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Hydroa Vacciniforme Medication

  • Author: Gregory Toy; Chief Editor: Dirk M Elston, MD  more...
Updated: Jun 20, 2016

Medication Summary

To date, no oral therapy reliably prevents the appearance of hydroa vacciniforme (HV) lesions. Oral antimalarials[29] and beta-carotene[30, 31, 32] may be used and are occasionally reported to be useful, especially when combined with a strict sun avoidance program. Other therapies that have been used with varying success include thalidomide, azathioprine, cyclosporine,[33] and fish oil supplementation.[34, 35, 36] Given the association with EBV, there may be some benefit to the use of antivirals such as acyclovir and valacyclovir.[3]



Class Summary

These agents suppress cutaneous lesions associated with many photodermatoses.

Hydroxychloroquine (Plaquenil)


Hydroxychloroquine can be used for the suppression of lesions in sun-sensitive disorders; its mechanism of action in HV is unknown.

Chloroquine (Aralen)


Chloroquine has anti-inflammatory activity by suppressing lymphocyte transformation and may have a photoprotective effect. It can be used for the suppression of lesions; its mechanism of action in HV is unknown.



Class Summary

These agents are yellow-orange pigments that may have photoprotective properties in selected photodermatoses.

Beta-carotene (Lumitene, B-Caro-T, A-Caro-25)


Beta-carotene's mechanism of action is not completely elucidated but it may relate to the ability of carotenoids to quench photoexcited molecular species. It reduces the severity of photosensitivity reactions in some patients with photodermatoses, especially erythropoietic protoporphyria (EPP).



Class Summary

After intercalating with DNA and irradiation by UV-A, methoxsalen leads to formation of DNA psoralen adducts that cross-link DNA. This affects gene expression by inhibiting DNA replication, mitosis, and cell division. 5-Methoxypsoralen (5-MOP, Bergapten, Psoraderm 5) has also been used, although it is not currently available in the United States.

Methoxsalen (8-MOP, Oxsoralen)


Methoxsalen inhibits mitosis by binding covalently to pyrimidine bases in DNA when photoactivated by UV-A.


Antivirals, Other

Class Summary

Given the association with EBV, there may be some benefit to the use of antivirals such as acyclovir and valacyclovir.

Acyclovir (Zovirax)


Acyclovir is a synthetic purine nucleoside analogue with activity against a number of herpesviruses, including herpes simplex and varicella-zoster. It is highly selective for virus-infected cells because of its high affinity for viral thymidine kinase enzyme. This effect serves to concentrate acyclovir monophosphate into virus-infected cells. The monophosphate then is metabolized into the triphosphate active form by cellular kinases.

Valacyclovir (Valtrex)


Valacyclovir is a prodrug rapidly converted to the active drug acyclovir. It is more expensive but has a more convenient dosing regimen than acyclovir.

Contributor Information and Disclosures

Gregory Toy State University of New York Downstate College of Medicine

Disclosure: Nothing to disclose.


Marjon Vatanchi, MD Pediatric Dermatology Research Fellow, Department of Dermatology, SUNY Downstate Medical Center

Marjon Vatanchi, MD is a member of the following medical societies: American Academy of Dermatology, Houston Dermatological Society, Medical Dermatology Society, National Psoriasis Foundation, Texas Dermatological Society

Disclosure: Nothing to disclose.

Jeannette Rachel Jakus, MD, MBA Clinical Assistant Professor, Director of Clinical Research, Assistant Program Director, Department of Dermatology, SUNY Downstate Medical Center; Dermatologist, Brody Dermatology

Jeannette Rachel Jakus, MD, MBA is a member of the following medical societies: American Academy of Dermatology, American Academy of Pediatrics, American Skin Association, Society for Pediatric Dermatology, Women's Dermatologic Society

Disclosure: Nothing to disclose.

Specialty Editor Board

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

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

Disclosure: Nothing to disclose.

Van Perry, MD Assistant Professor, Department of Medicine, Division of Dermatology, University of Texas School of Medicine at San Antonio

Van Perry, MD is a member of the following medical societies: American Academy of Dermatology

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.

Additional Contributors

Maureen B Poh-Fitzpatrick, MD Professor Emerita of Dermatology and Special Lecturer, Columbia University College of Physicians and Surgeons

Maureen B Poh-Fitzpatrick, MD is a member of the following medical societies: Alpha Omega Alpha, American Academy of Dermatology, New York Academy of Medicine, New York Dermatological Society

Disclosure: Nothing to disclose.

Quynh L Sebastian, MD Clinical Instructor, Division of Dermatology, UCLA David Geffen School of Medicine

Quynh L Sebastian, MD is a member of the following medical societies: American Academy of Dermatology, American Society for Dermatologic Surgery, American Society for Laser Medicine and Surgery

Disclosure: Nothing to disclose.

Raul Del Rosario, MD Consulting Staff, Dermatopathology, Mission Hospital at Laguna Beach

Raul Del Rosario, MD is a member of the following medical societies: American Society for Clinical Pathology

Disclosure: Nothing to disclose.

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Characteristic vesicular lesions occur on sun-exposed skin and heal with varioliform scarring.
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