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Drug Eruptions Clinical Presentation

  • Author: Jonathan E Blume, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Oct 09, 2015
 

History

The first step is to review the patient's complete medication list, including over-the-counter supplements. Document any history of previous adverse reactions to drugs or foods. Consider alternative etiologies, especially viral exanthems and bacterial infections. Exanthematous eruptions in children are more likely to be due to a viral infection than another infection; however, most such reactions in adults are due to medications.

Note any concurrent infections, metabolic disorders, or immunocompromise (eg, due to HIV infection, cancer, chemotherapy) because these increase the risk of drug eruptions. Immunocompromised persons have a 10-fold higher risk of developing a drug eruption than the general population. Although HIV infection causes profound anergy to other immune stimuli, the frequency of drug hypersensitivity reactions, including severe reactions (eg, TEN), is markedly increased in HIV-positive individuals. Patients with advanced HIV infection (CD4 count < 200 cells/µL) have a 10- to 50-fold increased risk of developing an exanthematous eruption to sulfamethoxazole.

Note and detail the following:

  • All prescription and over-the-counter drugs, including topical agents, vitamins, and herbal and homeopathic remedies
  • The interval between the introduction of a drug and onset of the eruption
  • Route, dose, duration, and frequency of drug administration
  • Use of parenterally administered drugs, which are more likely than oral agents to cause anaphylaxis
  • Use of topically applied drugs, which are more likely than other drugs to induce delayed-type hypersensitivity reactions
  • Use of multiple courses of therapy and prolonged administration of a drug, which can cause allergic sensitization
  • Any improvement after drug withdrawal and any reaction with readministration
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Physical

Although most drug eruptions are exanthematous, different types of drug eruptions are described.

With every drug eruption, it is important to evaluate for certain clinical features that may indicate a severe, potentially life-threatening drug reaction, such as TEN or hypersensitivity syndrome. Such features include the following:

  • Mucous membrane erosions
  • Blisters (Blisters herald a severe drug eruption.)
  • Nikolsky sign (epidermis sloughs with lateral pressure; indicates serious eruption that may constitute a medical emergency)
  • Confluent erythema
  • Angioedema and tongue swelling
  • Palpable purpura
  • Skin necrosis (see the image below)
    Warfarin (Coumadin) necrosis involving the leg. Warfarin (Coumadin) necrosis involving the leg.
  • Lymphadenopathy
  • High fever, dyspnea, or hypotension

Appreciating the morphology and features of drug eruptions is important. This can help the clinician determine the causative medication and the most appropriate treatment. See the following:

  • Acneiform: This is characterized by inflammatory papules or pustules that have a follicular pattern. They are localized primarily on the upper body. In contrast to acne vulgaris, comedones are absent in acneiform eruptions.
  • Acral erythema (erythrodysesthesia): This is a relatively common reaction to chemotherapy and is characterized by symmetric tenderness, edema, and erythema of the palms and soles. It is thought to be a direct toxic effect on the skin. Acral erythema often resolves 2-4 weeks after chemotherapy is discontinued.
  • Acute generalized exanthematous pustulosis (AGEP): Acute-onset fever and generalized scarlatiniform erythema occur with many small, sterile, nonfollicular pustules. The clinical presentation is similar to pustular psoriasis, but AGEP has more marked hyperleukocytosis with neutrophilia and eosinophilia. Most cases are caused by drugs (primarily antibiotics) often in the first few days of administration. A few cases are caused by viral infections, mercury exposure, or UV radiation. AGEP resolves spontaneously and rapidly, with fever and pustules lasting 7-10 days then desquamation over a few days.
  • Dermatomyositis like: Cutaneous findings include dermatomyositis (eg, Gottron papules), but patients tend to lack muscle involvement, associated malignancy, and antinuclear antibodies. Improvement is usually noted after the drug is withdrawn.
  • DRESS (ie, drug reaction with eosinophilia and systemic symptoms) syndrome or DIHS drug-induced hypersensitivity syndrome: These are characterized by the triad of fever, skin eruption, and internal organ involvement, and they usually are associated with intake of anticonvulsant drugs.
  • EM: This includes a spectrum of diseases (eg, EM minor, EM major), as described below; however, many authorities categorize SJS and TEN as EM major and differentiate them by body surface involvement
    • EM minor - Overall, this is a mild disease; patients are healthy. It is characterized by target lesions distributed predominantly on the extremities (see the images below). Mucous membrane involvement may occur but is not severe. Patients with EM minor recover fully, but relapses are common. Most cases are due to infection with herpes simplex virus, and treatment and prophylaxis with acyclovir is helpful.
      Erythema multiforme. Erythema multiforme.
      Target lesions of erythema multiforme. Target lesions of erythema multiforme.
    • SJS: This is characterized by widespread skin involvement, large and atypical targetoid lesions, significant mucous membrane involvement, constitutional symptoms, and sloughing of 10% of the skin. SJS can be caused by drugs and infections (especially those due to Mycoplasma pneumoniae).
    • SJS/TEN overlap: Epidermal detachment involves 10-30% of body surface area.
    • TEN: This is a severe skin reaction that involves a prodrome of painful skin (not unlike sunburn) quickly followed by rapid, widespread, full-thickness skin sloughing. It typically affects 30% or more the total body surface area (see the images below). Secondary infection and sepsis are major concerns, and pneumonia may develop from aspiration of sloughed mucosa. Most cases are due to drugs. The risk of TEN in HIV-positive patients is 1000-fold higher than in the general population.
      Toxic epidermal necrolysis. Toxic epidermal necrolysis.
      Stevens-Johnson syndrome. Stevens-Johnson syndrome.
  • Erythema nodosum: This is characterized by tender, red, subcutaneous nodules that typically appear on the anterior aspect of the legs. Lesions do not suppurate or become ulcerated (see the image below). It is a reactive process often secondary to infection, but it may be due to medications, especially oral contraceptives and sulfonamides.
    Erythema nodosum. Erythema nodosum.
  • Erythroderma: This is widespread inflammation of the skin (see the image below), and it may result from an underlying skin condition, drug eruption, internal malignancy, or immunodeficiency syndrome. Lymphadenopathy is often noted, and hepatosplenomegaly, leukocytosis, eosinophilia, and anemia may be present.
    Erythroderma. Erythroderma.
  • Fixed drug eruptions: Lesions recur in the same area when the offending drug is given (see the image below). Circular, violaceous, edematous plaques that resolve with macular hyperpigmentation is characteristic. Lesions occur 30 minutes to 8 hours after drug administration. Perioral and periorbital lesions may occur, but the hands, feet, and genitalia are the most common locations.
    Fixed drug eruption. Fixed drug eruption.
  • Hypersensitivity syndrome: This is a potentially life-threatening complex of symptoms often caused by anticonvulsants. Patients have fever, sore throat, rash, lymphadenopathy, hepatitis, nephritis, and leukocytosis with eosinophilia. It usually begins within 1-3 weeks after a new drug is started, but it may develop 3 months or later into therapy. Aromatic anticonvulsant drugs cross-react (ie, phenytoin, phenobarbital, carbamazepine); valproic acid is a safe alternative.
  • Leukocytoclastic vasculitis: This is the most common severe drug eruption seen in clinical practice (see the image below). It is characterized by blanching erythematous macules quickly followed by palpable purpura. Fever, myalgias, arthritis, and abdominal pain may be present. It typically appears 7-21 days after the onset of drug therapy, and a laboratory evaluation to exclude internal involvement is mandatory.
    Vasculitic reaction on the legs. Vasculitic reaction on the legs.
  • Lichenoid: This reaction appears similar to lichen planus and may be severely pruritic (see the image below). The eruption may include eczematous or psoriasiform papules.
    Lichen planus on the neck. Lichen planus on the neck.
  • Lupus: Drug-induced systemic lupus erythematosus (SLE) produces symptoms identical to those of SLE, but skin findings are uncommon. Lesions are also identical to drug-induced subacute cutaneous lupus erythematosus (SCLE), which is characterized by annular, psoriasiform, nonscarring lesions in a photodistributed pattern.
  • Morbilliform or exanthematous: This is the most common pattern of drug eruptions; it is the quintessential drug rash. Exanthem is typically symmetric, with confluent erythematous macules and papules that spare the palms and soles. It typically develops within 2 weeks after the onset of therapy.
  • Pseudoporphyria [1] : While largely a drug-induced condition, it can also occur with use of tanning beds and hemodialysis. Patients have blistering and skin fragility that is clinically and pathologically (see the image below) identical to that of porphyria cutanea tarda, but hypertrichosis and sclerodermoid changes are absent and urine and serum porphyrin levels are normal. Treatment is sun protection and withdrawal of the medication.
    Confluent necrosis of the epidermis in toxic epide Confluent necrosis of the epidermis in toxic epidermal necrolysis.
  • Serum sickness and serum sickness–like: These are type III hypersensitivity reactions mediated by the deposition of immune complexes in small vessels, activation of complement, and recruitment of granulocytes. Cutaneous signs typically begin with erythema on the sides of the fingers, hands, and toes and progress to a widespread eruption (most often morbilliform or urticarial). Viscera may be involved, and fever, arthralgia, and arthritis are common. Serum sickness–like reactions have a clinical presentation similar to that of serum sickness reactions, without the immune complex deposition. Renal involvement is rare. Serum sickness–like reactions usually occur with antibiotic therapy, especially with cefaclor.
  • Sweet syndrome ( acute febrile neutrophilic dermatosis): Tender erythematous papules and plaques occur most often on the face, neck, upper trunk, and extremities. The surface of the lesions may become vesicular or pustular. Systemic findings are common and include fever (most often), arthritis, arthralgias, conjunctivitis, episcleritis, and oral ulcers. Laboratory evaluation usually reveals an elevated sedimentation rate, neutrophilia, and leukocytosis. Sweet syndrome often occurs in association with cancers, inflammatory disorders, pregnancy, and medication use.
  • Urticaria: This usually occurs as small wheals that may coalesce or may have cyclical or gyrate forms. Lesions usually appear shortly after the start of drug therapy and resolve rapidly when the drug is withdrawn (see the image below). Giant urticaria is easily mistaken for EM.
    Perivascular mixed inflammatory infiltrate with eo Perivascular mixed inflammatory infiltrate with eosinophils characteristic of drug-induced urticaria.
  • Vesiculobullous: These reactions can resemble pemphigus, bullous pemphigoid, linear immunoglobulin A (IgA) dermatosis, dermatitis herpetiformis, herpes gestationis, or cicatricial pemphigoid. Most causative drugs have a thiol group, disulfide bonds, or sulfur-containing rings that are metabolized to thiol forms. Thiol-induced pemphigus tends to resemble pemphigus foliaceus or pemphigus erythematosus; nonthiol eruptions may resemble pemphigus vulgaris or pemphigus vegetans. Mucosal findings may be most common with nonthiol drugs. Results from direct and indirect immunofluorescence may be positive in persons with drug-induced pemphigus and bullous pemphigoid. Eruptions usually resolve after the inducing drug is discontinued, but D-penicillamine–induced pemphigus may take months to resolve and corticosteroids are often needed.

(Also see the Pill Identifier tool.)

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Causes

Fibrosing reactions have been associated with a variety of chemical exposures. Nephrogenic systemic fibrosis has been associated with gadolinium contrast agents used for MRI studies. Individuals with renal failure may have a buildup gadolinium in the skin and other organs and may recruit CD34-positive bone marrow–derived fibrocytes into lesional areas. Toxic oil ingestion has been associated with morphea, and Texier disease has been associated with phytomenadione (vitamin-K1) injections.

Rates of reactions to commonly used drugs are as follows:

  • Amoxicillin - 5.1%
  • Trimethoprim sulfamethoxazole - 4.7%
  • Ampicillin - 4.2%
  • Semisynthetic penicillin - 2.9%
  • Blood (whole human) - 2.8%
  • Penicillin G - 1.6%
  • Cephalosporins - 1.3%
  • Quinidine - 1.2%
  • Gentamicin sulfate - 1%
  • Packed red blood cells - 0.8%
  • Mercurial diuretics - 0.9%
  • Heparin - 0.7%

Cutaneous reaction rates in patients with HIV infection are as follows[6] :

  • Sulfasalazine - 20%
  • Trimethoprim-sulfamethoxazole - 14.9%
  • Dapsone - 3.1%
  • Aminopenicillins - 9.3%
  • Penicillins - 3.8%
  • Anticonvulsants - 3.4%
  • Penicillinase-resistant penicillins - 2.9%
  • Cephalosporins - 2.7%
  • Quinolones - 2.1%
  • Ketoconazole - 2%
  • Clindamycin - 1.8%
  • Primaquine - 1.8%
  • Tetracycline - 1.2%
  • Pentamidine - 1%
  • NSAIDs - 0.9%
  • Erythromycin - 0.6%
  • Zidovudine - 0.3%

Drugs that commonly cause serious reactions are as follows:

  • Allopurinol
  • Anticonvulsants
  • NSAIDs
  • Sulfa drugs
  • Bumetanide
  • Captopril
  • Furosemide
  • Penicillamine
  • Piroxicam
  • Thiazide diuretics

Drugs unlikely to cause skin reactions are as follows:

  • Digoxin
  • Meperidine
  • Acetaminophen
  • Diphenhydramine hydrochloride
  • Aspirin
  • Aminophylline
  • Prochlorperazine
  • Ferrous sulfate
  • Prednisone
  • Codeine
  • Tetracycline
  • Morphine
  • Regular insulin
  • Warfarin
  • Folic acid
  • Methyldopa
  • Chlorpromazine
  • Serotonin-specific reuptake inhibitors
  • Topical gels (eg, 4% tetracaine gel may cause serious cutaneous adverse reactions) [7]

Drugs associated with specific morphologic patterns are described below. The following is a list of medications that have been reported to cause specific types of cutaneous reactions. However, not every possible type of drug eruption has been listed. In addition, exclusion of a drug from the following list does not imply that it is not the cause of a patient's eruption. A high index of suspicion must always be maintained when confronted with a new onset eruption in a patient on multiple medications. Note the following:

  • Acneiform - Amoxapine, corticosteroids (see the image below), halogens, haloperidol, hormones, isoniazid, lithium, phenytoin, and trazodone
    Steroid acne. Note pustules and absence of comedon Steroid acne. Note pustules and absence of comedones.
  • AGEP - Most commonly beta-lactam antibiotics, macrolides, and mercury; less commonly acetaminophen, allopurinol, bufexamac, buphenine, carbamazepine, carbutamide, celecoxib, chloramphenicol, clindamycin, co-trimoxazole, clobazam, cyclins (eg, tetracycline), cytarabine, diltiazem, famotidine, furosemide, ginkgo biloba, hydrochlorothiazide, hydroxychloroquine, ibuprofen, imatinib, imipenem, isoniazid, IV contrast dye, lopinavir-ritonavir, mexiletine, morphine, nadoxolol, nifedipine, nystatin, olanzapine, phenytoin, pipemidic acid, piperazine, pseudoephedrine, pyrimethamine, quinidine, ranitidine, rifampicin, salbutiamine, sertraline, simvastatin, streptomycin, terbinafine, thallium, vancomycin, calcium channel blockers, ACE inhibitors (eg, captopril, ramipril), glyburide, and gemfibrozil. [8]
  • Alopecia - ACE inhibitors, allopurinol, anticoagulants, azathioprine, bromocriptine, beta-blockers, cyclophosphamide, didanosine, hormones, indinavir, NSAIDs, phenytoin, methotrexate (MTX), retinoids, and valproate
  • Bullous pemphigoid - Ampicillin, D-penicillamine, captopril, chloroquine, ciprofloxacin, enalapril, furosemide, neuroleptics, penicillins, phenacetin, psoralen plus UV-A, salicylazosulfapyridine, sulfasalazine, and terbinafine
  • Dermatomyositislike [9] - BCG vaccine, hydroxyurea (most common [10] ), lovastatin, omeprazole, penicillamine, simvastatin, and tegafur
  • DRESS syndrome - Most commonly, aromatic anticonvulsants (phenytoin, phenobarbital [phenobarbitone], carbamazepine), sulfonamides, minocycline, and doxycycline [11]
  • Erythema nodosum - Echinacea, halogens, oral contraceptives (most common), penicillin, sulfonamides, and tetracycline
  • Erythroderma - Allopurinol, anticonvulsants, aspirin, barbiturates, captopril, carbamazepine, cefoxitin, chloroquine, chlorpromazine, cimetidine, diltiazem, griseofulvin, lithium, nitrofurantoin, omeprazole, phenytoin, St. John's wort, sulfonamides, and thalidomide
  • Fixed drug eruptions - Acetaminophen, ampicillin, anticonvulsants, aspirin/NSAID, barbiturates, benzodiazepines, butalbital, cetirizine, ciprofloxacin, clarithromycin, dapsone, dextromethorphan, doxycycline, fluconazole, hydroxyzine, lamotrigine, loratadine, metronidazole, oral contraceptives, penicillins, phenacetin, phenolphthalein, phenytoin, piroxicam, saquinavir, sulfonamides, tetracyclines, ticlopidine, tolmetin, vancomycin, and zolmitriptan
  • Hypersensitivity syndrome - Allopurinol, amitriptyline, carbamazepine, dapsone, lamotrigine, minocycline, NSAIDs, olanzapine, oxcarbazepine, phenobarbital, phenytoin, saquinavir, spironolactone, sulfonamides, zalcitabine, and zidovudine
  • Lichenoid [12] - Amlodipine, antimalarials, beta-blockers, captopril, diflunisal, diltiazem, enalapril, furosemide, glimepiride, gold, leflunomide, levamisole, L-thyroxine, orlistat, penicillamine, phenothiazine, pravastatin, proton pump inhibitors, rofecoxib, salsalate, sildenafil, tetracycline, thiazides, and ursodeoxycholic acid
  • Linear IgA dermatosis [13] - Atorvastatin, captopril, carbamazepine, diclofenac, glibenclamide, lithium, phenytoin, and vancomycin
  • Lupus erythematosus [14] : Drug-induced SLE is most commonly associated with hydralazine, procainamide, and minocycline. Beta-blockers, chlorpromazine, cimetidine, clonidine, estrogens, isoniazid, lithium, lovastatin, methyldopa, oral contraceptives, quinidine, sulfonamides, tetracyclines, and tumor necrosis factor (TNF)–alpha inhibitors have been reported. Drug-induced SCLE is most commonly associated with hydrochlorothiazide. Calcium channel blockers, cimetidine, griseofulvin, leflunomide, terbinafine, and TNF-alpha inhibitors have been reported.
  • Morbilliform (exanthematous) - ACE inhibitors, allopurinol, amoxicillin, ampicillin, anticonvulsants, barbiturates, carbamazepine, cetirizine, ginkgo biloba, hydroxyzine, isoniazid, nelfinavir, NSAIDs, phenothiazine, phenytoin, quinolones, sulfonamides, thalidomide, thiazides, trimethoprim-sulfamethoxazole, and zalcitabine
  • Pemphigus [15] : Thiols include captopril, D-penicillamine, gold sodium thiomalate, mercaptopropionylglycine, pyritinol, thiamazole, and thiopronine. Nonthiols include aminophenazone, aminopyrine, azapropazone, cephalosporins, heroin, hydantoin, imiquimod, indapamide, levodopa, lysine acetylsalicylate, montelukast, oxyphenbutazone, penicillins, phenobarbital, phenylbutazone, piroxicam, progesterone, propranolol, and rifampicin.
  • Photosensitivity - ACE inhibitors, amiodarone, amlodipine, celecoxib, chlorpromazine, diltiazem, furosemide, griseofulvin, lovastatin, nifedipine, phenothiazine, piroxicam, quinolones, sulfonamides, tetracycline, and thiazide
  • Pseudoporphyria - Amiodarone, bumetanide, chlorthalidone, cyclosporine, dapsone, etretinate, 5-fluorouracil, flutamide, furosemide, hydrochlorothiazide/triamterene, isotretinoin, NSAIDs (including nalidixic acid and naproxen), oral contraceptive pills, and tetracycline
  • Psoriasis [16, 17, 18] - ACE inhibitors, angiotensin receptor antagonists, antimalarials, beta-blockers, bupropion, calcium channel blockers, carbamazepine, interferon (IFN) alfa, lithium, metformin, NSAIDs, terbinafine, tetracyclines, valproate sodium, and venlafaxine
  • Serum sickness [19] - Antithymocyte globulin for bone marrow failure, human rabies vaccine, penicillin, pneumococcal vaccine (in AIDS patients), and vaccines containing horse serum derivatives
  • Serum sickness–like - Beta-lactam antibiotics, cefaclor (most common), minocycline, propranolol, streptokinase, sulfonamides, and NSAIDs
  • SJS [20, 21, 22] - Allopurinol, anticonvulsants, aspirin/NSAIDS, barbiturates, carbamazepine, cimetidine, ciprofloxacin, codeine, didanosine, diltiazem, erythromycin, furosemide, griseofulvin, hydantoin, indinavir, nitrogen mustard, penicillin, phenothiazine, phenylbutazone, phenytoin, ramipril, rifampicin, saquinavir, sulfonamides, tetracyclines, and trimethoprim-sulfamethoxazole
  • Sweet syndrome - All- trans -retinoic acid, celecoxib, granulocyte colony-stimulating factor, nitrofurantoin, oral contraceptives, tetracyclines, and trimethoprim-sulfamethoxazole
  • TEN - Alfuzosin, allopurinol, anticonvulsants, aspirin/NSAIDs, sulfadoxine and pyrimethamine (Fansidar), isoniazid, lamotrigine, lansoprazole, letrozole, penicillins, phenytoin, prazosin, sulfonamides, tetracyclines, thalidomide, trimethoprim-sulfamethoxazole, and vancomycin
  • Urticaria - ACE inhibitors, alendronate, aspirin/NSAIDs, blood products, cephalosporins, cetirizine, clopidogrel, dextran, didanosine, infliximab, inhaled steroids, nelfinavir, opiates, penicillin, peptide hormones, polymyxin, proton pump inhibitors, radiologic contrast material, ranitidine, tetracycline, vaccines, and zidovudine
  • Vasculitis - Adalimumab, allopurinol, aspirin/NSAIDs, cimetidine, gold, hydralazine, indinavir, leflunomide, levofloxacin, minocycline, montelukast, penicillin, phenytoin, propylthiouracil, proton pump inhibitors, quinolones, ramipril, sulfonamide, tetracycline, thiazides, and thioridazine
  • Vesiculobullous (other) - ACE inhibitors, aspirin/NSAIDs, barbiturates, captopril, cephalosporins, entacapone, estrogen, furosemide, griseofulvin, influenza vaccine, penicillamine, penicillins, sertraline sulfonamides, and thiazides
  • Photosensitivity reaction - Long-term use of voriconazole causes significantly increased photosensitivity, resulting in some patients developing squamous cell carcinoma [23] and melanoma. [24] Recent studies have shown dose-dependent increased risk for squamous cell carcinoma: 5.6% with each 60-day exposure at a standard dose of 200 mg twice daily. At 5 years after transplantation, voriconazole conferred an absolute risk increase for squamous cell carcinoma of 28%.

Psychotropic drugs associated with specific morphologic patterns are as follows[25] :

  • Alopecia - Carbamazepine, fluoxetine, lamotrigine, lithium, gabapentin, and valproic acid
  • EM - Barbiturates, carbamazepine, diazepam overdose, fluoxetine, gabapentin, lithium plus trazodone concurrently, phenobarbital, risperidone, sertraline, and valproic acid
  • Morbilliform (exanthematous) - Alprazolam, barbiturates, bupropion, carbamazepine, chlorpromazine, desipramine, fluoxetine, lithium, maprotiline, nefazodone, risperidone, and trazodone
  • Photosensitivity - All antipsychotics, barbiturates, carbamazepine, chlorpromazine, doxepin, imipramine, thioridazine, and valproic acid
  • Pigmentation - Amitriptyline, carbamazepine, chlorpromazine, clozapine, diazepam following dermabrasion, gabapentin, haloperidol, lamotrigine, perphenazine, and thioridazine
  • Urticaria - Bupropion, carbamazepine, chlordiazepoxide, fluoxetine, imipramine, lamotrigine, lithium, paroxetine, and trazodone
  • Vasculitis - Fluoxetine, maprotiline, paroxetine, and trazodone

Chemotherapeutic agents associated with specific morphologic patterns are as follows:

  • Acneiform - Cetuximab, [26] dactinomycin, erlotinib, [26] fluoxymesterone, gefitinib, medroxyprogesterone, and vinblastine
  • Acral erythema (erythrodysesthesia) - Capecitabine, cisplatin, clofarabine, cyclophosphamide, cytarabine, docetaxel, doxorubicin, fluorouracil, gemcitabine, MTX, tegafur, and vinorelbine
  • Alopecia: All classes of chemotherapeutic agents are associated with alopecia. Commonly associated drugs include alkylating agents, anthracyclines, bleomycin, doxorubicin, hydroxyurea, MTX, mitomycin, mitoxantrone, vinblastine, and vincristine. Busulfan and cyclophosphamide administered in combination can cause permanent hair loss. Nilotinib (Tasigna) is a potent and selective bcr-abl kinase inhibitor currently used to treat imatinib-resistant chronic myeloid leukemia. Clinically, the reaction can present as pink/fleshy perifollicular papules with diffuse alopecia, without follicular drop-out. Histologically, it can demonstrate scarring or nonscarring alopecia with mixed features. [27, 28] Note the images below.
    Male-pattern diffuse hair loss. Male-pattern diffuse hair loss.
    Pink/fleshy perifollicular papules with diffuse al Pink/fleshy perifollicular papules with diffuse alopecia.
    Horizontal section shows perifollicular fibrosis c Horizontal section shows perifollicular fibrosis consistent with scarring alopecia.
  • EM - Busulfan, chlorambucil, cyclophosphamide, diethylstilbestrol (DES), etoposide, hydroxyurea, mechlorethamine, MTX, mitomycin C, mitotane, paclitaxel, and suramin
  • Erythema nodosum - Busulfan, DES, and imatinib
  • Fixed drug eruptions - Dacarbazine, hydroxyurea, paclitaxel, and procarbazine
  • Hyperpigmentation - Bischloroethylnitrosourea (BCNU; carmustine), bleomycin, busulfan, brequinar, cisplatin, cyclophosphamide, dactinomycin, daunorubicin, docetaxel, doxorubicin, fluorouracil, fotemustine, hydroxyurea, ifosfamide, MTX, mithramycin, mitoxantrone, nitrogen mustard, procarbazine, tegafur, thiotepa, and vinorelbine
  • Lichenoid - Hydroxyurea, imatinib, and tegafur
  • Lupus - Aminoglutethimide, DES, hydroxyurea, leuprolide, and tegafur
  • Morbilliform (exanthematous) - Bleomycin, carboplatin, cis -dichloro- trans -dihydroxy- bis -isopropylamine platinum (CHIP), chlorambucil, cytarabine, docetaxel, DES, doxorubicin, etoposide, 5-fluorouracil, hydroxyurea, MTX, mitomycin C, mitotane, mitoxantrone, paclitaxel, pentostatin, procarbazine, suramin, and thiotepa
  • TEN - Asparaginase, bleomycin, chlorambucil, cladribine, cytarabine, doxorubicin, 5-fluorouracil, MTX, plicamycin, procarbazine, and suramin
  • Urticaria [29] - Amsacrine, bleomycin, busulfan, carboplatin, chlorambucil, cisplatin, cyclophosphamide, cytarabine, daunorubicin, diaziquone, didemnin, DES, docetaxel, doxorubicin, epirubicin, etoposide, 5-fluorouracil, mechlorethamine, melphalan, MTX, mitomycin C, mitotane, mitoxantrone, paclitaxel, pentostatin, procarbazine, teniposide, thiotepa, trimetrexate, vincristine, and zinostatin
  • Vasculitis - Busulfan, cyclophosphamide, cytarabine, hexamethylene bisacetamide (HMBA), hydroxyurea, imatinib, levamisole, 6-mercaptopurine, MTX, mitoxantrone, rituximab, and tamoxifen

Cutaneous reactions to targeted chemotherapy are as follows:

  • Epidermal growth factor receptor inhibitors (eg, gefitinib, cetuximab, erlotinib [30] - Abnormal scalp, face hair, and/or eyelash growth, anaphylactic infusion reaction (cetuximab), papules and annular plaques, paronychia with/without pyogenic granulomas, telangiectasias, and xerosis. [31] See the images below.
    Paronychia. Paronychia.
    Papules and annular plaques. Papules and annular plaques.
    Superficial and mid-dermal perivascular infiltrate Superficial and mid-dermal perivascular infiltrate of lymphocytes and eosinophils. Foci of extravasation of erythrocytes.
  • Sorafenib [32] (a novel multikinase inhibitor) - Hand-foot skin reaction, facial and scalp eruption, scalp dysesthesia, subungual splinter hemorrhages, alopecia, body hair loss, stomatitis, nipple hyperkeratosis or pain, and eruptive facial cysts
  • Vemurafenib is a systemic medication recently approved by the Food and Drug Administration (FDA) for the treatment of metastatic melanoma. Vemurafenib selectively targets a specific BRAF mutation, V600E, in melanoma cells that allows unchecked proliferation of malignant cells. An unintended consequence of this medication has been the development of squamous cell carcinomas and keratoacanthomas in approximately a fourth of patients receiving the drug. There are some reports discussing the development of nonmalignant milia in a patient treated with vemurafenib. [33] See the images below.
    Numerous milia in a patient treated with vemurafen Numerous milia in a patient treated with vemurafenib.
    Dilated infundibular cyst. Dilated infundibular cyst.
  • Ipilimumab and vemurafenib each improve the overall survival of patients with metastatic melanoma. Patients with stage IV melanoma harboring a BRAF V600E mutation treated with vemurafenib after receiving ipilimumab can develop a pruritic, grade 3 (severe), maculopapular within 6-8 days after the start of treatment with vemurafenib. [34] .
  • Tamoxifen, an antiestrogenic agent, has been widely used as adjuvant hormonal therapy in the treatment of breast cancer. Distinctive cutaneous eruptions present clinically as papules and plaques and histopathologically are characterized by squamous metaplasia of eccrine ductal epithelium. The condition has varied etiologies and can occur as a drug reaction, with chemotherapeutic drugs being frequently implicated. [35]

Cutaneous reactions to cytokine therapy are as follows[36] :

  • Erythropoietin - Abnormal hair growth, localized rash, palpebral edema, and widespread eczema
  • Granulocyte colony stimulating factor - Exacerbation of preexisting psoriasis, leukocytoclastic, localized erythema, localized pruritus, Sweet syndrome, and vasculitis
  • Granulocyte macrophage colony-stimulating factor - Alopecia, epidermolysis, exacerbation of vasculitis, exfoliative dermatitis, flushing, localized erythema, localized wheals, maculopapular eruptions, pruritus, purpura, and urticaria
  • IFN-alfa - Alopecia, anasarca, cutaneous vascular lesions, eosinophilic fasciitis, exacerbation of preexisting herpes labialis, facial erythema, fixed drug eruption, hyperpigmentation, nummular eczema, paraneoplastic pemphigus, pruritus, psoriasis, sarcoidosis, SLE, urticaria, and xerostomia
  • IFN-beta - Fatal pemphigus vulgaris (when used in combination with interleukin (IL)–2, localized reactions (common), and urticaria
  • IFN-gamma - Increased relapses in melanoma and localized inflammation
  • IL-1alpha - Mucositis, phlebitis, Shwartzman reaction, and xerostomia
  • IL-1beta - Erythema at surgical wound sites, phlebitis, and rash
  • IL-2 - Blisters, cutaneous ulcers, desquamation, erythema, erythema nodosum, erythroderma, exacerbation of autoimmune skin disorders, flushing, hypersensitivity to iodine contrast material, necrosis, pruritus, telogen effluvium, TEN, and urticaria
  • IL-3 - Facial flushing, hemorrhagic rash, thrombophlebitis, and urticaria
  • IL-4 - Facial and peripheral edema, Grover disease, and papular rash
  • IL-6 - Diffuse erythematous scaling macules and papules
  • TNF-alpha antagonists can also cause Sweet-like hypersensitivity reactions and neutrophilic eccrine hidradenitis in addition to pustular folliculitis, psoriasis, interface dermatitis, lupus, vasculitis, and palmoplantar pustulosis. [37]
  • IL-12 and IL-23 monoclonal antibodies [38] - Injection site reactions
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Contributor Information and Disclosures
Author

Jonathan E Blume, MD Instructor in Clinical Dermatology, Columbia University College of Physicians and Surgeons; Dermatologist, Westwood Dermatology and Dermatologic Surgery Group PA

Jonathan E Blume, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, American Society for Dermatologic Surgery, International Society of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Michelle Ehrlich, MD Director of Cosmetic Dermatology and Surgery Residency Program, Harbor-UCLA Medical Center; Clinical Instructor, Department of Dermatology, University of California, Los Angeles, David Geffen School of Medicine

Michelle Ehrlich, MD is a member of the following medical societies: American Academy of Cosmetic Surgery, American Academy of Dermatology

Disclosure: Nothing to disclose.

Thomas N Helm, MD Clinical Professor of Dermatology and Pathology, University of Buffalo, State University of New York School of Medicine and Biomedical Sciences; Director, Buffalo Medical Group Dermatopathology Laboratory

Thomas N Helm, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Society for Dermatologic Surgery, American Society of Dermatopathology

Disclosure: Nothing to disclose.

Liaqat Ali, MD Assistant Professor, Department of Dermatology, Wayne State University School of Medicine; Dermatopathologist, Pinkus Dermatopathology Laboratory, Monroe, MI

Liaqat Ali, MD is a member of the following medical societies: American Society for Clinical Pathology, American Society of Dermatopathology, College of American Pathologists, United States and Canadian Academy of Pathology

Disclosure: Nothing to disclose.

Specialty Editor Board

Richard P Vinson, MD Assistant Clinical Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine; Consulting Staff, Mountain View Dermatology, PA

Richard P Vinson, MD is a member of the following medical societies: American Academy of Dermatology, Texas Medical Association, Association of Military Dermatologists, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeffrey P Callen, MD Professor of Medicine (Dermatology), Chief, Division of Dermatology, University of Louisville School of Medicine

Jeffrey P Callen, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American College of Physicians, American College of Rheumatology

Disclosure: Received income in an amount equal to or greater than $250 from: XOMA; Biogen/IDEC; Novartis; Janssen Biotech, Abbvie, CSL pharma<br/>Received honoraria from UpToDate for author/editor; Received honoraria from JAMA Dermatology for associate editor and intermittent author; Received royalty from Elsevier for book author/editor; Received dividends from trust accounts, but I do not control these accounts, and have directed our managers to divest pharmaceutical stocks as is fiscally prudent from Stock holdings in various trust accounts include some pharmaceutical companies and device makers for i inherited these trust accounts; for: Celgene; Pfizer; 3M; Johnson and Johnson; Merck; Abbott Laboratories; AbbVie; Procter and Gamble; Amgen.

Chief Editor

Dirk M Elston, MD Professor and Chairman, Department of Dermatology and Dermatologic Surgery, Medical University of South Carolina College of Medicine

Dirk M Elston, MD is a member of the following medical societies: American Academy of Dermatology

Disclosure: Nothing to disclose.

Additional Contributors

Neil Shear, MD Professor and Chief of Dermatology, Professor of Medicine, Pediatrics and Pharmacology, University of Toronto Faculty of Medicine; Head of Dermatology, Sunnybrook Women's College Health Sciences Center and Women's College Hospital, Canada

Neil Shear, MD is a member of the following medical societies: Canadian Medical Association, Ontario Medical Association, Royal College of Physicians and Surgeons of Canada, Canadian Dermatology Association, American Academy of Dermatology, American Society for Clinical Pharmacology and Therapeutics

Disclosure: Nothing to disclose.

Acknowledgements

Charles Camisa, MD Head of Clinical Dermatology, Vice-Chair, Department of Dermatology, Cleveland Clinic Foundation

Charles Camisa, MD is a member of the following medical societies: American Academy of Dermatology and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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Morbilliform drug eruption.
Warfarin (Coumadin) necrosis involving the leg.
Toxic epidermal necrolysis.
Stevens-Johnson syndrome.
Erythroderma.
Erythema multiforme.
Fixed drug eruption.
Fixed drug eruption involving the penis.
Oral ulcerations in a patient receiving cytotoxic therapy.
Phototoxic reaction after use of a tanning booth. Note sharp cutoff where clothing blocked exposure.
Vasculitic reaction on the legs.
Lichen planus on the neck.
Steroid acne. Note pustules and absence of comedones.
Drug reaction to hydroxychloroquine (Plaquenil).
Urticaria.
Erythema nodosum.
Confluent necrosis of the epidermis in toxic epidermal necrolysis.
Perivascular mixed inflammatory infiltrate with eosinophils characteristic of drug-induced urticaria.
Biopsy of pseudoporphyria shows a subepidermal blister with little to no inflammation.
Confluent necrosis of the epidermis in toxic epidermal necrolysis.
Superficial perivascular inflammatory infiltrate with numerous eosinophils characteristic of an exanthematous drug eruption.
Target lesions of erythema multiforme.
Papules and annular plaques.
Superficial and mid-dermal perivascular infiltrate of lymphocytes and eosinophils. Foci of extravasation of erythrocytes.
Numerous milia in a patient treated with vemurafenib.
Dilated infundibular cyst.
Paronychia.
Male-pattern diffuse hair loss.
Pink/fleshy perifollicular papules with diffuse alopecia.
Horizontal section shows perifollicular fibrosis consistent with scarring alopecia.
 
 
 
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