Chapter 056. Cutaneous Drug Reactions (Part 7)

These reactions are characterized by one or more sharply demarcated, erythematous lesions, sometimes leading to a blister. Hyperpigmentation results after resolution of the acute inflammation. With rechallenge, the lesion recurs in the same (i.e., fixed) location. Lesions often involve the lips, hands, legs, face, genitalia, and oral mucosa and cause a burning sensation. Most patients have multiple lesions. Fixed drug eruptions have been associated with phenolphthalein, sulfonamides, cyclines, dipyrone, NSAIDs, and barbiturates. Patch testing has been used in Europe to help establish the etiology.Immune Cutaneous Reactions: SevereVASCULITIS Cutaneous necrotizing vasculitis often presents as palpable purpuric lesions that may be...
Nội dung trích xuất từ tài liệu:
Chapter 056. Cutaneous Drug Reactions (Part 7) Chapter 056. Cutaneous Drug Reactions (Part 7) FIXED DRUG ERUPTIONS These reactions are characterized by one or more sharply demarcated,erythematous lesions, sometimes leading to a blister. Hyperpigmentation resultsafter resolution of the acute inflammation. With rechallenge, the lesion recurs inthe same (i.e., fixed) location. Lesions often involve the lips, hands, legs, face,genitalia, and oral mucosa and cause a burning sensation. Most patients havemultiple lesions. Fixed drug eruptions have been associated with phenolphthalein,sulfonamides, cyclines, dipyrone, NSAIDs, and barbiturates. Patch testing hasbeen used in Europe to help establish the etiology. Immune Cutaneous Reactions: Severe VASCULITIS Cutaneous necrotizing vasculitis often presents as palpable purpuric lesionsthat may be generalized or limited to the lower extremities or other dependentareas (Chap. 319). Urticarial lesions, ulcers, and hemorrhagic blisters also occur.Vasculitis may involve other organs, including the liver, kidney, brain, and joints.Drugs are an infrequent cause of vasculitis. Infection and collagen vasculardisease are responsible for the majority of cases. Propylthiouracil induces a cutaneous vasculitis that is accompanied byleukopenia and splenomegaly. Direct immunofluorescent changes in these lesionssuggest immune-complex deposition. Drugs implicated in vasculitis includeallopurinol, thiazides, sulfonamides, other antimicrobials, and several NSAIDs.The presence of eosinophils in the perivascular infiltrate of skin biopsy mayindicate a higher probability of a drug etiology. PUSTULAR ERUPTIONS AGEP is a rare reaction pattern, often associated with exposure to drugs.Usually beginning on the face or intertriginous areas, small nonfollicular pustulesoverlying erythematous and edematous skin may coalesce and lead to superficialulceration. Differentiating this eruption from TEN in its initial stages may bedifficult. A skin biopsy is important and shows scattered pustules in the upper partof the epidermis instead of the full-thickness necrosis that characterizes TEN.Fever is present with elevated neutrophil counts, and sepsis is often suspected.Acute pustular psoriasis is the principal differential diagnostic consideration.AGEP often begins within a few days of initiating drug treatment, most notablyantibiotics. For other associated drugs, diltiazem, chloroquine,hydroxychloroquine or terbinafine, AGEP begins later: 7–14 days after initiationof treatment. HYPERSENSITIVITY SYNDROME Initially described with phenytoin, hypersensitivity syndrome—amultiorgan drug-induced reaction—is also known as DRESS and drug-inducedhypersensitivity syndrome (DIHS). It presents as a widespread erythematouseruption that may become purpuric or lichenoid and is accompanied by many ofthe following features: fever, facial and periorbital edema, tender generalizedlymphadenopathy, leukocytosis (often with atypical lymphocytes andeosinophils), hepatitis, and sometimes nephritis or pneumonitis. The cutaneousreaction usually begins 2–8 weeks after the drug is started and lasts longer thanmild eruptions after drug cessation. Symptoms may persist for several weeks,especially hepatitis. The eruption recurs with rechallenge, and cross-reactionsamong aromatic anticonvulsants, including phenytoin, carbamazepine, andbarbiturates, are frequent. Other drugs causing this syndrome include lamotrigine,minocycline, dapsone, allopurinol, and sulfonamides, as well as abacavir andzalcitabine in HIV-infected patients. Reactivation of herpes viruses, especially ofherpes virus 6, has been reported to be frequent in this syndrome. The role of virusinfection is still unclear; it may contribute to long-lasting manifestations such ashepatitis or encephalitis. Mortality as high as 10% has been reported. In life-threatening situations such as pneumonitis or nephritis, systemic glucocorticoids(prednisone, 0.5–1.0 mg/kg) seem to reduce symptoms. Topical high-potencyglucocorticoids may also be helpful. In all cases, rapid withdrawal of thesuspected drug is required. STEVENS-JOHNSON SYNDROME AND TOXIC EPIDERMALNECROLYSIS SJS and TEN are terms that, most believe, describe the same usually drug-induced disorder, which is characterized by blisters and epidermal detachmentresulting from epidermal necrosis in the absence of substantial dermalinflammation. The term SJS is now used to describe cases with blisters developingon dusky or purpuric macules in which total body surface area blistering andeventual detachment is 30% detachment.Erythema multiforme major is now ...