Topical Corticosteroid Abuse - Copy

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Introduction

TCS, introduced into dermatologic therapy in1952, (hydrocortisone by Sulzberger andWitten)

Most commonly used drugs in dermatologicalpractice

Play a vital role in dermatologists’ armory fortreatment of a large number of inflammatorydisorders

However, they can act as double-edged swordif misused

Need judicious handling by both prescriber aswell as patient



Chief seduction of TC lies in rapidity ofsymptomatic relief in almost any dermatosis

This often prompts busy physician to reversenatural order of diagnosis followed by treatment

Even incorrect use, for instance in infectiousdermatoses, produces an initial improvement insymptoms

Apart from their anti-inflammatory effect, TC alsohave potent antipruritic, vasoconstrictive,antiproliferative, melanopenic, sex-hormonelikeand immunosuppressive effects on skin

All these can lead to significant local adverseeffects if TCs are used indiscriminately

IJDVL | March-April 2011 | Vol 77 | Issue 2



TCS are misused both by prescribing doctor andpatient 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 usedas fairness cream

Sequence events that lead to steroid abuse is asfollows- Doctor will prescribe moderately potent steroid to get

benefit and avoid side effects of potent steroid, for somedermatosis

Impressed by response, patient continues to use it andoften refer to friends also

Effect of steroid reduces due to tachyphylaxis andpatient is forced to use potent steroid and cyclecontinues





Brand names and composition of topical

corticosteroid-containing products

IJDVL | March-April 2011 | Vol 77 | Issue 2



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 intertriginousareas,

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 forpalms 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 infantsand elderly because of concerns about an increasedsurface-to-weight ratio and increased skin fragility,

respectively.



Penetration varies between eyelid and plantarskin about 300-fold







HUMAN MODELS OF TESTING CORTICOSTEROID

EFFICACY AND STRENGTH

Vasoconstriction test

After applying a defined quantity (eg, 5 mg) of Cs preparation toa defined skin area, vasoconstriction is assessed visually or bymeans 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 andtreated 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 topicalcorticosteroid is evaluated at 12 hours



ADVERSE EFFECTS OF TOPICAL

CORTICOSTEROIDS

Under normal conditions, up to 99% of appliedtopical 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 cutaneouscandidiasis, 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 shininessof skin, as well as appearance of striae

Atrophy recognized as M/c adverse effect of TCS

Dermal atrophy is probably caused by decreasedfibroblast growth and reduced synthesis of collagenand acid mucopolysaccharides

Intertriginous areas are particularly susceptible,

probably owing to thinner skin, increased moisture,elevated temperature, and partial occlusionprovided by skin in these sites



Telangiectasia

CS stimulate human dermal microvascular

endothelial cells, leading to the occurrence oftelangiectasia.

Characterized by an abnormal dilatation of capillaryvessels and arterioles

Striae

Visible linear scars, form in areas of dermal damage,presumably during mechanical stress

Develop with an initial inflammation and edema ofdermis, followed by deposition of dermal collagenalong 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 atrophyand loss of intercellular substance occur, causingblood vessels to lose their surrounding dermal matrix.

Fragility of dermal vessels leads to purpuric,irregularly shaped, hypopigmented, depressed scars

stellate pseudoscars most frequently develop overextremities, 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 pseudoscarsand 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 anddo not require potent formulations

Classical history of steroid rosacea begins in a middleaged woman with intermittent papules and pustulesthat are initially controlled with steroids of low potency

Subsequently lesions may reappear and promptcontinued use of greater- potency topical corticosteroid

Hypertrichosis

Promote growth of vellus hair by means of an unknownmechanism

Darker hairs may persist for months after withdrawal ofsteroids



(a) Marked atrophy and telangiectasia, (b) Severe exacerbation of acne with crustedand nodular lesions, (c) Tinea incognito after prolonged application of a super-potentTCs, (d) TCs-induced hypertrichosis, IJDVL | March-April 2011 | Vol 77 | Issue 2





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 offollicular papules and pustuleson an erythematousbackground

Begin in a perioral distribution,

with prominent sparing of skinadjacent to vermilion border

Most frequently observed inyoung women,may be seen inmen and children

Caused by long-term use ofpotent 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-dependentface" with bright erythema and monomorphic papules

IJDVL | Mar-Apr 2011 |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 aftertopical use is quitecommon

• Steroids probablyinterfere withsynthesis of melaninby smallermelanocytes, leadingto patchy areas of

hypopigmentation• Generally reversible

upondiscontinuation



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, anddisseminated cutaneous Alternaria infection

Tinea incognito Marked tinea infections, transformed into unrecognizable cutaneous

eruptions

Prolongation or mitigation of herpes simplex, molluscumcontagiosum, 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 delayedbarrier recovery (ie, increased transepidermal water loss)

May theoretically worsen barrier impairment in atopicdermatitis and psoriasis



Contact sensitization to TCS

Generally rare, 0.2% and 6%.

Nonfluorinated corticosteroids (eg, hydrocortisone,hydrocortisone17-butyrate, and budesonide) result in ahigher prevalence of contact allergy

Binding to amino acid arginine as part of certain proteins

seems to be a prerequisite for allergic reactions tocorticosteroids

A classification scheme based on structural relation ofsteroid molecule has been devised for cross-reactivity

Representative agents hydrocortisone (group A),triamcinolone acetonide (group B), betamethasone (groupC), and hydrocortisone butyrate (group D), is useful forclinical 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 achievedisease control.

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

To taper off treatment upon complete remission of skindiseases.

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



Optimizing the use of TCS

To be especially considerate when prescribing to elderlyand children.

To be aware of adverse effects and act immediately tocounteract them.

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

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



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