Pityriasis Rosea Medication

Updated: Jun 02, 2016
  • Author: Robert A Schwartz, MD, MPH; Chief Editor: Dirk M Elston, MD  more...
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Medication

Medication Summary

Pityriasis rosea (PR) is a self-limited disease; treatment is supportive. Drug therapy for PR primarily consists of symptomatic treatment of pruritus. Topical zinc oxide and calamine lotion may be helpful. Oral antihistamines and topical corticosteroids can be used as needed. For patients in whom superficial tinea infection is a concern or possibility, topical antifungal therapy can be used. There is no evidence-based medicine for pityriasis rosea, a self-limited disorder. [63]

Management of PR in patients with evidence of group A streptococcal infection may be warranted. The possible risk of scarlet fever and poststreptococcal sequelae should be considered. Acyclovir may hasten resolution, especially if given within 1 week of rash, but the data are not conclusive.

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Corticosteroids

Class Summary

Corticosteroids have anti-inflammatory properties and cause profound and varied metabolic effects. In addition, these agents modify the body’s immune response to diverse stimuli. Over-the-counter (OTC) steroid preparations of low-to-medium potency steroids may help relieve the itching associated with PR.

Hydrocortisone topical (Westcort, U-Cort, Ala-Cort, Caldecort)

Topical hydrocortisone is an adrenocorticosteroid derivative that is suitable for application to skin or external mucous membranes and is used to treat inflammatory dermatosis that is responsive to steroids. It decreases inflammation by suppressing the migration of polymorphonuclear leukocytes (PMNs) and reversing capillary permeability.

Betamethasone topical (Diprolene, Luxiq)

Topical betamethasone is used to treat inflammatory dermatoses responsive to steroids. It decreases inflammation by suppressing migration of PMNs and reversing capillary permeability. It affects production of lymphokines and has an inhibitory effect on Langerhans cells.

Clobetasol (Temovate, Temovate E, Olux, Olux-E)

Clobetasol is a class I superpotent topical steroid. It suppresses mitosis and increases synthesis of proteins that decrease inflammation and cause vasoconstriction.

Triamcinolone topical (Kenalog, Triderm)

Topical triamcinolone decreases inflammation by suppressing migration of PMNs and reversing capillary permeability.

Prednisone (Rayos)

Prednisone may decrease inflammation by reversing increased capillary permeability and suppressing PMN activity.

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Antihistamines

Class Summary

Antihistamines may control PR-related itching by blocking effects of endogenously released histamine.

Diphenhydramine (Benadryl, Aler-Cap, Altaryl)

Diphenhydramine, which is available as an OTC product, is a very safe oral antihistamine that can be used safely in pregnancy. It is highly effective for controlling pruritus symptoms caused by release of histamine in allergic reactions.

Hydroxyzine (Vistaril)

Hydroxyzine is a sedating agent that antagonizes H1 receptors in the periphery and may suppress histamine activity in the subcortical region of the central nervous system (CNS). It is effective against PR-related pruritus.

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Antibiotics, Other

Class Summary

Empiric antimicrobial therapy must be comprehensive and should cover all likely pathogens in the context of the clinical setting.

Erythromycin (E.E.S., Ery-Tab, Erythrocin, EryPed)

Erythromycin inhibits bacterial growth, possibly by blocking dissociation of peptidyl tRNA from ribosomes and causing RNA-dependent protein synthesis to arrest. It may have anti-inflammatory and immunomodulatory effects. In children, age, weight, and severity of infection determine the proper dosage. When twice-daily dosing is desired, half of the total daily dose may be taken every 12 hours.

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Antiviral Agents

Class Summary

Antiviral agents may improve the rate of resolution if given within 1 week of the appearance of the rash.

Acyclovir (Zovirax)

Acyclovir is a prodrug activated through phosphorylation by a virus-specific thymidine kinase that inhibits viral replication. Herpesvirus thymidine kinase (TK), but not host-cell TK, converts acyclovir into acyclovir monophosphate, a nucleotide analogue. Guanylate kinase converts the monophosphate into diphosphate and triphosphate analogues that inhibit viral DNA replication. Once phosphorylated, the drug causes DNA chain termination when acted on by DNA polymerase. It interferes with DNA replication within the virions.

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