Mastocytosis Medication

  • Author: Daniel J Hogan, MD; Chief Editor: Dirk M Elston, MD   more...
 
Updated: Jun 4, 2010
 

Medication Summary

Tailor therapy according to the patient's specific needs for symptomatic relief. Patients may be started on oral H1 antihistamine and/or oral disodium cromoglycate with or without the use of a potent topical steroid for selected cutaneous lesions. In patients with a limited number of lesions, intralesional corticosteroid injections are an additional therapeutic option. Oral histamine H2 antagonists may be administered in addition to an oral H1 antihistamine.

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Antihistamines

Class Summary

Relieve pruritus and flushing.

Hydroxyzine (Atarax, Atozine, Vistaril)

 

Antagonizes H1 receptors in periphery. May suppress histamine activity in subcortical region of CNS.

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Mast cell stabilizers

Class Summary

Cromolyn is a mast cell stabilizer that improves diarrhea, flushing, headaches, vomiting, urticaria, abdominal pain, nausea, and itching in some patients.

Cromolyn sodium (Gastrocrom)

 

Inhibits degranulation of sensitized mast cells following exposure to specific antigens. Available as an oral concentrate solution in 5-mL ampules to mix with water and is administered at least 30 min ac. Each 5-mL ampule contains 100 mg of cromolyn sodium, USP, in purified water. Each foil pouch contains 8 ampules.

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Histamine H2 antagonists

Class Summary

Addition of H2 antagonist to H1 antagonist helps control pruritus and whealing. In addition, GI symptoms associated with hyperchlorhydria, such as peptic ulcer disease and gastritis, respond well to this medication.

Cimetidine (Tagamet)

 

H2 antagonist that when combined with an H1 type may be useful in treating itching and flushing in urticaria and contact dermatitis that do not respond to H1 antagonists alone. Use in addition to H1 antihistamines.

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Vasopressors

Class Summary

For patients with systemic disease or extensive symptoms.

Epinephrine (EpiPen)

 

DOC for treating anaphylactoid reactions. Has alpha-agonist effects that include increased peripheral vascular resistance, reversed peripheral vasodilatation, systemic hypotension, and vascular permeability. Beta-agonist effects include bronchodilatation, chronotropic cardiac activity, and positive inotropic effects.

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Contributor Information and Disclosures
Author

Daniel J Hogan, MD  Clinical Professor of Internal Medicine (Dermatology), Nova Southeastern University College of Osteopathic Medicine; Investigator, Hill Top Research, Florida Research Center

Daniel J Hogan, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, American Contact Dermatitis Society, and Canadian Dermatology Association

Disclosure: Nothing to disclose.

Coauthor(s)

Christin M Mastrodomenico  Louisiana State University School of Medicine-Shreveport

Christin M Mastrodomenico is a member of the following medical societies: American Medical Association, Louisiana State Medical Society, and Student National Medical Association

Disclosure: Nothing to disclose.

Specialty Editor Board

Timothy McCalmont, MD  Director, UCSF Dermatopathology Service, Professor of Clinical Pathology and Dermatology, Departments of Pathology and Dermatology, University of California at San Francisco; Editor-in-Chief, Journal of Cutaneous Pathology

Timothy McCalmont, MD is a member of the following medical societies: Alpha Omega Alpha, American Medical Association, American Society of Dermatopathology, California Medical Association, College of American Pathologists, and United States and Canadian Academy of Pathology

Disclosure: Apsara Consulting fee Independent contractor

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.

Rosalie Elenitsas, MD  Herman Beerman Associate Professor of Dermatology, University of Pennsylvania School of Medicine; Director, Penn Cutaneous Pathology Services, Department of Dermatology, University of Pennsylvania Health System

Rosalie Elenitsas, MD is a member of the following medical societies: American Academy of Dermatology and American Society of Dermatopathology

Disclosure: Lippincott Williams Wilkins Royalty Textbook editor; DLA Piper Consulting fee Consulting

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.

Acknowledgments

The authors and editors of eMedicine gratefully acknowledge the contributions of previous author, Virginia Pylant Lewis, MD, to the development and writing of this article.

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Urticaria pigmentosa lesions on the face of a child. Courtesy of Lee H. Grafton, MD.
Urticaria pigmentosa lesions on the back of a child. Courtesy of Lee H. Grafton, MD.
Lesion on the scalp of an infant.
Lesion on the arm. Courtesy of Lee H. Grafton, MD.
Blistering lesion.
Hematoxylin and eosin stain revealing mast cells in the papillary dermis.
Giemsa stain revealing mast cells.
 
 
 
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