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Most individuals with G6PD deficiency are asymptomatic.When it induces hemolysis, it is usually is short-lived. [5]Most people who develop symptoms are male, due to the X-linked pattern of inheritance, but female carriers can be affected due to unfavorable lyonization or skewed X-inactivation, where random inactivation of an X-chromosome in certain cells creates a population of G6PD-deficient ...
The congenital form of methemoglobinemia has an autosomal recessive pattern of inheritance. Due to a deficiency of the enzyme diaphorase I (cytochrome b5 reductase), methemoglobin levels rise and the blood of met-Hb patients has reduced oxygen-carrying capacity. Instead of being red in color, the arterial blood of met-Hb patients is brown.
Methemoglobinemia; Anemias (lack of red blood cells or hemoglobin) Iron-deficiency anemia; Megaloblastic anemia. Vitamin B 12 deficiency Pernicious anemia; Folate deficiency; Hemolytic anemias (destruction of red blood cells) Genetic disorders of RBC membrane Hereditary spherocytosis; Hereditary elliptocytosis; Congenital dyserythropoietic anemia
G6PD deficiency by itself is usually asymptomatic, but when combined with external stress such as an infection, fava beans, or oxidative drugs like primaquine. [ 25 ] Primaquine and tafenoquine can pass through the placenta, causing hemolytic anemia in utero if the fetus has G6PD deficiency.
Many patients with 6-phosphogluconate dehydrogenase deficiency are carriers and have no symptoms. It has been discovered that symptoms manifest more frequently in female carriers. Depending on how severe the deficiency is, it has been demonstrated that enzyme activity is reduced by 35–65%. [citation needed]
G6PD reduces NADP + to NADPH while oxidizing glucose-6-phosphate. [2] Glucose-6-phosphate dehydrogenase is also an enzyme in the Entner–Doudoroff pathway, a type of glycolysis. Clinically, an X-linked genetic deficiency of G6PD makes a human prone to non-immune hemolytic anemia. [3]
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If drug-induced nonautoimmune hemolytic anemia occurs secondarily to drug induced methemoglobinemia, methylene blue can be used as a first-line therapy. However methylene blue should be avoided in those with a concomitant G6PD deficiency as methylene blue may cause further oxidative hemolysis.