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Solar Urticaria Medication

  • Author: Ani L Tajirian, MD; Chief Editor: Dirk M Elston, MD  more...
 
Updated: Aug 11, 2014
 

Medication Summary

Because solar urticaria involves IgE-mediated mast cell degranulation with consequent histamine release, the first line of treatment for this disease consists of long-acting, nonsedating H1-receptor blockers. Often, such agents achieve a protective factor of 10 or more. The H2-receptor antagonist ranitidine and others may aid in treatment when an H1 blocker is not effective on its own.

Antimalarial agents can treat certain photosensitive eruptions, including those of solar urticaria, but their efficacy is unpredictable.

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Antihistamines, 2nd Generation

Class Summary

The extent to which antihistamines are useful against solar urticaria 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, while 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 should be explained to the patient.

Cetirizine (Zyrtec)

 

Cetirizine forms a complex with histamine for H1-receptor sites in the blood vessels, gastrointestinal (GI) tract, and respiratory tract.

Fexofenadine (Allegra)

 

Fexofenadine competes with histamine for H1 receptors in the GI tract, blood vessels, and respiratory tract, reducing hypersensitivity reactions. The drug does not sedate.

Loratadine (Claritin, Alavert)

 

Loratadine selectively inhibits peripheral H1 receptors.

Desloratadine (Clarinex)

 

Desloratadine is a long-acting tricyclic histamine antagonist selective for H1 receptors. It relieves nasal congestion and systemic effects of seasonal allergy. The drug is a major metabolite of loratadine, which, after ingestion, is metabolized extensively to active metabolite 3-hydroxydesloratadine.

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Antimalarials

Class Summary

Antimalarials are used to treat certain photosensitive eruptions, including solar urticaria, but their efficacy is unpredictable.

Hydroxychloroquine (Plaquenil)

 

Hydroxychloroquine inhibits chemotaxis of eosinophils and the locomotion of neutrophils. It impairs complement-dependent antigen-antibody reactions. Hydroxychloroquine sulfate 200mg is equivalent to 155mg hydroxychloroquine base and 250mg chloroquine phosphate.

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Histamine H2-Receptor Antagonists

Class Summary

These agents are usually given in addition to H1 blockers.

Ranitidine (Zantac)

 

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

Famotidine (Pepcid)

 

Famotidine competitively inhibits histamine at the H2 receptors in gastric parietal cells, reducing gastric acid secretion, gastric volume, and hydrogen concentrations.

Nizatidine (Axid, Axid AR)

 

This agent competitively inhibits histamine at the H2 receptor of the gastric parietal cells, resulting in reduced gastric acid secretion, gastric volume, and reduced hydrogen concentrations.

Cimetidine (Tagamet HB 200)

 

This agent inhibits histamine at H2 receptors of gastric parietal cells, which results in reduced gastric acid secretion, gastric volume, and hydrogen concentrations.

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Contributor Information and Disclosures
Author

Ani L Tajirian, MD Procedural Fellow, Division of Dermatology, University of Vermont College of Medicine

Disclosure: Nothing to disclose.

Coauthor(s)

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

Disclosure: Nothing to disclose.

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.

Acknowledgements

Elma D Baron, MD Assistant Professor of Dermatology, Case Western Reserve University, University Hospitals of Cleveland; Director of Skin Study Center, University Hospitals Research Institute; Acting Chief of Dermatology, Veterans Affairs Medical Center, Cleveland

Elma Baron, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Photobiology, Photomedicine Society, and Society for Investigative Dermatology

Disclosure: Nothing to disclose.

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.

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.

Charles R Taylor, MD Associate Professor of Dermatology, Harvard Medical School; Director of Phototherapy Unit, Department of Dermatology, Massachusetts General Hospital

Charles Taylor, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Laser Medicine and Surgery, Massachusetts Medical Society, New England Dermatological Society, and Society for Investigative Dermatology

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.

References
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