Drug Eruptions Medication

  • Author: Jonathan E Blume, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: May 15, 2012
 

Medication Summary

Therapy for most drug eruptions is mainly supportive in nature. Morbilliform eruptions are treated with oral antihistamines and topical steroids. IVIG is currently the most common agent used to treat TEN. Cyclosporine may also have a role in the treatment of TEN. Prednisone may be used in the treatment of hypersensitivity syndrome with heart and lung involvement, severe serum sickness–like reaction, and Sweet syndrome.

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First-generation antihistamines

Class Summary

These agents antagonize H1 receptors and block release of histamine. They provide symptomatic relief of pruritus and help improve eruptions.

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Hydroxyzine HCl (Anxanil, Atarax, Atozine, Durrax, Vistaril)

 

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical CNS. Available as 10-, 25-, 50-, or 100-mg tab.

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Diphenhydramine HCl (Benadryl, Benylin, Diphen, AllerMax)

 

For symptomatic relief of allergic symptoms caused by release of histamine in immune reactions.

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Second-generation antihistamines, nonsedating

Class Summary

These agents cause less, if any, drowsiness than first-generation agents.

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Loratadine (Claritin)

 

Selectively inhibits peripheral histamine H1 receptors.

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Corticosteroids

Class Summary

Topical agents provide symptomatic relief of pruritus. Systemic steroids are used in persons with hypersensitivity syndrome, severe serum sickness–like reactions, and Sweet syndrome.

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Desonide

 

For inflammatory dermatosis responsive to steroids; decreases inflammation by suppressing migration of PMN leukocytes and reversing capillary permeability.

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Prednisone (Deltasone, Orasone, Sterapred)

 

Immunosuppressant for treatment of immune disorders; may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity; available in 2.5-, 5-, 10-, 20-, or 50-mg tab.

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Immunoglobulins

Class Summary

These agents are used to treat TEN.

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Intravenous immunoglobulin (Gammagard, Gamimune)

 

Blood product prepared from pooled plasma of healthy donors. Following features are possibly relevant to efficacy: neutralization of circulating myelin antibodies through anti-idiotypic antibodies; down-regulation of proinflammatory cytokines, including IFN-gamma; blockade of Fc receptors on macrophages; suppression of inducer T and B cells and augmentation of T-suppressor cells; blockade of complement cascade; promotion of remyelination; and 10% increase in CSF IgG.

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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, and International Society of Dermatology

Disclosure: Nothing to disclose.

Coauthor(s)

Liaqat Ali, MD  Fellow, Division of Dermatopathology, Department of Dermatology and Pathology, Pennsylvania State University College of Medicine

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

Disclosure: Nothing to disclose.

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 and American Academy of Dermatology

Disclosure: Nothing to disclose.

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.

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, and American Society of Dermatopathology

Disclosure: Nothing to disclose.

Specialty Editor Board

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: American Academy of Dermatology, American Society for Clinical Pharmacology and Therapeutics, Canadian Dermatology Association, Canadian Medical Association, Ontario Medical Association, and Royal College of Physicians and Surgeons of Canada

Disclosure: Nothing to disclose.

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, Association of Military Dermatologists, Texas Dermatological Society, and Texas Medical Association

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, and American College of Rheumatology

Disclosure: Amgen Honoraria Consulting; Celgene Honoraria Safety Monitoring Committee

Catherine M Quirk, MD  Clinical Assistant Professor, Department of Dermatology, University of Pennsylvania

Catherine M Quirk, MD is a member of the following medical societies: Alpha Omega Alpha and American Academy of Dermatology

Disclosure: Nothing to disclose.

Chief Editor

Dirk M Elston, MD  Director, Ackerman Academy of Dermatopathology, New York

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