Introduction
Use of prescription drugs in the United States
Incidence of cutaneous reactions
Pathogenesis of drug reactions
Nonimmunologic drug reactions
Immunologic drug reactions
Genetic factors and cutaneous drug reactions
Global considerations
Clinical presentation of cutaneous drug reactions
Nonimmune cutaneous reactions
Exacerbation or induction of dermatologic diseases
Photosensitivity eruptions
Pigmentation changes
Warfarin necrosis of skin
Drug-induced hair disorders
Drug-induced nail disorders
Toxic erythema of chemotherapy and other chemotherapy reactions
Immune cutaneous reactions: common
Maculopapular eruptions
Pruritis
Urticaria/angioedema/anaphylaxis
Anaphylactoid reactions
Irritant/allergic contact dermatitis
Fixed drug eruptions
Immune cutaneous reactions: rare and severe
Drug-induced hypersensitivity syndrome
- Etiology
- Type 1 reaction: beta lactam drugs (m/c), neuromuscular blocking agents, quinolones, platinum-containing chemotherapeutic agents, and foreign proteins (eg, chimeric antibodies)
- Pathophysiology
- Some patients can form drug-specific IgE on exposure to a medication, although most do not.
- Once formed, the drug-specific IgE occupies receptors on mast cells and basophils
- If the drug is encountered again, these cells may activate, resulting in symptoms.
- Clinical features
- Type 1 reaction: onset is rapid (seconds to minutes) and symptoms can range from mild (eg, urticaria, pruritus, flushing) to more severe (eg, angioedema of the larynx, anaphylaxis)
- Management
- Urticaria and pruritus without systemic symptoms are usually treated with antihistamines
Stevens-Johnson syndrome (SJS) and toxic epidermal necrolysis (TEN)
- SJS: <10% of BSA / TEN: >30% of BSA
- Clinical features
- 4-28 days after exposure to trigger (2 days after repeat exposure)
- Acute influenza-like prodrome
- Rapid-onset erythematous macules, vesicles, bullae
- Necrosis & sloughing of epidermis
- Mucosal involvement
- Common triggers
- Drugs
- Allopurinol, antibiotics (eg, sulfonamides), anticonvulsants (eg, carbamazepine, lamotrigine, phenytoin), NSAIDs (eg, piroxicam), sulfasalazine
- Other
- M.pneumoniae, vaccination, graft-vs-host disease
- Drugs
- Treatment
- Aggressive fluid support d/t poor oral intake and profound cutaneous fluid loss.
- Secondary infections are common ? antiseptic precautions
Pustular eruptions (AGEP)
Overlap hypersensitivity syndrome
Vasculitis
Management of the patient with suspected drug eruption
Early diagnosis of severe eruptions
| DIAGNOSIS | MUCOSALLESIONS | TYPICAL SKIN LESIONS | FREQUENT SIGNSAND SYMPTOMS | MOST COMMONCULPRIT DRUGS |
| Stevens-Johnson syndrome(SJS) | Erosionsusually attwo ormore sites | Small blisters form from dusky maculesor atypical targets; rare areas ofconfluence; detachment ?10% bodysurface area | Most cases involve fever | Sulfonamides,anticonvulsants,allopurinol, nonsteroidalanti- inflammatory drugs(NSAIDs) |
| Toxic epidermal necrolysis (TEN) | Erosionsusually attwo ormore sites | Individual lesions like those seen in SJS;confluent dusky erythema; large sheetsof necrotic epidermis; total detachmentof >30% body surface area | Nearly all cases involvefever, “acute skin failure,”leukopenia | Same as for SJS |
| Drug-induced hypersensitivity syndrome/drug rash witheosinophilia and systemicsymptoms (DIHS/DRESS) | Mucositisreported inas many as30% | Diwuse, deep red morbilliform eruptionwith facial involvement; facial and acralswelling | Fever, lymphadenopathy,hepatitis, nephritis,myocarditis, eosinophilia,atypical lymphocytosis | Anticonvulsants,sulfonamides,allopurinol, minocycline |
| Acute generalizedexanthematous pustulosis(AGEP) | Oralerosions inperhaps20% | Innumerable pinpoint pustules overlyinga diwuse erythematous eruption; maydevelop superficial erosions | High fever, leukocytosis(neutrophilia),hypocalcemia | ?-Lactamantibiotics, calciumchannel blockers,macrolide antibiotics |
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