lotion, hydrogel, and shampoo
formulations have been developed to improve patient convenience and acceptance, without sacrificing the efficacy, safety and tolerability of the
traditional ointment and cream formulations. A recent systematic review of the literature found that while there are few direct comparison studies
between clobetasol propionate, a class 1 steroid, in different vehicles, the efficacy rates for more recent formulations is roughly comparable to that of
clobetasol ointment in the treatment of psoriasis. The most common adverse effect was mild and transient stinging/burning at the lesion site, which
may be due to the alcohol content found in these formulations.29 None of the clinical trials directly compared these formulations with one
another.30,31
Increasing hydration of the stratum corneum can enhance absorption of topical corticosteroids by four to five times. Absorption is also enhanced by
ten times with occlusion.32 A retrospective study of wet dressings used with topical corticosteroids (hydrocortisone 1% cream to the face and folds
and triamcinolone 0.1% cream from the neck down) for adults with recalcitrant pruritic dermatoses of different etiologies, alleviated the pruritus in
98% of the patients at dismissal. The enhanced corticosteroid penetration is only one of the numerous benefits of the wet dressings.33
Indications
Topical corticosteroids are recommended for their antiinflammatory activity in inflammatory skin diseases, but they can also be used for their
antimitotic effects and their capacity to decrease the synthesis of connective tissue molecules.1 Certain variables must be considered when treating
skin disorders with topical glucocorticoids. For example, the responsiveness of diseases to topical glucocorticoids varies. In this setting, diseases can
be divided into the three categories shown in Table 2161: (1) highly responsive, (2) moderately responsive, and (3) least responsive.
Table 2161 Responsiveness of Dermatoses to Topical Application of Corticosteroids
Pediatric Uses
Topical glucocorticoids are highly effective, and few side effects are observed when a lowpotency preparation is used for brief periods of time without
occlusion in children. However, children and, in particular, infants, are at an increased risk of absorbing topical corticosteroids for several reasons.
They have a higher ratio of skin surface area to body weight and application to a given area results in a greater potentially systemic dose of steroid.
Infants may also be less able to metabolize potent glucocorticoids rapidly.34 Premature infants are especially at risk because their skin is thinner and
the penetration rate of topically applied drugs is greatly increased.35 Application of topical steroids to the diaper area results in occlusion of the
steroid by the diaper, and increased penetration occurs. Excess absorption of topical glucocorticoids can suppress endogenous cortisol production.
Consequently, subsequent cessation of topical steroid therapy after an extended treatment period can, albeit rarely, result in an addisonian crisis.
Deaths from addisonian crisis have been reported with the use of topical steroids, and the risk of this occurring is greater in children.36 Chronic
suppression of cortisol production can also lead to growth retardation. A morning plasma cortisol level can be performed to screen for adrenal
suppression, although ACTH stimulation testing with cosyntropin is more accurate. If suppression is present, the child should be slowly weaned from
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the steroids to prevent these complications.
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Corticosteroids have been used with success for atopic dermatitis for several decades. Placebocontrolled trials have found them effective in 75% or
more of patients with atopic dermatitis when compared with fewer than 30% of placebotreated patients.37 They are important for managing acute
the penetration rate of topically applied drugs is greatly increased.35 Application of topical steroids to the diaper area results in occlusion of the
steroid by the diaper, and increased penetration occurs. Excess absorption of topical glucocorticoids can suppress endogenous cortisol production.
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Consequently, subsequent cessation of topical steroid therapy after an extended treatment period can, albeit rarely, result in an addisonian crisis.
Deaths from addisonian crisis have been reported with the use of topical steroids, and the risk of this occurring is greater in children.36 Chronic
suppression of cortisol production can also lead to growth retardation. A morning plasma cortisol level can be performed to screen for adrenal
suppression, although ACTH stimulation testing with cosyntropin is more accurate. If suppression is present, the child should be slowly weaned from
the steroids to prevent these complications.
Corticosteroids have been used with success for atopic dermatitis for several decades. Placebocontrolled trials have found them effective in 75% or
more of patients with atopic dermatitis when compared with fewer than 30% of placebotreated patients.37 They are important for managing acute
flares. As with other skin conditions, selecting the appropriate strength according to the body site, the extent of involvement and the flare intensity is
essential for treatment success.27 Education of the patients and caregivers is critical to improve adherence to the prescribed medication and optimize
compliance. Results from largescale surveys show that patients/caregivers overestimate the actual risks of topical corticosteroids (“steroid phobias”)
leading to treatment noncompliance.38,39 Adequate time should be spent transmitting the important role of intermittent topical corticosteroid
therapy, and the beneficial riskbenefit ratio with their appropriate use.40
Hemangiomas of infancy show a good or partial response to treatment with ultrapotent topical glucocorticoids in 74% of infants. The majority
reported accelerated cessation of growth. Small, superficial hemangiomas, particularly at sites prone to ulceration, disfigurement or both, and small
periocular lesions that have not yet caused significant visual impairment are the best candidates for therapy.41 The mechanism of action by which
corticosteroids act in hemangiomas to decrease proliferation is unknown. Intralesional corticosteroid injection of hemangiomas before and after
treatment, have revealed an increase in mast cells, reduced transcription in several cytokines and enhanced transcription of cytochrome b gene.42
Geriatric Uses
Elderly patients similarly can have thin skin, which allows for increased penetration of topical glucocorticoids. They are also more likely to have
preexisting skin atrophy secondary to aging and may be diaper dependent, so the same precautions used in the treatment of infants should be used
when treating elderly patients.
Uses in Pregnancy
Appropriate human studies using topical glucocorticoids in pregnancy have never been undertaken. Studies in animals, however, show that topical
steroids are systemically absorbed and may cause fetal abnormalities, especially when used in excessive amounts, under occlusive dressings, for
prolonged periods of time, or when the more potent agents are used. Most topical steroids are rated by the US Food and Drug Administration as
category C drugs, which imply that caution must be exercised when used in pregnancy. A recent, systematic review of the safety of topical
corticosteroids in pregnancy performed by Chi et al, found that the current data is inconclusive and limited and unable to detect an association
between topical corticosteroids and congenital abnormalities, preterm delivery, mode of delivery or stillbirth. The current evidence shows no
statistically significant effects for pregnant women who use topical corticosteroids compared with unexposed women. However, in a small cohort
study of participants from a single maternity center, there appears to be an association of highly potent corticosteroids with low birth weight. Most of
the previous studies only assessed the risk for congenital abnormality or orofacial cleft. Further cohort studies with comprehensive outcome
measures (including fetal growth, preterm birth, and birth death), consideration of corticosteroid potency, dosage and indications, and a large sample
size are required in order to detect a small risk.43 It is currently unknown whether topical glucocorticoids are excreted in breast milk; however, they
should be used with caution in breastfeeding mothers and should never be used on the breasts before breastfeeding.
Dosing Regimen
The frequency of topical application of corticosteroids was developed in an empirical manner, with most textbooks and physicians recommending
twicedaily use. For superpotent corticosteroids, oncedaily application is considered as beneficial as twicedaily application. Likewise, there is at best
a slight difference with once versus twice daily application of potent or moderately potent corticosteroids. These observations suggest that oncedaily
application of topical corticosteroids may be as effective as twice daily, while decreasing the risks of side effects, tachyphylaxis, and cost of therapy,
and improving patient compliance.44 Tachyphylaxis has been demonstrated in experimental conditions by diminished vasoconstriction, rebound of
DNA synthesis, and recovery of histamine wheals after application of topical steroids in patients with a history of longterm topical steroid usage.45
As a working rule in adults, no more than 45 g/week of potent or 100 g/week of weak or moderately potent topical corticosteroid should be applied
(without occlusion) if systemic absorption is to be avoided.46
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Clinical Formulations
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Topical steroids come in many different vehicles and dosage forms. The clinical potency of a topical corticosteroid depends not only on the
application of topical corticosteroids may be as effective as twice daily, while decreasing the risks of side effects, tachyphylaxis, and cost of therapy,
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and improving patient compliance.44 Tachyphylaxis has been demonstrated in experimental conditions by diminished vasoconstriction, rebound of
DNA synthesis, and recovery of histamine wheals after application of topical steroids in patients with a history of longterm topical steroid usage.45
As a working rule in adults, no more than 45 g/week of potent or 100 g/week of weak or moderately potent topical corticosteroid should be applied
(without occlusion) if systemic absorption is to be avoided.46
Clinical Formulations
Topical steroids come in many different vehicles and dosage forms. The clinical potency of a topical corticosteroid depends not only on the
inherent potency of the molecule but also on factors such as the vehicle and the nature of the skin onto which it is applied. The vehicle in which the
steroid is incorporated may be as important as the steroid molecule itself because the vehicle affects the amount of steroid that is released in any
given period of time. Very occlusive vehicles, such as ointments, potentiate glucocorticoid effects because they provide increased hydration of the
stratum corneum and increase its permeability. By covering the skin with an occlusive dressing such as plastic wrap, this effect can be heightened
as much as 100fold. The solubility of the glucocorticoid in the vehicle also affects penetration into the epidermis. Propylene glycol is one agent
commonly used to dissolve the glucocorticoid in the vehicle, and it is found in many topical glucocorticoid preparations.32 In general, compounds
that contain higher amounts of propylene glycol tend to be more potent.
Treatment of the skin before application of the topical steroid may also affect the absorption of the compounds into the skin. For example, use of
keratolytics or fat solvents such as acetone enables increased penetration by disrupting the epidermal barrier. Tape stripping of the skin also
increases the absorption of hydrocortisone by 78% to 90%.33
The major classes of formulations for corticosteroids are ointments, creams, lotions, and gels. Ointments are the best preparation when treating
dry skin conditions because they provide the most moisture and are useful for treating conditions on areas of the body with thick skin, such as the
palms and soles. Peanut oil has also been combined with steroids to form a preparation that is thinner and easier to apply while retaining the
hydrating capability of ointments. However, patients may feel that ointments and oils are too greasy and prefer the use of creams that are
cosmetically more acceptable, but provide less hydration of the skin. New emollient creams have been devised that contain an increased amount
of petrolatum but with less greasiness than ointments, and some patients find them more cosmetically appealing.
Certain body areas require the use of specific vehicles to obtain good compliance. For example, lotions and creams are preferred in acute
eczema as well as dermatoses that involve large surface body areas. Lotions, solutions, and gels have less penetration than ointments but are
useful in treating hairbearing areas, such as the scalp, where greasiness is cosmetically displeasing to the patient. Steroidimpregnated tapes are
useful because they provide occlusion with increased penetration and provide protection of the skin lesion from manipulation, such as scratching,
by the patient. Sprays containing steroids are available and represent a convenient mode of applying these agents. Additionally, foam products
have been added to currently available topical formulations. They are highly efficacious, cosmetically superior, and well tolerated. (For more
discussion on vehicles for topical preparations, see Chapter 214.)
Initiating Therapy
Some general principles should be remembered when initiating topical corticosteroids; these are outlined in Box 2161.1,47
Box 2161 Principles When Initiating Topical Steroid Therapy
Initiate lowest potency to sufficiently control disease.
Prolonged use of an agent of insufficient potency should be avoided.
When large surface areas are involved, treatment with low to medium potency preparations is recommended.
Highly responsive diseases will usually respond to weak steroid preparations, whereas lessresponsive diseases require medium or highpotency
topical steroids.
Lowpotency, ideally nonhalogenated preparations should be used on the face and intertriginous areas.
Very potent corticosteroids, frequently under occlusion, are usually required for hyperkeratotic or lichenified dermatoses and for involvement of
palms and soles.
Because of increased body surface area to body mass index ratio and increased risk of systemic absorption, high potency preparations and
halogenatedmedium potency preparations, should be avoided in infants and young children, other than for shortterm application.
See reference 40.
Monitoring Therapy
Application of corticosteroids to large surface areas, occlusion, higher concentrations, or more potent derivatives directly increases the risk of
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hypothalamic–pituitary–axis (HPA) suppression. If the latter is suspected, laboratory analyses that include a complete blood cell count, a chemistry
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panel, and a baseline morning cortisol level should be performed. In a patient with confirmed HPA suppression, gradual reduction of potency and
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amount of topical steroid, and possibly the simultaneous institution of oral steroid supplementation, are needed.48
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Monitoring Therapy
Application of corticosteroids to large surface areas, occlusion, higher concentrations, or more potent derivatives directly increases the risk of
hypothalamic–pituitary–axis (HPA) suppression. If the latter is suspected, laboratory analyses that include a complete blood cell count, a chemistry
panel, and a baseline morning cortisol level should be performed. In a patient with confirmed HPA suppression, gradual reduction of potency and
amount of topical steroid, and possibly the simultaneous institution of oral steroid supplementation, are needed.48
Risks and Precautions
Local as well as systemic side effects have been documented with the use of topical corticosteroids. Under normal conditions, up to 99% of the applied
topical corticosteroid is cleared from the skin, and only 1% is therapeutically active. Cutaneous adverse effects can result from the small percentage of
percutaneously absorbed corticosteroid or may also result from its transient presence onto the skin. Continued use of topical corticosteroids may also
lead to tachyphylaxis.49
Considerations for prescribing topical corticosteroids to prevent side effects should be followed1,47,50,51 (Box 2162).
Box 2162 Continuing Use of Topical Steroids
Highly potent formulations should be used for short periods (2 to 3 weeks) or intermittently.
Once disease control is partially achieved, the use of a less potent compound should be initiated.
Reduce frequency of application (e.g., application only in the morning, alternateday therapy, weekend use) once disease control is partially achieved.
Topical corticosteroids should be avoided on ulcerated or atrophic skin, and on skin with coexistent infectious dermatoses.
Sudden discontinuation should be avoided after prolonged use to prevent rebound phenomena.
Special guidelines should be followed when treating certain body areas (e.g., intertriginous areas) or certain populations (e.g., children or the elderly)
to prevent the occurrence of local or systemic adverse effects.
Laboratory tests should be considered if systemic absorption of corticosteroids is suspected.
Use combination therapy when clinically indicated (e.g., addition of topical calcineurin inhibitor, tretinoin or calcipotriene).
Complications
Local adverse effects of topical corticosteroid use are more prevalent than systemic reactions. They are largely due to the antiproliferative effects of
these agents.49
Atrophic Changes
Skin atrophy is the most prominent cutaneous adverse effect, and involves both the epidermis and dermis. Dermal atrophy develops from the direct
antiproliferative effects of topical corticosteroids on fibroblasts, with inhibition of collagen and mucopolysaccharide synthesis, resulting in loss of
dermal support. Decreased synthesis of types I and III collagens after topical glucocorticoid use has been shown in numerous studies.52–54 Reduction
of glycosaminoglycan production has also been described.55 Levels of hyaluronan, the major glycosaminoglycan in the skin, are also rapidly
decreased after shortterm glucocorticoid treatment, because of decreased of hyaluronan synthesis.56 Fragmentation and thinning of elastic fibers
develop on the upper layers, whereas deeper fibers form a compact and dense network. As a result of these atrophic changes, there is vascular
dilatation, telangiectasias, purpura, easy bruising, stellate pseudoscars (purpuric, irregularly shaped, and hypopigmented atrophic scars), and
ulceration. Although atrophy is, to some extent, reversible, formation of striae, visible linear scars that form in areas of dermal damage presumably
during mechanical stress, are permanent.46
Acneiform Reactions
The development or exacerbation of dermatoses of the face, including steroid rosacea, acne, and perioral dermatitis, is a wellknown side effect of
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topical corticosteroids. Although steroids initially lead to the suppression of inflammatory papules and pustules, patients become addicted because
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they notice that the lesions flare when treatment is withdrawn. This frequently leads to the continued use of greater potency topical corticosteroids.
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For these reasons, steroid use should be discouraged in the treatment of rosacea and perioral and periocular dermatitis.
Prolonged corticosteroid treatment can also result in “steroid acne,” which is characterized by crops of dense, inflamed pustules in the same
ulceration. Although atrophy is, to some extent, reversible, formation of striae, visible linear scars that form in areas of dermal damage presumably
during mechanical stress, are permanent.46
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Acneiform Reactions
The development or exacerbation of dermatoses of the face, including steroid rosacea, acne, and perioral dermatitis, is a wellknown side effect of
topical corticosteroids. Although steroids initially lead to the suppression of inflammatory papules and pustules, patients become addicted because
they notice that the lesions flare when treatment is withdrawn. This frequently leads to the continued use of greater potency topical corticosteroids.
For these reasons, steroid use should be discouraged in the treatment of rosacea and perioral and periocular dermatitis.
Prolonged corticosteroid treatment can also result in “steroid acne,” which is characterized by crops of dense, inflamed pustules in the same
developmental stage. These lesions occur on the face, chest, and back (see Chapter 80). Patients with psoriasis are also susceptible to a
papulopustular flare after withdrawal of highpotency, topical corticosteroid therapy to an extensive surface area for a prolonged period of time.40
Hypertrichosis
Hypertrichosis occurs rarely in women and children who apply potent corticosteroids to the face. The mechanism is still unknown.1
Pigmentary Changes
Decreased pigmentation is a common side effect of topical steroid use. The pigment generally returns after discontinuation of therapy.
Development of Infections
Topical corticosteroids are responsible for exacerbating and/or masking cutaneous infectious diseases. The incidence of skin infection during
corticosteroid therapy varies but is probably between 16% and 43%.57 Tinea versicolor, disseminated Alternaria infection, and dermatophytosis,
including tinea incognito (masked dermatophyte infection), can develop. Granuloma gluteale infantum, characterized by reddish–purplish
granulomatous lesions on the diaper area, is a wellknown complication of diaper dermatitis that is being treated with corticosteroids. Candida
albicans is commonly recovered in these patients. Topical corticosteroids have also an effect on prolongation or worsening of herpes simplex,
molluscum contagiosum, and scabies infection.
Allergic Reactions
Allergic contact dermatitis from steroids should be suspected when its use worsens the dermatitis, does not lead to improvement or changes the
clinical pattern of disease. It occurs more commonly in patients with an impaired barrier function, such as patients with stasis dermatitis, leg ulcers and
atopic dermatitis.58 The prevalence of topical corticosteroid sensitization ranges between 0.2% and 6.0%, and increases with prolonged exposure and
selection of certain drugs.49,59,60 In a 6year retrospective study, 127 of 1,188 patients (10.7%) patch tested with topical corticosteroids showed a
positive reaction to at least one agent, with 56 patients reacting to multiple topical corticosteroids.61 Topical corticosteroids were recognized as the
American Contact Dermatitis Society's 2005 allergen of the year based on their prevalence.62 A classification has been created to determine cross
reactivity among the various available preparations. This classification has four groups on the basis of structure and crossreactivity patterns (Table
2162). Each class is represented by an agent.63 Class A is represented by the hydrocortisone type, class B by the acetonide steroids, class C by the
betamethasone type and class D, subdivided into two groups, D1 represented by betamethasone dipropionate and D2 by methylprednisolone
aceponate. Patchtest reactions to class A steroids are most common, whereas patchtest reactions to class C steroids are extremely rare. When an
allergy to a topical corticosteroid is highly suspected and patch testing is not available, the clinician should prescribe a class C steroid with a vehicle
that contains no allergens. Desoximethasone 0.25% ointment and 0.05% gel are the only two products that meet these criteria.64 The vehicle or the
preservative can also be responsible for the allergy to the corticosteroid preparation. A systematic review of ingredients in corticosteroid vehicles was
recently published. The authors found seven vehicle ingredients that are commonly used in topical corticosteroid preparations and are wellknown
allergens: (1) propylene glycol, (2) sorbitan sesquioleate, (3) formaldehydereleasing preservatives (imidazolidinylurea and diazolidinylurea), (4)
parabens, (5) methylchloroisothiazolinone/methylisothiazolinone, (6) lanolin, and (7) fragrance (see Box 2163). Of 166 topical corticosteroids, 128
(including all creams) had at least one of these vehicle components. More generic products were free of allergens than were the branded products.
Solutions and ointments were the least allergenic vehicles. The most commonly present potential allergens were propylene glycol and sorbitan
sesquioleate.64
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Table 2162 Classification of Corticosteroids by CrossReactivity
Chapter 216. Topical Corticosteroids, Isabel C. Valencia; Francisco A. Kerdel Page 9 / 14
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Structural
A B C D1 D2
Class
parabens, (5) methylchloroisothiazolinone/methylisothiazolinone, (6) lanolin, and (7) fragrance (see Box 2163). Of 166 topical corticosteroids, 128
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(including all creams) had at least one of these vehicle components. More generic products were free of allergens than were the branded products.
Solutions and ointments were the least allergenic vehicles. The most commonly present potential allergens were propylene glycol and sorbitan
sesquioleate.64
Table 2162 Classification of Corticosteroids by CrossReactivity
Structural
A B C D1 D2
Class
Adapted from Jacob SE, Steele T: Corticosteroid classes: a quick reference guide including patch test substances and crossreactivity. J Am Acad Dermatol 5 4(4):723727, 2006
Box 2163 Potential Allergens in Topical Corticosteroids Vehicles
Propylene glycol
Sorbitan sesquioleate
Methylchloroisothiazolinone/methylisothiazolinone
Lanolin
Parabens
Formaldehyde releasing preservatives (imidazolidinylurea/diazolidinylurea)
Fragrance
Systemic Adverse Effects
Ocular Effects
The development of glaucoma from the use of topical corticosteroids around the eye has been described.65–67 Prolonged corticosteroid use has also
led to vision loss.68
Suppression of the Hypothalamic–Pituitary–Adrenal Axis
Suppression of the HPA axis has been described with the use of potent topical corticosteroids. Iatrogenic Cushing syndrome and corticosteroid
related Addison crises have been described after prolonged use of potent topical corticosteroid preparations. A dose of 14 g/week of clobetasol
propionate or 49 g/week of betamethasone dipropionate is sufficient to suppress plasma cortisol levels.19 It is generally assumed that systemic effects
are more prevalent with high potency topical corticosteroids; however, a recent case report described a pediatric patient with Netherton syndrome
who developed Cushing syndrome from percutaneous absorption of hydrocortisone 1%, a lowpotency corticosteroid agent.69 Literature reviewing
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the potential effect of topical corticosteroids and vertical growth in atopic dermatitis is overall reassuring but has mixed results. Crosssectional
Chapter 216. Topical Corticosteroids, Isabel C. Valencia; Francisco A. Kerdel Page 10 / 14
studies have demonstrated that children with atopic dermatitis have diminished growth, 70,71 while others have found that temporary changes in
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cortisol levels do not affect eventual adult height.72 A recent controlled questionnaire study found that the overall height of children with atopic
73
Suppression of the HPA axis has been described with the use of potent topical corticosteroids. Iatrogenic Cushing syndrome and corticosteroid
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related Addison crises have been described after prolonged use of potent topical corticosteroid preparations. A dose of 14 g/week of clobetasol
propionate or 49 g/week of betamethasone dipropionate is sufficient to suppress plasma cortisol levels.19 It is generally assumed that systemic effects
are more prevalent with high potency topical corticosteroids; however, a recent case report described a pediatric patient with Netherton syndrome
who developed Cushing syndrome from percutaneous absorption of hydrocortisone 1%, a lowpotency corticosteroid agent.69 Literature reviewing
the potential effect of topical corticosteroids and vertical growth in atopic dermatitis is overall reassuring but has mixed results. Crosssectional
studies have demonstrated that children with atopic dermatitis have diminished growth,70,71 while others have found that temporary changes in
cortisol levels do not affect eventual adult height.72 A recent controlled questionnaire study found that the overall height of children with atopic
dermatitis treated with topical corticosteroids was unaffected.73
Metabolic Side Effects
Increased glucose production and decreased glucose use induce hyperglycemia and may lead to diabetes mellitus. Femoral avascular necrosis rarely
has been associated with the use of topical corticosteroids.74–76
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