Any reason a white female is G6pd deficient?!
Question:
Military told me I was G6pd defecient, supposedly affects mostly males of black, middle eastern or mediteranian orgin, of which i am none, so why me? is it a shady ancestor or rogue genes
Answers:
Believe it or not, G6PD is the most common enzyme deficiency worldwide. Some epidemiologists feel that this is due to the fact that G6PD offers some protection against malarial infections which are an important cause of death in some areas of the world. While the incidence is very low in Caucasians, it certaily isn't nonexistent. The other thing that is interesting is that G6PD deficiency is an X-linked recessive disease, so it is relatively unusual for a woman to get it. In theory, you would need to inherit one abnormal gene from your mother and one from your father to get the full-blown condition. However, some women with just one abnormal gene out of two can have a mild form of the disease. I suspect that either you have a mild form of the disease and inherited the gene from your mother (if it were from your father, he would have had the disease) OR that you had a false positive test. This can happen when patients are hemolyzing (breaking down blood cells) for other reasons. I would recommend that you see your physician and make sure they confirm the test by repeating it. By the way. I hope your reference to a "shady ancestor" isn't a negative reference to people of African, Middle Eastern or Mediterranean origin!
Other Answers:
Hope this helps the web page was informative. worth a look. does not sound like shady ancestor genes.LOL.
Many mutations of the housekeeping gene encoding glucose-6-phosphate dehydrogenase (G6PD) cause G6PD deficiency in humans. Some underlie severe forms of chronic nonspherocytic hemolytic anemia (CNSHA) for which there is no definitive treatment. By using retroviral vectors pseudotyped with the vesicular stomatitis virus G glycoprotein that harbor the human G6PD (hG6PD) complementary DNA, stable and lifelong expression of hG6PD was obtained in all the hematopoietic tissues of 16 primary bone marrow transplant (BMT) recipient mice and 14 secondary BMT recipients.
Most of these mutations cause little or no disease, except when patients are challenged by oxidative drugs or fava beans. However, some mutations cause severe instability of the dimeric molecule and, as a result, lifelong chronic nonspherocytic hemolytic anemia (CNSHA).7,8 Patients with CNSHA are, by definition, anemic and jaundiced, but often tolerate their condition well. However, in the more severe cases, patients have anemia that impairs their quality of life, requiring periodic blood transfusions; they are also at risk from life-threatening exacerbation of hemolysis concomitant with infections
Source(s):
http://www.bloodjournal.org/cgi/content/full/96/13/4111
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