New antimalarial drug approved In US & Australia for prevention and treatment.

It is tafenoquine. It is marketed in the US as Arakoda (for prevention) and Krintafel (for. treatment) and Australia as Kodatef (for prevention) and Kozenis (for treatment). It appears that approval in Canada is pending.

Big caveat: Some people are genetically predisposed to have a life threatening reaction to this drug. It is not at all suitable for self-treatment, as you must be first tested to be sure you don't have the genetic problems.

It is a relative of primaquine, which also has the genetic issues. Like primaquine, it is active against the persistent liver stage that occurs with a couple of species of malaria, that can cause the disease to flare up months after you were first infected.

Tafenoquine has advantages over primaquine and other antimalarial like chloroquine, mefloquine (Lariam), atovaquone/proguanil (Malarone), and doxycycline. In particular, it stays loner in the body, so you take fewer pills. You take it for three days before arriving int he malaria area; once a week while in the area; and only once after leaving. Chloroquine is not effective against P. falciparum, but tafenoquine is.

There is insufficient safety data for children, so it can only be used by people over 16. Women who are pregnant, breastfeeding or trying to conceive should not use it, except under close medical supervision to treat malaria. (The child may have the genetic problem even if the mother doesn't.) Women should use contraception for three months after using tafenoquine. It should not be used by people with a history of severe psychosis, such as hallucinations, delusions, or grossly disorganized thinking or behavior.

In clinical trials, the most common adverse events were headache, back pain, dizziness, nausea, and diarrhea. These were not common or severe, around 3% of users. There were a couple of reports of psychiatric problems in people with a history of psychosis, who were given extra high doses as apart of clinical trials. Hence the caution for people with a history of psychiatric problems.

Once there is more experience with actual use of the drug, these precautions may change of course.

Such a pleasure to read your posts, Nutrax! Always clear, informative, complete, and accurate.

I've been wondering: I've taken primaquine (after G6PD testing) a couple of times. Does this put me in the clear forever, or can the deficiency show up later in life? And if I am in the clear in relation to primaquine, does this mean I'm ok to take tafenoquine, as it appears (based on the fact that the test is the same)? Last, do you know if the genetic testing which is supposed to be more definitive than the blood test is easy, common, and/or cheap?

No worries if no answers; this is more along the lines of idea curiosity than anything urgent.

best,

Mark

Glucose-6-phosphate dehydrogenase deficiency is an enzyme disorder. G6PD catalyzes nicotinamide adenine dinucleotide phosphate (NADP) to its reduced form, NADPH, in the pentose phosphate pathway. Erythrocytes are dependent on NADPH from this source to prevent oxidative stress. When G6PD is deficient, the erythrocytes are subject to acute hemolysis due to oxidative stress. The deficiency can also cause neonate hyperbilirubinemia. The cause is mutations on the distal long arm of the X chromosome, which are X-recessive.

I trust that makes it all perfectly clear.

OK. G6PD is an enzyme that red blood cells need to keep from self-destructing under certain conditions. If the enzyme levels are too low, things like serious infection, eating fava beans, or taking certain drugs, cause the conditions that result in destruction. The deficiency can be the cause of a serious problem in newborns, where there is too much bilirubin (a byproduct of the removal of old red blood cells)in the blood.

G6PD deficiency is a genetic disorder, not an allergy. It results from mutations of genes on the X chromosome. Over 400 different mutations are known; each causes different levels of deficiency. Total deficiency is fatal. Most cases are mild to moderate. Because it's on the X chromosome and because it is recessive, almost all people with it are male. A female would have to have a mutation on both X chromosomes. So, unlike some allergies, it can't come & go, get better with time, or suddenly appear.

There are also geographic and racial patterns. From the American Family Physician Journal:

G6PD deficiency occurs with increased frequency throughout Africa, Asia, the Mediterranean, and the Middle East. In the United States, black males are most commonly affected, with a prevalence of approximately 10 percent. Prevalence of the deficiency is correlated with the geographic distribution of malaria, which has led to the theory that carriers of G6PD deficiency may incur partial protection against malarial infection. Cases of sporadic gene mutation occur in all populations.

Since the issue is a deficiency in red blood cells, the usual way to test for it is a blood test. The most common test involves mixing blood with chemical stuff and looking at fluorescence under UV light. Another mixes it with different stuff and measures it with a spectrophotometer. It's more costly & requires a specialized lab. There are some other complex tests as well, plus DNA tests. The spectrophotometer and the complex tests are usually reserved for when you have to have some exact numbers and the DNA for genetic studies.

Most of the time, anemia due to G6PD takes care of itself. Older red cells are the ones most affected and they are soon replaced by new ones. If the problem is removed (Sorry, Dr. Lecter, lay off the fava beans) the new cells take over and all is well. Just don't take primaquine or eat fava beans again. Sometimes, though, it can be serious enough that transfusion is needed.

A person with G6PD deficiency who is diagnosed with P. vivax or P. ovale would probably get quantitative testing, to see if they could be given primaquine under medical supervision. If the deficiency level is too severe, then tropical disease specialists get to have debates.

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