Atovaquone

Atovaquone is a naphthoquinone whose mechanism of action involves inhibition of the mitochondrial electron transport system in the protozoa. Malaria parasites depend on de novo pyrimidine biosynthesis through dihy-droorotate dehydrogenase coupled to electron transport. Plasmodia are unable to salvage and recycle pyrimidines as do mammalian cells.

Atovaquone is poorly absorbed from the gastrointestinal tract, but absorption is increased with a fatty meal. Excretion of the drug, mostly unchanged, occurs in the feces. The elimination half-life is 2 to 3 days. Low plasma levels persist for several weeks. Concurrent administration of metoclopramide, tetracycline, or ri-fampin reduces atovaquone plasma levels by 40 to 50%.

Atovaquone has good initial activity against the blood but not the hepatic stage of P. vivax and P. ovale malaria parasites. It is effective against erythrocytic and exoerythrocytic P. falciparum, and therefore, daily suppressive doses need to be taken for only 1 week upon leaving endemic areas. When used alone, it has an unacceptable (30%) rate of recrudescence and selects for resistant organisms. It and proguanil are synergistic when combined and no atovaquone resistance is seen. This combination (Malarone) is significantly more effective than mefloquine, amodiaquine, chloroquine, and combinations of chloroquine, pyrimethamine, and sulfadox-ine. In addition to using the combination of atovaquone and proguanil for the treatment and prophylaxis of P. falciparum malaria, atovaquone is also used for the treatment and prevention of P. carinii pneumonia and babesiosis therapy.

Atovaquone is well tolerated and produces only rare instances of nausea, vomiting, diarrhea, abdominal pain, headache, and rash of mild to moderate intensity.

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