Primaquine is a medication used to treat and prevent malaria and to treat Pneumocystis pneumonia.

Specifically it is used for malaria due to Plasmodium vivax and Plasmodium ovale along with other medications and for prevention if other options cannot be used.

It is an alternative treatment for Pneumocystis pneumonia together with clindamycin.

It is taken by mouth.

Common side effects include nausea, vomiting, and stomach cramps.

Primaquine should not be given to people with glucose-6-phosphate dehydrogenase (G6PD) deficiency due to the risk of red blood cell breakdown.

It is recommended that primaquine not be used during pregnancy.

The mechanisms of action is is believed to involve effects on the malaria parasites’ DNA.

Primaquine is primarily used to prevent relapse of malaria due to Plasmodium vivax and Plasmodium ovale.

It eliminates hypnozoites, the dormant liver form of the parasite, after the organisms have been cleared from the bloodstream.

Use of primaquine in combination with quinine or chloroquine each of which is very effective at clearing P. vivax from blood, improves outcomes; they appear to also potentiate the action of primaquine.

It is recommended for primary prophylaxis prior to travel to areas with a high incidence of P. vivax, and for terminal prophylaxis (anti-relapse therapy) after travel.

A single dose of primaquine has the  ability to kill gametocytes of P. falciparum and P. vivax in blood; it also kills asexual trophozoites of P. vivax in blood, but not of P. falciparum.

Because of its action against gametocytes, it is recommended for use in reducing transmission to control P. falciparum infections.

Primaquine is also used in the treatment of Pneumocystis pneumonia (PCP), a fungal infection commonly occurring in people with AIDS and, more rarely, in those taking immunosuppressive drugs. 

To treat PCP effectively, it is usually combined with clindamycin.

Primaquine should not be administered to anyone with G6PD deficiency because a severe reaction can occur, resulting in hemolytic anemia.

However, a single dose of primaquine (0.25 mg/kg) is safe to give even in individuals with G6PD deficiency, for the purpose of preventing transmission of P. falciparum malaria.

Primaquine is contraindicated in pregnancy, because the glucose-6-phosphate dehydrogenase status of the fetus would be unknown.

Primaquine overdose can cause a dangerous reduction in various blood cell counts, and should be avoided in people at risk for agranulocytosis, which include people with conditions such as rheumatoid arthritis and lupus erythematosus, and those taking concurrent medications that also decrease blood cell counts.

Hemolytic reactions may occur in individuals with G6PD deficiency and in individuals with a family or personal history of favism. 

Areas of high prevalence of G6PD deficiency are Africa, Southern Europe, Mediterranean region, Middle East, South-East Asia, and Oceania. 

Common side effects of primaquine administration include:  nausea, vomiting, and stomach cramps.

In persons with cytochrome b5 reductase deficiency, primaquine causes methemoglobinemia, a condition in which the blood carries less oxygen that it does normally.

Overdosing can reduce the number of function of various kinds of blood cells, including loss of red blood cells, methemoglobinemia, and loss of white blood cells.

Persons with glucose-6-phosphate dehydrogenase deficiency (G6PD) may develop hemolytic anemia from primaquine.

Primaquine is lethal to P. vivax and P. ovale in the liver stage, and also to P. vivax in the blood stage through its ability to do oxidative damage to the cell. 

Primaquine can possibly eliminate P. vivax merozoites in bone marrow as a result of accumulation there of hydrogen peroxide.

It  is well-absorbed in the gut and extensively distributed in the body without accumulating in red blood cells. 

Administration of primaquine with food or grapefruit juice increases its oral bioavailibity.

In blood, about 20% of circulating primaquine is protein-bound.

It has preferential binding to the acute phase protein orosomucoid. 

It as a half-life on the order of 6 hours, 

It is quickly metabolized by liver enzymes to carboxyprimaquine, which does not have anti-malarial activity. 

Renal excretion of the parent drug is less than 4%.

It is a generic drug,

A clinical trial demonstrated the efficacy of higher-dose primaquine in preventing relapse of P. vivax malaria.

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