Solar Urticaria Medication

Author: Ani L Tajirian, MD; Chief Editor: Dirk M Elston, MD more...

Updated: Jan 11, 2012

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Medication Summary
Antihistamines
Antimalarials
Histamine H2-receptor antagonists
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Medication Summary

Treatment of solar urticaria can be frustrating. A combination of different modalities is often necessary, but the success of these methods is highly variable. Taking measures to avoid or minimize sun exposure is the most important step for patients with solar urticaria. Unfortunately, this often requires major adjustments in lifestyle, which might be impractical for some patients.

Class Summary

Because solar urticaria involves IgE-mediated mast cell degranulation with consequent histamine release, the first line of treatment consists of long-acting, nonsedating H1-receptor blockers. Often, such agents achieve a protective factor of 10 or more. The extent to which this is useful depends on the severity of the disease itself. For example, someone who gets hives after just a few seconds of sun exposure is unlikely to benefit from antihistamine monotherapy. A patient requiring 10 minutes or more of exposure would show more benefit. Antihistamines seem to block wheal response and minimize pruritus, but they do not entirely eliminate an erythematous reaction. This tendency should be explained to the patient.

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Cetirizine (Zyrtec)

Forms complex with histamine for H1-receptor sites in blood vessels, GI tract, and respiratory tract.

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Fexofenadine (Allegra)

Competes with histamine for H1 receptors in GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. Does not sedate.

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Loratadine (Claritin)

Selectively inhibits peripheral H1 receptors.

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Desloratadine (Clarinex)

Long-acting tricyclic histamine antagonist selective for H1 receptor. Relieves nasal congestion and systemic effects of seasonal allergy. A major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine.

Class Summary

Used to treat certain photosensitive eruptions, including solar urticaria. Efficacy is unpredictable.

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Hydroxychloroquine (Plaquenil)

Inhibits chemotaxis of eosinophils and locomotion of neutrophils. Impairs complement-dependent antigen-antibody reactions.

Hydroxychloroquine sulfate 200 mg is equivalent to 155 mg hydroxychloroquine base and 250 mg chloroquine phosphate.

Class Summary

Usually given in addition to H1 blockers.

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Ranitidine (Zantac)

H2 antagonist that, when combined with H1 type, may be useful in treating allergic reactions that do not respond to H1 antagonists alone.

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Contributor Information and Disclosures

Author

Ani L Tajirian, MD Resident Physician, Department of Dermatology, University of Medicine and Dentistry of New Jersey-New Jersey Medical School

Disclosure: Nothing to disclose.

Coauthor(s)

Philip J Cohen, MD Chief, Section of Dermatology, New Jersey Veterans Affairs Medical Center

Disclosure: Nothing to disclose.

Specialty Editor Board

Donald Belsito, MD Professor of Clinical Dermatology, Department of Dermatology, Columbia University Medical Center

Donald Belsito, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, Dermatology Foundation, New York County Medical Society, New York Dermatological Society, Noah Worcester Dermatological Society, and Phi Beta Kappa

Disclosure: Nothing to disclose.

Michael J Wells, MD Associate Professor, Department of Dermatology, Texas Tech University Health Sciences Center, Paul L Foster School of Medicine

Michael J Wells, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Medical Association, and Texas Medical Association

Disclosure: Nothing to disclose.

Jeffrey Meffert, MD Assistant Clinical Professor of Dermatology, University of Texas School of Medicine at San Antonio

Jeffrey Meffert, MD is a member of the following medical societies: American Academy of Dermatology, American Medical Association, Association of Military Dermatologists, and Texas Dermatological Society

Disclosure: Nothing to disclose.

Joel M Gelfand, MD, MSCE Medical Director, Clinical Studies Unit, Assistant Professor, Department of Dermatology, Associate Scholar, Center for Clinical Epidemiology and Biostatistics, University of Pennsylvania

Joel M Gelfand, MD, MSCE is a member of the following medical societies: Society for Investigative Dermatology

Disclosure: AMGEN Consulting fee Consulting; AMGEN Grant/research funds Investigator; Genentech Grant/research funds investigator; Centocor Consulting fee Consulting; Abbott Grant/research funds investigator; Abbott Consulting fee Consulting; Novartis investigator; Pfizer Grant/research funds investigator; Celgene Consulting fee DMC Chair; NIAMS and NHLBI Grant/research funds investigator

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.

Additional Contributors

The authors and editors of eMedicine gratefully acknowledge the contributions of previous authors, Elma Baron, MD, and Charles Taylor, MD, to the development and writing of this article.

References

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