Introduction

TCS, introduced into dermatologic therapy in

1952, (hydrocortisone by Sulzberger and
Witten)
Most commonly used drugs in dermatological
practice
Play a vital role in dermatologists armory for
treatment of a large number of inflammatory
disorders
However, they can act as double-edged sword
if misused
Need judicious handling by both prescriber as
well as patient
Chief seduction of TC lies in rapidity of
symptomatic relief in almost any dermatosis
This often prompts busy physician to reverse
natural order of diagnosis followed by treatment
Even incorrect use, for instance in infectious
dermatoses, produces an initial improvement in
symptoms
Apart from their anti-inflammatory effect, TC also
have potent antipruritic, vasoconstrictive,
antiproliferative, melanopenic, sex-hormonelike
and immunosuppressive effects on skin
All these can lead to significant local adverse
effects if TCs are used indiscriminately

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TCS are misused both by prescribing doctor and
patient themselves, as it gives instant relief to
signs and symptoms
Face is the commonest site of such misuse as its
effect is cosmetically appreciable, most often used
as fairness cream
Sequence events that lead to steroid abuse is as
follows-
Doctor will prescribe moderately potent steroid to get
benefit and avoid side effects of potent steroid, for some
dermatosis
Impressed by response, patient continues to use it and
often refer to friends also
Effect of steroid reduces due to tachyphylaxis and
patient is forced to use potent steroid and cycle
continues
Nonmedical advisers
Friends, neighbors, beauticians, barbers, etc.
Telling use it as fairness/cosmetic creams, anti-acne, anti-
fungal therapy and for skin eruptions
Tendency to reuse old prescription for a recurrent or
new rash
Prescription sharing with relatives and friends on
presumption that similar looking skin problems can
be self-treated
Easy availability, asking without a valid prescription
at chemist shop
To prescribe rationally, India has only a little over
6500 qualified dermatologists to cater to a population
of over 1.2 billion


Brand names and composition of topical
corticosteroid-containing products
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Source and reason for using preparation in 140
patients who misused topical corticosteroids
Effects and side-effects of TCs depend mainly
on
Thickness of skin
Potency of TC
Amount of absorption
Factors affecting absorption of the drug
Vehicle,
site and
frequency of application,
duration of therapy,
barrier function and condition of skin
GUIDELINES FOR SELECTION OF AN APPROPRIATE TCS

Low to medium potency agents generally are used to treat
acute inflammatory skin lesions of face and intertriginous
areas,
High potent agents are often required to treat chronic,
hyperkeratotic, or lichenified lesions on palms and soles
Applied once or twice daily
Greater frequency of application may be necessary for
palms or soles
Every-other-day or week- end-only application may be
effective in treatment of several chronic conditions
Lower-potency agents are preferentially used in infants
and elderly because of concerns about an increased
surface-to-weight ratio and increased skin fragility,
respectively.
Penetration varies between eyelid and plantar
skin about 300-fold

HUMAN MODELS OF TESTING CORTICOSTEROID
EFFICACY AND STRENGTH
Vasoconstriction test
After applying a defined quantity (eg, 5 mg) of Cs preparation to
a defined skin area, vasoconstriction is assessed visually or by
means of infrared reflection photometry
Ultraviolet erythema test
TCS is applied 24 hours prior to UVA or UVB light exposure
Erythema is induced by applying 3 fold MED
7 hr after UV exposure, extent of the erythema is scored and
treated sites are compared with untreated ones
Pyrexial erythema test
Intracutaneous injection of a defined quantity of bacterial pyrogen
(purified lipopolysaccharide of Salmonella abortus equiis)
Local inflammation with and without application of topical
corticosteroid is evaluated at 12 hours

ADVERSE EFFECTS OF TOPICAL
CORTICOSTEROIDS

Under normal conditions, up to 99% of applied
topical corticosteroid is removed , only 1% is
therapeutically active
Local adverse events of corticosteroid use are far
more prevalent than systemic reactions
Adverse effects of TCS

Atrophic changes
Steroid atrophy
Telangiectasia
Striae
Purpura
Stellate pseudoscars
Ulceration
Easy bruising
Infections
Masked microbial infections
(tinea incognito)
Aggravation of cutaneous
candidiasis, herpes or demodex
Reactivation of Kaposi sarcoma
Granuloma gluteale infantum

Ocular changes
Ocular hypertension
Glaucoma
cataract
Pharmacologic effects
Steroid rebound, steroid
addiction, tachyphylaxis
Miscellaneous
Steroid acne
Perioral dermatitis
Steroid rosacea
Topical steroid-dependent face
(TSDF) or red face syndrome
Hirsutism
Hyperpigmentation
Hypopigmentation
Photosensitization
Rebound flare (psoriasis)
Atrophy

Reflected by increased transparency and shininess
of skin, as well as appearance of striae
Atrophy recognized as M/c adverse effect of TCS
Dermal atrophy is probably caused by decreased
fibroblast growth and reduced synthesis of collagen
and acid mucopolysaccharides
Intertriginous areas are particularly susceptible,
probably owing to thinner skin, increased moisture,
elevated temperature, and partial occlusion
provided by skin in these sites
Telangiectasia
CS stimulate human dermal microvascular
endothelial cells, leading to the occurrence of
telangiectasia.
Characterized by an abnormal dilatation of capillary
vessels and arterioles

Striae
Visible linear scars, form in areas of dermal damage,
presumably during mechanical stress
Develop with an initial inflammation and edema of
dermis, followed by deposition of dermal collagen
along lines of mechanical stress
Histologically, represent scar tissue and therefore,
once developed, are permanent.


Purpura, stellate pseudoscars, and
ulcerations

Arise when severe steroid induced dermal atrophy
and loss of intercellular substance occur, causing
blood vessels to lose their surrounding dermal matrix.
Fragility of dermal vessels leads to purpuric,
irregularly shaped, hypopigmented, depressed scars
stellate pseudoscars most frequently develop over
extremities, mostly on severely atrophic,
telangiectatic purpuric skin
True ulceration from continued abuse of
corticosteroids has also been reported
A, Steroid atrophy on dorsum of hand
with hyperpigmentation as a consequence
of easy bruising caused by rarefaction of
connective tissue. Stellate pseudoscars
and increased wrinkling are also apparent

B, Thickened lichenified skin, severe
epidermal atrophy, and erythema after
inappropriate use of high-potency
corticosteroids on eyelids.
Striae


Steroid rosacea
Dermatoses of the face are usually steroid-sensitive and
do not require potent formulations
Classical history of steroid rosacea begins in a middle
aged woman with intermittent papules and pustules
that are initially controlled with steroids of low potency
Subsequently lesions may reappear and prompt
continued use of greater- potency topical corticosteroid

Hypertrichosis
Promote growth of vellus hair by means of an unknown
mechanism
Darker hairs may persist for months after withdrawal of
steroids

(a) Marked atrophy and telangiectasia, (b) Severe exacerbation of acne with crusted
and nodular lesions, (c) Tinea incognito after prolonged application of a super-potent
TCs, (d) TCs-induced hypertrichosis,
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Acne

Can rapidly induce an acneiform eruption
Attributed to degradation of follicular epithelium,
resulting in extrusion of follicular content
Initially lead to suppression of inflammatory papules
and pustules
Become more resistant upon recurrence, producing
clinical picture of TCS induced acnelike lesion

Steroid abuse in a patient with atopic dermatitis showing generalized
facial erythema, patchy hyperpigmentation on the forehead, increased
atrophy, and wrinkles around eyes. This patient has continued treatment
with stronger derivatives because of loss of effect (tachyphylaxis).
Perioral dermatitis

A facial eruption, composed of
follicular papules and pustules
on an erythematous
background
Begin in a perioral distribution,
with prominent sparing of skin
adjacent to vermilion border
Most frequently observed in
young women,may be seen in
men and children
Caused by long-term use of
potent CS on face
A, Long-term inadvertent use of corticosteroids for treatment of perioral and
cheek dermatitis. B, atrophic skin and white scarring, along with telangiectases
(e) hypopigmentation: sparing of the periorbital area (f) topical steroid-dependent
face" with bright erythema and monomorphic papules
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Vol 77 | Issue 2
Steroid addiction
Patients continue treatment because of
concerns that acne, rosacea, perioral
dermatitis, or telangiectasia may flare up
when treatment is withdrawn
Some cases may also present as red
burning skin syndrome
Hypopigmentation

Decreased
pigmentation after
topical use is quite
common
Steroids probably
interfere with
synthesis of melanin
by smaller
melanocytes, leading
to patchy areas of
hypopigmentation
Generally reversible
upon
discontinuation

Hypopigmentation and
hyperpigmentation, easy bruising,
telangiectases and atrophy on left
forearm.
Tinea incognito
of leg
Bruising, brownish discoloration of skin,
and scarring in a 74- year-old woman with
atopic dermatitis.
Aggravation of cutaneous infections

Common and often occur early in therapy
P. versicolor, onychomycosis, dermatophytosis, and
disseminated cutaneous Alternaria infection
Tinea incognito
Marked tinea infections, transformed into unrecognizable cutaneous
eruptions
Prolongation or mitigation of herpes simplex, molluscum
contagiosum, and scabies infection have been reported
Granuloma gluteale infantum
A persistent reddish-purple, granulomatous, papulonodular eruption
that rarely occurs on buttocks, thighs, or inguinal fold in children
Well-known consequence of diaper dermatitis that is being treated
with corticosteroids
Delayed wound healing
keratinocytes (epidermal atrophy, delayed re-
epithelialization)
Fibroblasts (reduced collagen and ground substance,
resulting in dermal atrophy and striae)
Vascular connective tissue support (telangiectasia, purpura,
easy bruising), and
Impaired angiogenesis (delayed granulation tissue
formation)
Decreases in skin elasticity
Epidermal barrier disturbance
Decreased formation of lipid lamellar bodies and delayed
barrier recovery (ie, increased transepidermal water loss)
May theoretically worsen barrier impairment in atopic
dermatitis and psoriasis


Contact sensitization to TCS
Generally rare, 0.2% and 6%.
Nonfluorinated corticosteroids (eg, hydrocortisone,
hydrocortisone17-butyrate, and budesonide) result in a
higher prevalence of contact allergy
Binding to amino acid arginine as part of certain proteins
seems to be a prerequisite for allergic reactions to
corticosteroids
A classification scheme based on structural relation of
steroid molecule has been devised for cross-reactivity
Representative agents hydrocortisone (group A),
triamcinolone acetonide (group B), betamethasone (group
C), and hydrocortisone butyrate (group D), is useful for
clinical tests of contact allergy
Rare systemic adverse events of TCS

Optimizing the use of TCS

To prescribe for appropriate dermatoses.

To use appropriate potency and strength of TC to achieve
disease control.

To maintain with a less potent preparation or reduce
frequency of application after satisfactory response.

To taper off treatment upon complete remission of skin
diseases.

To be extra careful when prescribing topical steroid over
certain locations (e.g. scrotum, face, and flexures).

Optimizing the use of TCS

To be especially considerate when prescribing to elderly
and children.

To be aware of adverse effects and act immediately to
counteract them.

To avoid home-made dilutions of TC and prescribing TC in
combination with antimicrobial and antifungal.

To resist temptation to use TC for an undiagnosed rash; this
makes possibility of correct diagnosis even bleaker in future