17
Drug Reactions
• The skin is one of the most common targets for adverse drug reactions.
• Adverse cutaneous drug reactions (ACDR) affect 2–3% of all hospitalized patients.
• Pathogenesis of ACDR not totally understood but can involve immunologic, nonimmunologic, and idiosyncratic mechanisms (Table 17.1).
Table 17.1
Mechanisms of cutaneous drug-induced reactions.
DRESS, drug reaction with eosinophilia and systemic symptoms (also known as DIHS, drug-induced hypersensitivity syndrome); SJS, Stevens–Johnson syndrome; TEN, toxic epidermal necrolysis.
• Some of the most and least likely culprit drugs are listed in Table 17.2.
Table 17.2
Selected most and least likely drugs to cause adverse cutaneous drug reactions.
* With the exception of urticaria with narcotics and aspirin.
NSAIDs, nonsteroidal anti-inflammatory drugs; EGFR, epidermal growth factor receptor.
Adapted from: Arndt KA, Jick H. Rates of cutaneous reactions to drugs. J. Am. Med. Assoc. 1976;235:918–923.
• Most common types of ACDR: morbilliform > urticaria > vasculitis (Table 17.3).
Table 17.3a
Characteristics of selected adverse cutaneous drug reactions (ACDR).
* Aromatic anticonvulsants, e.g. phenytoin, phenobarbital, and carbamazepine, are most often implicated.
SJS, Stevens–Johnson syndrome; TEN, toxic epidermal necrolysis; BSA, body surface area; URI, upper respiratory tract infection; LABD, linear IgA bullous dermatosis; SSSS, staphylococcal scalded skin syndrome; AGEP, acute generalized exanthematous pustulosis; GVHD, graft-versus-host disease; FDE, fixed drug eruption; ICU, intensive care unit; IV, intravenous; SC, subcutaneous; BUN/Cr, blood urea nitrogen/creatinine; ANCA, antineutrophil cytoplasmic antibodies; DIC, disseminated intravascular coagulation; GI, gastrointestinal; H&E, hematoxylin and eosin; DIF, direct immunofluorescence; LMWH, low-molecular-weight heparin; FDA, Food and Drug Administration; NSAIDs, nonsteroidal anti-inflammatory drugs; ACE, angiotensin-converting enzyme; 5-FU, 5-fluorouracil.
