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Drug Eruptions Workup

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

Laboratory Studies

History and physical examination are often sufficient for diagnosing mild asymptomatic eruptions. Severe or persistent eruptions may require further diagnostic testing, as follows:

  • Biopsy can be helpful in confirming the diagnosis of a drug eruption (eg, by showing eosinophils in morbilliform eruptions or numerous neutrophils without vasculitis in persons with Sweet syndrome).
  • CBC count with differential may show leukopenia, thrombocytopenia, and eosinophilia in patients with serious drug eruptions.
  • Serum chemistry studies may be useful. Liver involvement leading to death can occur in persons with hypersensitivity syndromes. Special attention should be paid to the electrolyte balance and renal and/or hepatic function indices in patients with severe reactions such as SJS, TEN, or vasculitis.
  • Antibody and/or immunoserology tests may be ordered. Antihistone antibodies are noted in persons with drug-induced SLE, whereas anti-Ro/SS-A antibodies are most common in persons with drug-induced SCLE.
  • Direct cultures may be needed to investigate a primary infectious etiology or secondary infection.
  • Urinalysis, stool guaiac tests, and chest radiography are important for patients with vasculitis.
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Imaging Studies

Chest radiography, along with urinalysis and stool guaiac tests, is important for patients with vasculitis.

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Other Tests

Rechallenge tests by means of skin prick or patch testing to confirm the causative agent is of limited value. Skin tests may be hazardous to patients who have had severe reactions. With the possible exception of acute generalized exanthematous pustulosis (AGEP), patch tests have a low sensitivity and specificity and are not useful.[39]

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Histologic Findings

In some cases, biopsy may be helpful in establishing a diagnosis of a drug reaction.

Histopathology of an exanthematous drug eruption may show both superficial and deep perivascular inflammatory cell infiltrates. Eosinophils in the infiltrate suggest such a drug eruption (see the image below).

Superficial perivascular inflammatory infiltrate wSuperficial perivascular inflammatory infiltrate with numerous eosinophils characteristic of an exanthematous drug eruption.

In patients with Sweet syndrome, biopsy reveals edema of the superficial dermis and a dense infiltrate of neutrophils. Leukocytoclasia may be present, but vasculitis is absent.

Histopathology of TEN shows subepidermal split, full-thickness epidermal necrosis and a sparse perivascular lymphocytic infiltrate (see the image below).

Confluent necrosis of the epidermis in toxic epideConfluent necrosis of the epidermis in toxic epidermal necrolysis.
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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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