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8/10/2019 Referensi FDE Gtr

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Fixed Drug Eruptions

FDEs usually appear as solitary, erythematous, bright red or dusky red macules that may evolve

into an edematous plaque; bullous-type lesions may be present. FOEs are most commonly found

on the genitalia and in the perianal area, although they can occur anywhere on the skin surface(Fig. 40-5). Some patients may complain of burning or stinging, and others may have fever,

malaise, and abdominal symptoms. FDE can develop from 30 minutes to 8 to 16 hours after

ingestion of the medication. After the initial acute phase lasting days to weeks, residual grayish

or slatecolored hyperpigmentation develops. On rechallenge, not only do the lesions recur in the

same location, but also new Iesions often appear. More than 100 drugs have been impUcatedin

causing FDEs, including ibuprofen, sulfonamides, naproxen, and tetracyclines. A haplotype

linkage in trimethoprim-sulfamethoxazole- induced FDE has been documented. 43"A challenge

or provocation test with the suspected drug may be useful in establishing the diagnosis. Patch

testing at the site of a previous lesion yields a positive response in up to 43 percent of patients.

Results of prick and intradermal skin tests may be positive in 24 percent and 67 percent of

patients, respectively.45

Fitzpatrick hal 397-398

Fixed Drug Reactions

Fixed drug reactions are common. Fixed drug erupttons are

so named because they recur at the same site wlth each

exposure to the med~cation. In most pattents, six or fewer

lesions occur, frequently only one. Uncommonly, fixed

eruptions may be multifocal with numerous lesions. They

may present anywhere on the body, but half occur on the

oral and genital mucosa. Fixed eruptions represent 2% of all

genital ulcers evaluated at clinics for sexually-transmitted

diseases (Fig. 6-37), and are not infrequent in young boys.

Clinically, a fixed eruption begins as a red patch that

soon evolves to an iris or target lesion identical to erythema

multlfome, and may eventually bltster and erode. Lesions of


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the genital and oral mucosa usually present as erosions. Most

lestons are 1 to several cm in diameter, but larger plaques

may occur, resembling cellulitts. Charactenstically, prolonged

or permanent postinflammatory hyperp~gmentahon

results, although a nonpigmenting variant of a fixed drug

eruphon is recognized. With repeated or continued ingestton

of the offending medication, new lesions may be added,

sometimes eventuating in a clinical picture similar to drug-

induced erythema multiforme major. Histologically, an interface

dermatitis occurs with intraepidermal and subepidermal

vesicle formation, necrosis of keratinocytes, and a mixed

superficial and deep infiltrate of neutrophils, eosinophils, and

mononuclear cells. Pigment incontinence is usually marked,

correlating with the pigmentation resulting from fixed drug

eruptions. As biopsies are generally performed during the

acute stage of a recurrence, the stratum corneum is normal.

Papillaly dermal fibrosis and deep perivascular pigment

incontinence are commonly present fmm prior episodes.

This contrast between a normal stratum corneum (suggesting

an acute process) and chronic dermal changes is virtually

pathognomonic of fixed drug eruption.

I

Medications inducing fixed drug eruptions are usually

those taken intermittently. Many of the NSAIDs, especially

pyrazolone derivatives, paracetamol, naproxen, oxicams, and

mefenamic acid cause fixed drug eruption, with a special

predilection for the lips. Sulfonamides, trimethoprim, or the

combination are now responsible for the majority of genital

fixed drug eruptions. Barbiturates, tetracyclines, phenolphthalein

(in laxatives), acetaminophen, ceterizine, celecoxib,

dextmmetbophan, hydroxyzine, lamotrigine, phenylpropanolamine,


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erythromycin, and Chinese and Japanese herbs

are other possible causes.The risk of developing a fixed drug

eruption has been linked to HLA-B22. Patch tests with various

concentrations of the offending medication can reproduce I

the lesion on affected but not unaffected skin.Tape stripping

the skin before applying the suspected medication in various

vehicles may increase the likelihood of a positive patch

test.This technique appears to be most useful in pyrazolone

derivative-related reactions that are reproduced in 85% or

more of cases.

Occasionally, fixed drug reactions do not result in longlasting

hyperpigmentation. The so-called nonpigmenting

fixed drug eruption is distinctive. It is characterized by large,

tender, often symmetrical erythematous plaques that resolve

completely within weeks, only to recur on reingestion of the

offending drug (Fig. 6-38). Pseudoepltedrine hydrochloride is

by far the most common culprit.?he baboon syndrome, where

the buttocks, groin, and axilla are preferentiaIly involved, is I

considered a nonpigmenting fured drug eruption by some.

Lesions of a fixed drug eruption contain intraepidermal

CD8tT-cells with the phenotypic markers of effector memory

T-cells. These skin-residentT-cells rapidly pmduce IFN-y on

exposure to the offending medication.

By Andrews disease of the skin hal 138

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