ACDR.pdf

1. Cutaneous Drug Eruptions
Dr Zahra Nikyar
Assistant Professor of Dermatology

2. The skin is one of the most
common targets for adverse drug
reactions.
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3. Risk factors:
1)Older age
2)Female gender
3)Immunosuppression; e.g. in patients with
AIDS,especially due to sulfonamides
4)Specifc HLA alleles
The risk increases as the number of drugs taken
increases
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7. Exanthematous (Maculopapular/Morbilliform):
• The most frequent of all cutaneous drug reactions, are often indistinguishable
from viral exanthems.
• Red macules and papules become confluent in a symmetric, generalized
distribution that often spares the Face and mucous membranes.
• Pruritus, low-grade fever and eosinophilia may be present.
• Onset is 14 to 21 days after starting the drug.
• Lesions clear rapidly following withdrawal of the implicated agent and may
progress to a generalized exfoliative dermatitis if the drug is continued.
• Are common with aminopenicilline(in patients with infectious mononucleosis),
and trimethoprim/sulfamethoxazole (TMP-SMX) (used in AIDS patients),
allopurinol and anticonvulsants.
• Identifying and discontinuing the causative drug are the most important steps in
management; symptomatic treatment with antipruritic agents and potent topical
• glucocorticoids may be helpful.
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10. Fixed drug eruptions (FDE):
The lesions develop 1 to 2 weeks after a first exposure. With subsequent
exposures, they appear within 24 hours(30 minutes to 8 hours).
Clinically, one or a few, round, sharply demarcated erythematous and edematous
plaques arc seen sometimes with a dusky, violaceous hue, central blister or
detached epidermis .
Lesions favor the lips, face, hands, feet and genitalia.
Upon readministration of the causative drug, the lesions recur at exactly the same
sites.
Fade over several days, often leaving a residual postinflammatory brown
pigmentation.
The drugs most frequently associated with FDE are sulfonamides (in some series,
up to 75% of cases), NSAIDs (in particular, phenazone derivatives), barbiturates,
tetracyclines and carbamazepine.
Topical steroids are effective. Drug avoidance prevents recurrence.
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17. Drug Induced Lichenoid Eruption
• lesions that are clinically and histologically indistinguishable from
those of idiopathic lichen planus
• often appear initially as eczematous with a purple hue and involve
large areas of the trunk.
• Usually the mucous membranes and nails are not involved
• Many drugs, including β-blockers, penicillamine, and ACE
inhibitors, especially captopril
• The mean latent period is between 2 months and 3 years
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20. Acneiform (Pustular)
Eruptions
• These pustular eruptions mimic acne
• Comedons are absent.
 Oral corticosteroids anabolic steroids
 Lithium
 Danazol
 OCP
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22. Lupus Erythematosus–Like
Drug Eruptions
• Drug-induced lupus (DIL) is a rare adverse reaction
• Older patients are more likely to suffer from DIL than from
idiopathic SLE.
• More frequently in females, with a 4:1 ratio
• More than 80 drugs have been implicated; the most common are
hydralazine, procainamide, isoniazid, methyldopa, quinidine,
minocycline, and chlorpromazine and anti–TNF-α
• DIL are usually milder than those seen in idiopathic SLE
• Cutaneous manifestations are much less common than in SLE.
• Renal involvement and CNS disease are rare.
• Antinuclear antibodies (ANAs), antihistone antibodies, and anti–
single stranded DNA antibodies are markers for lupus-like drug
eruptions.
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23. Drug-Induced Subacute Cutaneous
Lupus Erythematosus
• Annular or psoriasiform lesions on the
upper trunk and extensor surfaces of the
arms.
• Clinically and histologically identical to
those of subacute cutaneous lupus
erythematosus.
• Anti-Ro and anti-La antibodies
Hydrochlorothiazide,
Calcium channel blockers, terbinafne,
NSAIDs
Griseofulvin
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24. Lymphomatoid Drug
Eruption
• Any patient who develops an atypical
lymphoid infiltrate should have a
drug-based etiology excluded before
the diagnosis of cutaneous
lymphoma is made.
• Lesions that resemble mycosis
fungoides have been reported
• Phenytoin (Dilantin), phenothiazines,
barbiturates
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25. Drug Induced Vasculitis
• 10% of the acute cutaneous vasculitis
• Usually involves small vessels
• Hallmark: Palpable purpura
• Lower extremities.
• Onset: 7 to 21 days
• Urticaria can be a manifestation of small-vessel
vasculitis.
• Other features include hemorrhagic bullae,
ulcers, nodules, Raynaud disease, and digital
necrosis.
• May also affect internal organs, such as the
liver, kidney, gut, and CNS, and can be
potentially life threatening
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26. Drug Induced Photosensivity
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28. Drug Induced Hyperpigmentation
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32. Hydroquinone Induced Ochronosis
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33. Drug Induced
Hypertrichosis
• Antibiotics such as streptomycin.
• Anti-inflammatory drugs such as
benoxaprofen and corticosteroids.
• Vasodilators (diazoxide, minoxidil,
prostaglandin E1)
• Diuretics (acetazolamide)
• Anticonvulsants (phenytoin)
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34. Erlotinib induced Eyelash Trichomegally
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