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Tiêu đề Drugs and the Skin
Trường học University of Clinical Pharmacology
Chuyên ngành Clinical Pharmacology
Thể loại Tài liệu
Năm xuất bản 2003
Thành phố Hanoi
Định dạng
Số trang 18
Dung lượng 2,34 MB

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Nội dung

• Pharmacokinetics of the skin • Topical preparations:Vehicles for presenting drugs to the skin; Emollients, barrier preparations and dusting powders;Topical analgesics; Antipruritics; A

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Drugs and the skin

SYNOPSIS

This account is confined to therapy directed

primarily at the skin.

• Pharmacokinetics of the skin

• Topical preparations:Vehicles for presenting

drugs to the skin; Emollients, barrier

preparations and dusting powders;Topical

analgesics; Antipruritics; Adrenocortical

steroids; Sunscreens

• Cutaneous adverse drug reactions

• Individual disorders: Psoriasis.Acne,

Urticaria, Skin infections

It is easy to do more harm than good with

potent drugs, and this is particularly true in

skin diseases Many skin lesions are caused by

systemic or topical use of drugs, often taking

the form of immediate or delayed

hypersensitivity.

Pharmacokinetics

The stratum corneum (superficial keratin layer) is

both the principal barrier to penetration of drugs into

the skin and a reservoir for drugs; a corticosteroid

may be detectable even 4 weeks after a single

application

Drugs are presented in vehicles, e.g cream,

ointment, and their entry into the skin is determined

by the:

• rate of diffusion of drug from the vehicle to the surface of the skin (this depends on the type of vehicle, see below)

• partitioning of the drug between the vehicle and the stratum corneum (a physicochemical feature

of the individual drug) and

• degree of hydration of the stratum corneum (hydration reduces resistance to diffusion of drug)

Vehicles (bases1) are designed to vary in the extent to which they increase the hydration of the stratum corneum; e.g oil-in-water creams promote hydration (see below) Some vehicles also contain substances intended to enhance penetration, e.g squalane (p 306)

Absorption through normal skin varies with site; from the sole of the foot and the palm of the hand it

is relatively low, it increases progressively on the forearm, the scalp, the face until on the scrotum and vulva absorption is very high

Where the skin is damaged by inflammation, burn or exfoliation, absorption is further increased

If an occlusive dressing (impermeable plastic

membrane) is used, absorption increases by as much

as 10-fold (plastic pants for babies are occlusive, and some ointments are partially occlusive) Serious systemic toxicity can result from use of occlusive dressing over large areas

A drug readily diffuses from the stratum corneum into the epidermis and then into the dermls, where

1 The chief ingredient of a mixture.

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it enters the capillary microcirculation of the skin,

and thus the systemic circulation There may be a

degree of presystemic (first-pass) metabolism in the

epidermis and dermis, a desirable feature to the

extent that it limits systemic effects

Transdermal delivery systems are now used to

administer drugs via the skin for systemic effect

(see p 109)

Topical preparations

It is convenient to think of these under the following

headings:

• Vehicles for presenting drugs to the skin

• Emollients, barrier preparations and dusting

powders

• Topical analgesics

• Antipruritics

• Adrenocortical steroids

• Sunscreens

• Miscellaneous substances

VEHICLES FOR PRESENTING DRUGS

TO THE SKIN

The formulations are described in order of decreasing

water content All water-based formulations must

contain preservatives, e.g chlorocresol, but these

rarely cause allergic contact dermatitis

Lotions or wet dressings

Water is the most important component Wet

dressings are generally used to cleanse, cool and

relieve pruritus in acutely inflamed lesions, especially

where there is much exudation, e.g atopic eczema

The frequent reapplication and the cooling effect of

evaporation of the water reduce the inflammatory

response by inducing superficial vasoconstriction

Sodium chloride solution 0.9%, or solutions of

astringent2 substances, e.g aluminium acetate lotion,

or potassium permanganate soaks or compresses of

approx 0.05%, can be used The use of lotions or

2 Astringents are weak protein precipitants, e.g tannins, salts

of aluminium and zinc.

wet dressings over very large areas can reduce body temperature dangerously in the old or the very ill

Shake lotions, e.g calamine lotion, are essentially

a convenient way of applying a powder to the skin (see Dusting powders, p 301) with additional cooling due to evaporation of the water They are contraindicated when there is much exudate because crusts form Lotions, after evaporation, sometimes produce excessive drying of the skin, but this can be reduced if oils are included, as in oily calamine lotion

Creams

These are emulsions either of oil-in-water (washable; cosmetic 'Vanishing' creams) or water-in-oil The water content allows the cream to rub in well A cooling effect (cold creams) is obtained with both groups as the water evaporates

Oil-in-water creams, e.g aqueous cream (see emul-sifying ointment, below), mix with serous discharges and are especially useful as vehicles for water-soluble active drugs They may contain a wetting (surface tension reducing) agent (cetomacrogol) Aqueous cream is also used as an emollient (see below) Various other ingredients, e.g calamine, zinc, may

be added to it

Water-in-oil creams, e.g oily cream, zinc cream, behave like oils in that they do not mix with serous discharges, but their chief advantage over ointments (below) is that the water content makes them easier

to spread and they give a better cosmetic effect They act as lubricants and emollients, and can be used on hairy parts Water-in-oil creams can be used as vehicles for lipid-soluble substances A dry skin is mainly short of water, and oily substances are needed to provide a barrier that reduces evaporation of water, i.e the presence of oils contributes to epidermal hydration

Ointments

Ointments are greasy and are thicker than creams Some are both lipophilic and hydrophilic, i.e by occlusion they promote dermal hydration, but are also water miscible Other ointment bases are composed largely of lipid; by preventing water loss

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they have a hydrating effect on skin and are used in

chronic dry conditions Ointments contain fewer

preservatives and are less likely to sensitise There

are two main kinds:

Water-soluble ointments include mixtures of

mac-rogols and polyethylene glycols; their consistency can

be varied readily They are easily washed off and

are used in burn dressings, as lubricants and as

vehicles that readily allow passage of drugs into the

skin, e.g hydrocortisone

Emulsifying ointment is made from emulsifying

wax (cetostearyl alcohol and sodium lauryl sulphate)

and paraffins Aqueous cream is an oil-in-water

emulsion of emulsifying ointment

Nonemulsifying ointments do not mix with water

They adhere to the skin to prevent evaporation and

heat loss, i.e they can be considered a form of

occlusive dressing (with increased systemic absorption

of active ingredients); skin maceration may occur

Nonemulsifying ointments are helpful in chronic

dry and scaly conditions, such as atopic eczema,

and as vehicles; they are not appropriate where

there is significant exudation They are difficult to

remove except with oil or detergents and are messy

and inconvenient, especially on hairy skin Paraffin

ointment contains beeswax, paraffins and cetostearyl

alcohol

Collodions

Collodions are preparations of cellulose nitrate

(pyroxylin) dissolved in an organic solvent The

solvent evaporates rapidly and the resultant flexible

film is used to hold a medicament, e.g salicylic

acid, in contact with the skin They are irritant and

inflammable and are used to treat only small areas

of skin

Pastes

Pastes, e.g zinc compound paste, are stiff,

semi-occlusive ointments containing insoluble powders

They are very adhesive and give good protection to

circumscribed lesions, preventing spread of active

ingredients to surrounding skin Their powder

content enables them to absorb a moderate amount

T O P I C A L P R E P A R A T I O N S

of discharge They can be used as vehicles, e.g coal tar paste, which is zinc compound paste with 7.5% coal tar Lassar's paste is used as a vehicle for dithranol in the treatment of plaque psoriasis

EMOLLIENTS, BARRIER PREPARATIONS AND DUSTING POWDERS

Emollients hydrate the skin and soothe and smooth dry scaly conditions They need to be applied frequently as their effects are short-lived There is a variety of preparations but aqueous cream in addition

to its use as a vehicle (above) is effective when used

as a soap substitute Various other ingredients may

be added to emollients, e.g menthol, camphor or phenol for its mild antipruritic effect and zinc and titanium dioxide as astringents

Barrier preparations Many different kinds have been devised for use in medicine, in industry and in the home to reduce dermatitis They rely on water-repellent substances, e.g silicones (dimethicone cream), and on soaps, as well as on substances that form an impermeable deposit (titanium, zinc, cal-amine) The barrier preparations are useful in protecting skin from discharges and secretions (colostomies, napkin rash) but they are ineffective when used under industrial working conditions Indeed, the irritant properties of some barrier creams can enhance the percutaneous penetration

of noxious substances A simple after-work emollient

is more effective

Silicone sprays and occlusives, e.g hydrocolloid

dressings, may be effective in preventing and treating pressure sores

Masking creams (camouflaging preparations) for

obscuring unpleasant blemishes from view are greatly valued by the victims3 They may consist of titanium oxide in an ointment base with colouring appropriate to the site and the patient

Dusting powders, e.g zinc starch and talc,4 may

3 In the UK, the Red Cross offers a free cosmetic camouflage service through hospital dermatology departments.

4 Talc is magnesium silicate It must not be used for dusting surgical gloves as it causes granulomas if it gets into wounds

or body cavities.

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cool by increasing the effective surface area of the

skin and they reduce friction between skin surfaces

by their lubricating action Though usefully

absor-bent, they cause crusting if applied to exudative

lesions They may be used alone or as a vehicle for,

e.g fungicides

Gels or jellies are semisolid colloidal solutions or

suspensions used as lubricants and as vehicles for

drugs They are sometimes useful for treating the

scalp

TOPICAL ANALGESICS

Counterirritants and rubefacients are irritants

that stimulate nerve endings in intact skin to relieve

pain in skin (e.g postherpetic), viscera or muscle

supplied by the same nerve root All produce

inflammation of the skin which becomes flushed,

hence rubefacients They are often effective though

their precise mode of action is unknown

The best Counterirritants are physical agents,

especially heat Many drugs, however, have been

used for this purpose and suitable preparations

containing salicylates, nicotinates, menthol, camphor

and capsaicin (depletes skin substance P) are also

available

Topical NSAIDs (see p 290) are used to relieve

musculoskeletal pain

Local anaesthetics Lidocaine and prilocaine are

available as gels, ointments and sprays to provide

reversible block of conduction along cutaneous

nerves (see p 422) Benzocaine and amethocaine

(tetracaine) carry a high risk of sensitisation

Volatile aerosol sprays, beloved by sportspeople,

produce analgesia by cooling and by placebo effect

ANTIPRURITICS

Mechanisms of itch are both peripheral and central.

Impulses pass along the same nerve fibres as those

of pain, but the sensation experienced differs

qualitatively as well as quantitatively from pain In

the CNS endogenous opioid peptides are released

and naloxone can relieve some cases of intractable

itch Local liberation of histamine and other autacoids

in the skin also contributes and may be responsible for much of the itch of urticarial allergic reactions Histamine release by bile salts may explain some, but not all, of the itch of obstructive jaundice It is likely that other chemical mediators, e.g serotonin and prostaglandins, are involved

Generalised pruritus

In the absence of a primary dermatosis it is important

to search for an underlying cause, e.g iron deficiency, liver or renal failure and lymphoma, but there remain patients in whom the cause either cannot be removed or is not known

Antihistamines (Ha receptor), especially chlor-phenamine and hydroxyzine orally, are used for their sedative or anxiolytic effect (except in urticaria); they should not be applied topically over a prolonged period for risk of allergy

In severe pruritus, a sedative antidepressant may also help The itching of obstructive jaundice may

be relieved by androgens but they may increase the jaundice If obstruction is only partial, colestyramine and phototherapy can be useful Naltrexone offers short-term relief of the pruritus associated with haemodialysis

Localised pruritus

Scratching or rubbing seems to give relief by converting the intolerable persistent itch into a more bearable pain Firm pressure with a finger may relieve the itch A vicious cycle can be set up in which itching provokes scratching and scratching leads to skin lesions which itch, as in lichenified eczema Covering the lesion or enclosing it in a medicated bandage so as to prevent any further scratching or rubbing may help

Topical corticosteroid preparations are used to treat

the underlying inflammatory cause of pruritus, e.g

in eczema

A cooling application such as 0.5-2% menthol in aqueous cream is antipruritic, probably by weak local anaesthetic action

Calamine and astringents (aluminium acetate, tannic

acid) may help Local anaesthetics do not offer any long-term solution and since they are liable to sensitise the skin they are best avoided; lignocaine

is least troublesome in this respect Topical doxepin

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T O P I C A L P R E P A R A T I O N S

can be helpful in localised pruritus, but extensive

use induces sedation; like other topical antihistamines

it induces allergic contact dermatitis

Crotamiton, an acaricide, is reputed to have a

specific but unexplained antipruritic action, although

it is irritant

Pruritus ani is managed by attention to hygiene,

emollients, e.g washing with aqueous cream, and a

weak corticosteroid with antiseptic/anticandida

application used as briefly as practicable (some cases

are a form of neurodermatitis) Secondary contact

sensitivity, e.g to local anaesthetics, is common

ADRENOCORTICAL STEROIDS

Actions Adrenal steroids possess a range of actions

(see p 664) of which the following are relevant to

topical use:

• Inflammation is suppressed, particularly when

there is an allergic factor, and immune responses

are reduced

• Antimitotic activity suppresses proliferation of

keratinocytes, fibroblasts and lymphocytes

(useful in psoriasis, but also causes skin

thinning)

• Vasoconstriction reduces ingress of

inflammatory cells and humoral factors to the

inflamed area; this action (blanching effect on

human skin) has been used to measure the

potency of individual topical corticosteroids (see

below)

Penetration into the skin is governed by the

factors outlined at the beginning of this chapter

The vehicle should be appropriate to the condition

being treated: an ointment for dry, scaly conditions,

a water-based cream for weeping eczema

Uses Adrenal steroids should be considered a

symptomatic and sometimes curative, but not

preventive, treatment Ideally a potent steroid (see

below) should be given only as a short course and

reduced as soon as the response allows

Cortico-steroids are most useful for eczematous disorders

(atopic, discoid, contact) and other inflammatory

conditions save those due to infection Dilute

corticosteroids are useful in psoriasis (see p 309)

Adrenal steroids of highest potency are reserved for recalcitrant dermatoses, e.g lichen simplex, lichen planus, nodular prurigo and discoid lupus ery-thematosus

Topical corticosteroids are of no use for urticarial conditions and are contraindicated in infection, e.g fungal, herpes, impetigo, scabies, because the infection will exacerbate and spread Where ap-propriate, an adrenal steroid formulation may include

an antimicrobial, e.g miconazole, fusidic acid, in infected eczema

Topical corticosteroids should be applied sparingly ('Marmite rather than marmalade') The 'finger tip unit'5 is a useful guide in educating patients (see Table 16.1)

The difficulties and dangers of systemic adrenal steroid therapy are sufficient to restrict such use to serious conditions (such as pemphigus and generalised exfoliative dermatitis) not responsive to other forms of therapy

• Use for symptom relief and never prophylactically

• Choose the appropriate therapeutic potency (see Table 16.2), i.e mild for the face In cases likely to be resistant, use a very potent preparation, e.g for

3 weeks, to gain control, after which change to a less potent preparation.

• Choose the appropriate vehicle, i.e a water-based cream for weeping eczema, an ointment for dry scaly conditions.

• Use a combined adrenal steroid/antimicrobial formulation if infection is present.

• Advise the patient to apply the formulation very thinly, just enough to make the skin surface shine slightly.

• Prescribe in small but adequate amounts so that serious overuse is unlikely to occur without the doctor knowing, e.g weekly quantity by group (Table 16.2): very potent 15 g; potent 30 g; others 50 g.

• Occlusive dressing should be used only briefly Note that babies' plastic pants are an occlusive dressing as well as being a social amenity.

Choice Corticosteroids are classified according to

their therapeutic potency (efficacy), i.e according to

both drug and % concentration (see Table 16.2)

5 The distance from the tip of the adult index finger to the first crease.

16

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TABLE 16.1 Finger tip unit dosimetry for topical

corticosteroids

Age

3-6 months

1 -2 years

3-5 years

6-10 years

Adult

Face/

Neck

1

1.5

1.5

2

2.5

Arm/

Hand

1 1.5 2 2.5 Arm — 3 Hand— 1

Leg/

Foot

1.5 2 3 4.5 Foot — 2 Leg—6

Trunk (front)

1 2 3 3.5 7

Trunk (back, including buttocks) 1.5 3 3.5 5 7

TABLE 16.2 Topical corticosteroid formulations

conventionally ranked according to therapeutic

potency

Very potent Clobetasol (0.05%) [also formulations of

diflucortolone (0.3%), halcinonide]

Potent Beclomethasone (0.025%) [also

formulations of betamethasone, budesonide, desonide, desoxymethasone, diflucortolone (0.1 %), fluclorolone, fluocinolone (0.025%), fluocinonide, fluticasone, hydrocortisone butyrate, mometasone (once daily), triamcinolone]

Moderately potent Clobetasone (0.05%) [also formulations

of alclometasone, clobetasone, desoxymethasone, fluocinolone (0.00625%), fluocortolone, fluandrenolone, hydrocortisone plus urea (see p 307)]

Mildly potent Hydrocortisone (0.1-1.0%) [also

formulations of alclomethasone, fluocinolone (0.0025%), methylprednisolone]

Important note: the ranking is based on agent and its

concentration: the same drug appears in more than one rank.

Choice of preparation relates both to the disease

and the site of intended use High potency

preparations are commonly needed for lichen

planus and discoid lupus erythematosus; weaker

preparations (hydrocortisone 0.5-2.5%) are usually

adequate for eczema, use on the face and in

childhood

When a skin disorder requiring a corticosteroid

is already infected, a preparation containing an

antimicrobial is added, e.g fusidic acid or

clo-trimazole When the infection is eliminated the

corticosteroid may be continued alone

Intralesional injections are occasionally used to

provide high local concentrations without systemic effects in chronic dermatoses, e.g hypertrophic lichen planus and discoid lupus erythematosus Adverse effects Used with restraint topical cortico-steroids are effective and safe Adverse effects are more likely with formulations ranked therapeutically

as very potent or potent in Table 16.2

• Short-term use Infection may spread.

• Long-term use Skin atrophy can occur within

4 weeks and may or may not be fully reversible

It reflects loss of connective tissue which also causes striae (irreversible) and generally occurs

at sites where dermal penetration is high (face, groins, axillae)

Other effects include: local hirsutism; perioral dermatitis (especially in young women) responds

to steroid withdrawal and may be mitigated by tetracycline by mouth for 4-6 weeks; depigmentation

(local); acne (local) Potent corticosteroids should not

be used on the face unless this is unavoidable.

Systemic absorption can lead to all the adverse effects of systemic corticosteroid use Fluticasone propionate and mometasone furcate are rapidly metabolised following cutaneous absorption which may reduce the risk of systemic toxicity Suppression

of the hypothalamic/pituitary axis readily occurs with overuse of the very potent agents, and when 20% of the body is under an occlusive dressing with mildly potent agents Other complications of occlusive dressings include infections (bacterial, candidal) and even heat stroke when large areas are occluded Antifungal cream containing hydrocortisone and used for vaginal candidiasis may contaminate the urine and misleadingly suggest Cushing's syndrome.6 Applications to the eyelids may get into the eye and cause glaucoma

Rebound exacerbation of the disease can occur

after abrupt cessation of therapy This can lead the patient to reapply the steroid and so create a vicious cycle

Allergy Corticosteroids, particularly hydrocortisone and budesonide, or other ingredients in the

for-6 Kelly C J et al 2001 Raised cortisol excretion rate in urine and contamination by topical steroids British Medical Journal 322: 594.

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T O P I C A L P R E P A R A T I O N S

mulation, may cause allergic contact dermatitis and

the possibility of this should be considered where

expected benefit fails to occur

SUNSCREENS

(Sunburn and Photosensitivity)

Ultraviolet (UV) solar radiation consists of:

• UVA (320-400 nanometres): causes skin aging

(damage to collagen) and probably skin cancer

• UVB (290-320 nm): is 1000 times more active

than UVA, acutely causes sunburn and tanning,

and chronically skin cancer and skin aging

• UVC (200-290 nm) is prevented, at present, from

reaching the earth at sea level by the

stratospheric ozone layer, though it can cause

skin injury at high altitude

Protection of the skin

Protection from UV radiation is effected by:

Absorbent sunscreens These organic chemicals

absorb UVB and UVA at the surface of the skin

(generally more effective for UVB)

UVB protection: aminobenzoic acid and

aminobenzoates (padimate-O), cinnamates,

salicylates, camphors

UVA protection: benzophenones (mexenone,

oxybenzone), dibenzoylmethanes

Reflectant sunscreens Inert minerals such as

titanium dioxide, zinc oxide and calamine act as a

physical barrier to UVB and UVA: they are

cos-metically unattractive but the newer micronised

preparations are more acceptable

The performance of a sunscreen is expressed as

the sun protective factor (SPF) which refers to UVB

(UVA is more troublesome to measure and the

protection is indicated by a star rating system with

4 stars providing the greatest) A SPF of 10 means

that the dose of UVB required to cause erythema

must be 10 times greater on protected than on

unprotected skin The SPF should be interpreted

only as a rough guide; consumer use is more

haphazard and less liberal amounts are applied to

the skin in practice Sunscreens should protect against

both UVB and UVA Absorbent and reflectant

components are combined in some preparations The washability of the preparation (including removal by sweat and swimming) is also relevant to efficacy and frequency of application; some penetrate the stratum corneum (padimate-O) and are more persistent than others

Uses Sun screens are no substitute for light-impermeable clothing and sun avoidance They are, however, beneficial in protecting those who are photosensitive due to drugs (below) or to disease, i.e for photodermatoses such as photosensitivity dermatitis, polymorphic light eruption, cutaneous porphyrias and lupus erythematosus Methodical use of sunscreens appears to reduce the incidence of squamous cell carcinoma in vulnerable individuals The lower lip receives a substantial dose of UV but may be neglected when a sunscreen is applied (specific lip-blocks are available) Sunscreens can cause allergic dermatitis or photodermatitis (but not titanium dioxide, though its vehicle may) Treatment of mild sunburn is usually with a lotion such as oily calamine lotion Severe cases are helped by topical corticosteroids NSAIDs, e.g indometacin, can help if given early, by preventing the formation of prostaglandins

Photosensitivity

Drug photosensitivity means that an adverse effect occurs as a result of drug plus light, usually UVA; sometimes even the amount of ultraviolet radiation from fluorescent light tubes is sufficient

Systemically taken drugs that can induce photo-sensitivity are many Of the drug groups given below, those most commonly reported are:7

antimitotics: dacarbazine, vinblastine antimicrobials: demeclocycline, doxycycline,

nalidixic acid, sulphonamides

antipsychotics: chlorpromazine, prochlorperazine cardiac arrhythmic: amiodarone

diuretics: frusemide (furosemide),

chlorothiazide, hydrochlorothiazide

fibric acid derivatives, e.g fenofibrate hypoglycaemic: tolbutamide

' Data from The Medical Letter 1995 37: 35.

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nonsteroidal anti-inflammatory: piroxicam

psoralens (see below).

Topically applied substances that can produce

photosensitivity include:

pam-aminobenzoic acid and its esters (used as

sunscreens)

coal tar derivatives

psoralens from juices of various plants (e.g.

bergamot oil)

6-methylcoumarin (used in perfumes, shaving

lotions, sunscreens)

There are two forms of photosensitivity:

Phototoxicity, like drug toxicity, is a normal effect

of too high a dose of UV in a subject who has been

exposed to the drug The reaction is like severe

sunburn The threshold returns to normal when the

drug is withdrawn Some drugs, notably NSAIDs,

induce a 'pseudoporphyria', clinically resembling

porphyria cutanea tarda and presenting with skin

fragility, blisters, and milia on sun-exposed areas,

notably the backs of the hands

Photoallergy, like drug allergy, is a cell-mediated

immunological effect that occurs only in some

people, and which may be severe with a small dose

Photoallergy due to drugs is the result of a

photo-chemical reaction caused by UVA in which the drug

combines with tissue protein to form an antigen

Reactions may persist for years after the drug is withdrawn;

they are usually eczematous

Systemic protection, as opposed to application of

drug to exposed areas, should be considered when

the topical measures fail Antimalarials such as

hydroxychloroquine may be effective for short periods

in polymorphic light eruption and in cutaneous

lupus erythematosus

Psoralens (obtained from citrus fruits and other

plants), e.g methoxsalen, are used to induce

photo-chemical reactions in the skin After topical or

systemic administration of the psoralen and

sub-sequent exposure to UVA there is an erythematous

reaction that goes deeper than ordinary sunburn

and that may reach its maximum only after 48 h

(sunburn maximum is 12-24 h) Melanocytes are

activated and pigmentation occurs over the following week This action is used to repigment areas of disfiguring depigmentation, e.g vitiligo in black-skinned persons

In the presence of UVA the psoralen interacts with DNA, forms thymine dimers, and inhibits DNA synthesis Psoralen plus UVA (PUVA) treatment is used chiefly in severe psoriasis (a disease charac-terised by increased epidermal proliferation), and cutaneous T cell lymphoma

Severe adverse reactions can occur with psoralens

and ultraviolet radiation, including increased risk

of skin cancer (due to mutagenicity inherent in their action), cancer of the male genitalia, cataracts and accelerated skin aging; the treatment is used only

by specialists

Chronic exposure to sunlight induces wrinkling

and yellowing due to the changes in the dermal connective tissue Topical retinoids are widely used in an attempt to reverse some of these tissue changes

MISCELLANEOUS SUBSTANCES Keratolytics are used to destroy unwanted tissue,

including warts and corns Great care is obviously necessary to avoid ulceration They include trichloracetic acid, salicylic acid and many others Resorcinol and sulphur are mild keratolytics used

in acne

Squalane is a saturated hydrocarbon insoluble in

water but soluble in sebum It therefore penetrates the skin and is a vehicle for delivery of agents; it is water repellent and is used for incontinence and prevention of bed sores It appears in mixed formulations

Salicylic acid may enhance the efficacy of a topical

steroid in hyperkeratotoic disorders

Tars are mildly antiseptic, antipruritic and they

inhibit keratinisation in an ill-understood way They are safe in low concentrations and are used in psoriasis Photosensitivity occurs There are very many preparations, which usually contain other

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C U T A N E O U S A D V E R S E D R U G R E A C T I O N S

substances, e.g coal tar and salicylic acid ointment;

it is sometimes useful to add an adrenal steroid

Ichthammol is a sulphurous tarry distillation

product of fossilised fish (obtained in the Austrian

Tyrol); it has a weaker effect than coal tar

Zinc oxide provides mild astringent, barrier and

occlusive actions

Calamine is basic zinc carbonate that owes its pink

colour to added ferric oxide It has a mild astringent

action and is used as a dusting powder and in shake

and oily lotions It is of limited value

Urea is used topically to assist skin hydration, e.g

in ichthyosis

Insect repellents, e.g against mosquitoes, ticks,

fleas, such as deet (diethyl toluamide), dimethyl

phthalate These are applied to the skin and repel

insects principally by vaporisation They must be

applied to all exposed skin, and sometimes also to

clothes if their objective is to be achieved (some

damage plastic fabrics and spectacle frames) Their

duration of effect is limited by the rate at which they

vaporise (skin and ambient temperature), by washing

off (sweat, rain, immersion) and by mechanical

factors causing rubbing (physical activity) They can

cause allergic and toxic effects, especially with

prolonged use About 10% is absorbed Plainly the

vehicle in which they are applied is also important,

and an acceptable substance achieving persistence

of effect beyond a few hours has yet to be developed

But the alternative of spreading an insecticide in

the environment causing general pollution and

indiscriminate insect kill is unacceptable Selective

environmental measures against some insects, e.g

mosquitoes, are sometimes feasible

Benzyl benzoate may be used on clothes; it

resists one or two washings

the same drug may produce different rashes in different people

Irritant or allergic contact dermatitis is eczematous

and is often caused by antimicrobials, local ana-esthetics, topical antihistamines, and increasingly commonly by topical corticosteroids It is often due

to the vehicle in which the active drug is applied, particularly a cream

Reactions to systemically administered drugs are

commonly erythematous, like those of measles, scarlatina or erythema multiforme They give no useful clue as to the cause They commonly occur during the first 2 weeks of therapy, but some immu-nological reactions may be delayed for months Patients with the acquired immunodeficiency syndrome (AIDS) have an increased risk of adverse reactions, which are often severe

Though drugs may change, the clinical problems remain depressingly the same: a patient develops a rash; he is taking many different tablets; which, if any, of these caused his eruption, and what should

be done about it? It is no answer simply to stop all drugs, though the fact that this can often be done casts some doubt on the patient's need for them in the first place All too often potentially valuable drugs are excluded from further use on totally inadequate grounds Clearly some guidelines are needed but no simple set of rules exists that can cover this complex subject 8

The following questions should be asked in every case:

• Can other skin diseases be excluded?

• Are the skin changes compatible with a drug cause?

• Which drug is most likely to be responsible?

• Are any further tests worthwhile?

• Is any treatment needed?

These questions are deceptively simple but the answers are often difficult

Cutaneous adverse drug

reactions

DRUG-SPECIFIC RASHES

Despite great variability, some hints at drug-specific

Drugs applied locally or taken systemically often

cause rashes These take many different forms and

8 Hardie R A, Savin J A1979 British Medical Journal: 1935, to whom we are grateful for this quotation and classification.

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or characteristic rashes from drugs taken systemically,

can be discerned, as follows:

Acne and pustular: e.g corticosteroids,

androgens, ciclosporin, penicillins

Allergic vasculitis: e.g sulphonamides, NSAIDs,

thiazides, chlorpropamide, phenytoin, penicillin,

retinoids

Anaphylaxis: x-ray contrast media, penicillins,

ACE inhibitors

Bullous pemphigoid: frusemide (and other

sulphonamide-related drugs), ACE inhibitors,

penicillamine, penicillin, PUVA therapy

Eczema: e.g penicillins, phenothiazines.

Exanthematic/maculopapular reactions are the

most frequent; unlike a viral exanthem the eruption

typically starts on the trunk; the face is relatively

spared Continued use of the drug may lead to

erythroderma They commonly occur at about the

ninth day of treatment (or day 2-3 in previously

exposed patients), although onset may be delayed

until after treatment is completed; causes include

antimicrobials, especially ampicillin,

sulphonamides and derivatives (sulphonylureas,

frusemide (furosemide) and thiazide diuretics)

Morbilliform (measles-like) eruptions typically

recur on rechallenge

Erythema multiforme: e.g NSAIDs,

sulphonamides, barbiturates, phenytoin

Erythema nodosum: e.g sulphonamides, oral

contraceptives, prazosin

Exfoliative dermatitis and erythroderma: gold,

phenytoin, carbamazepine, allopurinol, penicillins,

neuroleptics, isoniazid

Fixed eruptions are eruptions that recur at the

same site, often circumoral, with each

administration of the drug: e.g phenolphthalein

(laxative self-medication), sulphonamides, quinine

(in tonic water), tetracycline, barbiturates,

naproxen, nifedipine

Hair loss: e.g cytotoxic anticancer drugs,

acitretin, oral contraceptives, heparin,

androgenic steroids (women), sodium valproate,

gold

Hypertrichosis: corticosteroids, ciclosporin,

doxasosin, minoxidil

Lichenoid eruption: e.g p-adrenoceptor blockers,

chloroquine, thiazides, frusemide (furosemide),

captopril, gold, phenothiazines

Lupus erythematosus: e.g hydralazine, isoniazid,

procainamide, phenytoin, oral contraceptives, sulfazaline

Purpura: e.g thiazides, sulphonamides,

sulphonylureas, phenylbutazone, quinine Aspirin induces a capillaritis (pigmented purpuric dermatitis)

Photosensitivity: see above.

Pemphigus: e.g penicillamine, captopril,

piroxicam, penicillin, rifampicin

Pruritus unassociated with rash: e.g oral

contraceptives, phenothiazines, rifampicin (cholestatic reaction)

Pigmentation: e.g oral contraceptives (chloasma

in photosensitive distribution), phenothiazines, heavy metals, amiodarone, chloroquine (pigmentations of nails and palate, depigmentation

of the hair), minocycline

Psoriasis may be aggravated by lithium and

antimalarials

Scleroderma-like: bleomycin, sodium valproate,

tryptophan contaminants (eosinophila-myalgia syndrome)

Serum sickness: immunoglobulins and other

immunomodulatory blood products

Stevens-Johnson syndrome and toxic epidermal

necrolysis:9 e.g anticonvulsants, sulphonamides, aminopenicillins, oxicam NSAIDs, allopurinol, chlormezanone, corticosteroids

Urticaria and angioedema: e.g penicillins, ACE

inhibitors, gold, NSAIDs, e.g aspirin, codeine

Recovery after withdrawal of the causative drug

generally begins in a few days, but lichenoid reactions may not improve for weeks

Diagnosis The patient's drug history may give clues Reactions are commoner during early therapy (days) than after the drug has been given for months Diagnosis by readministration of the drug (challenge)

is safe with fixed eruptions, but not with others, particularly those that may be part of a generalised effect, e.g vasculitis Patch and photopatch tests are useful in contact dermatitis, for they reproduce the causative process but should be performed only by those with special experience Fixed drug eruptions can sometimes be reproduced by patch testing with the drug over the previously affected site

9 Roujeau C-J et al 1995 New England Journal of Medicine 333:1600

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