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Griseofulvin (Gris-PEG, Grifulvin, Grisactin, Fulvicin) is an oral fungistatic agent used in the long-term treatment of dermatophyte infections caused by Epidermophyton, Microsporum, and Trichophyton spp. Produced by the mold Penicillium griseofulvin, this agent inhibits fungal growth by binding to the microtubules responsible for mitotic spindle formation, leading to defective cell wall development.
Ineffective topically, griseofulvin is administered orally but has poor gastrointestinal absorption; absorption can be improved by microcrystalline processing of the drug and by taking the drug with fatty meals. Peak serum levels occur 4 hours after dosing. Griseofulvin is metabolized in the liver and has a half-life of 24 to 36 hours. The drug binds to keratin precursor cells and newly synthesized keratin in the stratum corneum of the skin, hair, and nails, stopping the progression of der-matophyte infection.
In the treatment of ringworm of the beard, scalp, and other skin surfaces, 4 to 6 weeks of therapy is often required. Therapy failure may be to the result of an in-correct diagnosis; superficial candidiasis, which may re-semble a dermatophyte infection, does not respond to griseofulvin treatment. Onychomycosis responds very slowly to griseofulvin (1 year or more of treatment is commonly required) and cure rates are poor; itracona-zole and terbinafine hydrochloride are more effective than griseofulvin for onychomycosis.
Griseofulvin is usually well tolerated. Headache is common with initiation of therapy. Hepatotoxicity (es-pecially in patients with acute intermittent porphyria), dermatitis, and gastrointestinal distress also occur. Griseofulvin increases warfarin metabolism, and griseo-fulvin metabolism is increased by phenobarbital.
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