G6PD deficiency is an X-linked disorder characterized by an abnormal gene that leads to a shortage of G6PD, an essential enzyme responsible for glucose 6 phosphate dehydrogenase, within red blood cells. In individuals without this deficiency, the enzyme plays a crucial role in safeguarding the cells from harm during a chemical process. However, in those with G6PD deficiency, the red blood cells become susceptible to damage or destruction when exposed to infectious diseases, specific medications, or certain types of food.
The disorder primarily impacts southern European and black men. Women, on the other hand, are not directly affected by it, but they can be carriers of the abnormal gene. Consequently, they are at risk of passing the gene on to their sons, potentially leading to the disorder in the next generation.
Certain drugs, including specific antimalarial drugs and antibiotics, can trigger the destruction of red blood cells (haemolysis) in individuals with the abnormal gene of G6PD deficiency. The table below lists the drugs that may pose this risk. Additionally, a particular type of G6PD deficiency known as “favism” can be activated by a chemical found in broad beans, and individuals affected by this form must refrain from consuming them to prevent haemolysis.
Following the intake of a triggering drug or food, or during the course of an infectious illness, an individual with G6PD deficiency experiences symptoms of anemia. These symptoms may include jaundice, fatigue, headaches, and shortness of breath, which can even manifest after minimal physical exertion.
Diagnosing G6PD deficiency involves a blood test. While there is no targeted cure for the condition, symptoms triggered by certain drugs or foods can be prevented by simply avoiding those substances. Managing the disorder involves being cautious about potential triggers to minimize the risk of experiencing adverse effects.