Hydroa Vacciniforme Medication
- Author: Gregory Toy; Chief Editor: Dirk M Elston, MD more...
To date, no oral therapy reliably prevents the appearance of hydroa vacciniforme (HV) lesions. Oral antimalarials 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, 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.
These agents suppress cutaneous lesions associated with many photodermatoses.
Hydroxychloroquine can be used for the suppression of lesions in sun-sensitive disorders; its mechanism of action in HV is unknown.
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.
These agents are yellow-orange pigments that may have photoprotective properties in selected photodermatoses.
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).
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 inhibits mitosis by binding covalently to pyrimidine bases in DNA when photoactivated by UV-A.
Given the association with EBV, there may be some benefit to the use of antivirals such as acyclovir and valacyclovir.
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 is a prodrug rapidly converted to the active drug acyclovir. It is more expensive but has a more convenient dosing regimen than acyclovir.
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