Chapter 056. Cutaneous Drug Reactions (Part 5)

Onychomadesis Onychomadesis is caused by temporary arrest of nail matrix mitotic activity. Common drugs reported to induce onychomadesis includecarbamazepine, lithium, retinoids, and chemotherapeutic agents such as cyclophosphamide and vincristine.ParonychiaParonychia and multiple pyogenic granuloma with progressive and painful periungual abscess of fingers and toes are a side effect of systemic retinoids,lamivudine, indinavir, and anti-EGFR monoclonal antibodies (cetuximab, gefitinib).Nail DiscolorationSomedrugs,includinganthracyclines,taxanes,fluorouracil,andzidovudine, may induce nail bed hyperpigmentation through melanocyte stimulation. It appears to be reversible and dose-dependent. ...
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Chapter 056. Cutaneous Drug Reactions (Part 5) Chapter 056. Cutaneous Drug Reactions (Part 5) Onychomadesis Onychomadesis is caused by temporary arrest of nail matrix mitoticactivity. Common drugs reported to induce onychomadesis includecarbamazepine, lithium, retinoids, and chemotherapeutic agents such ascyclophosphamide and vincristine. Paronychia Paronychia and multiple pyogenic granuloma with progressive and painfulperiungual abscess of fingers and toes are a side effect of systemic retinoids,lamivudine, indinavir, and anti-EGFR monoclonal antibodies (cetuximab,gefitinib). Nail Discoloration Some drugs, including anthracyclines, taxanes, fluorouracil, andzidovudine, may induce nail bed hyperpigmentation through melanocytestimulation. It appears to be reversible and dose-dependent. PRURITUS Pruritus is a common symptom of most drug eruptions, but it may alsooccur without skin lesions as the only manifestation of drug intolerance. Severepruritus may occur in up to 50% of African patients treated with antimalarials andlead to poor compliance. It is much rarer in Caucasians. Immune Cutaneous Reactions: Benign MACULOPAPULAR ERUPTIONS Morbilliform or maculopapular eruptions are the most common of all drug-induced reactions, often start on the trunk or areas of pressure or trauma, andconsist of erythematous macules and papules that are frequently symmetric andmay become confluent. Involvement of mucous membranes is unusual, with theexception of scaly lips; the eruption may be associated with moderate to severepruritus and fever. Diagnosis is rarely assisted by laboratory testing. Skin biopsy isuseless because it shows normal skin or very mild and nonspecific changes. Aviral exanthem is the principal differential diagnostic consideration, especially inchildren. Absence of enanthems, absence of symptoms in ears, nose, and throatand upper respiratory tract, and polymorphism of the skin lesions support a drugrather than a viral eruption. Maculopapular reactions usually develop within 1 week of initiation oftherapy and last less than 2 weeks. Occasionally these eruptions may decrease orfade with continued use of the responsible drug. Since the eruption may alsoworsen, the suspect drug should be discontinued unless it is essential. Oralantihistamines, emollients, and soothing baths may help relieve pruritus. Shortcourses of potent topical glucocorticoids can reduce inflammation and symptoms.Systemic glucocorticoid treatment is rarely indicated. URTICARIA/ANGIOEDEMA Urticaria is the second most frequent type of cutaneous reaction to drugs.However, drug allergy explains no more than 10–20% of acute urticaria cases. Itis a skin reaction characterized by pruritic, red wheals of varying size. Individuallesions rarely last more than 24 h. Deep edematous dermal and subcutaneoustissues are known as angioedema. Angioedema may involve mucous membranes.Urticaria and angioedema may be part of a life-threatening anaphylactic reaction. Drug-induced urticaria may be caused by three mechanisms: an IgE-dependent mechanism, circulating immune complexes (serum sickness), andnonimmunologic activation of effector pathways. IgE-dependent urticarialreactions usually occur within 36 h of drug exposure but can occur within minutes.Immune complex–induced urticaria associated with serum sickness usually occurs6–12 days after first exposure. In this syndrome, the urticarial eruption may beaccompanied by fever, hematuria, arthralgias, hepatic dysfunction, and neurologicsymptoms. Certain drugs, such as NSAIDs, ACE inhibitors, angiotensin II antagonists,and radiographic dyes, may induce urticarial reactions, angioedema, andanaphylaxis in the absence of drug-specific antibody. Although ACE inhibitors,aspirin, penicillin, and blood products are the most frequent causes of urticarialeruptions, urticaria has been observed in association with nearly all drugs. Drugsmay also cause chronic urticaria, which lasts more than 6 weeks. Aspirinfrequently exacerbates this problem. The treatment of urticaria or angioedema depends on the severity of thereaction and the rate at which it is evolving. In severe cases, with respiratory orcardiovascular compromise, epinephrine is the mainstay of therapy, but its effectis reduced in patients using beta blockers. Treatment with systemicglucocorticoids, sometimes administered IV, is helpful. In addition to drugwithdrawal, for patients with only cutaneous symptoms and without symptoms ofangioedema or anaphylaxis, oral antihistamines are usually sufficient.[newpage]