G6PD deficiency is due to a problem with an enzyme (chemical) called G6PD found in the red blood cells of the blood. It is more common in males but females could be a carrier and remain asymptomatic- no symptoms at all.
This deficiency can cause hemolytic anemia-breaking up of the RBC , usually after exposure to certain medications, foods, or even infections.Most people with G6PD deficiency don’t have any symptoms, while others develop symptoms of anemia only after RBCs have been destroyed, a condition called hemolysis. In these cases, the symptoms disappear once the cause, or trigger, is removed.
A normal life is certainly possible, if the child is aware that the condition is lifelong and must be cautious of certain medicine and chemical exposure. Keeping the list of medicine, chemical and food to be avoided is always a wise thing to do. Always present the list to the medical doctor when seeking treatment.
Some children with G6PD must not take asprin. Check with your specialist or paediatrician first.
In conclusion, patients must always be informed this is not a life threatening disease and one can live a normal life provided he is not exposed to the triggering factors.
These are signs of glucose-6-phosphate dehydrogenase (G6PD) deficiency.
Be alert if the child presents with the following symptoms, including jaundice, pale skin/pallor (RBCs destroyed), persistent/severe tiredness (due to low oxygen carrying capacity as a result of low RBC after being destroyed) and dark urine.
Ernest Beutler, M.D. (a leading expert in this field) has to say about neonatal icterus (jaundice), “Icterus neonatorum with no evidence of immunologic incompatibility occurs in some infants with G6PD deficiency. The jaundice may be quite severe and, if untreated, may result in kernicterus. Thus G6PD deficiency is a preventable cause of mental retardation, and this aspect of the disorder has considerable public health significance.”
Jaundice in newborns is one of the most common conditions affecting newborn babies that causes concern to their mothers. New mothers are frequently caused worry by the yellowish discoloration of the skin and sclera (the whites of the eyes) in their babies.
Jaundice is caused by the accumulation of unconjugated (before conjugation process takes place in liver) bilirubin due to the immature development of the baby’s liver. This condition is deemed as a normal transitional condition in the 1st week of life and is known as Physiological jaundice.
However, if the serum bilirubin levels rise too excessively, it may be because for due concern. Unconjugated bilirubin can penetrate the blood-brain barrier and is neurotoxic (toxic to the brain-neuro). It can cause death in newborns. Infants who survive would have lifelong neurologic sequelae. Increased levels of unconjugated-indirect bilirubin which is free (not bound to albumin) may cause kernicterus damage to the brain centers of those infants.
Such conditions frequently warrants diagnostic evaluation to ensure that the neonatal jaundice does not turn fatal.
Be alert if the child presents with the following symptoms, including jaundice, pale skin/pallor (RBCs destroyed), persistent/severe tiredness (due to low oxygen carrying capacity as a result of low RBC after being destroyed) and dark urine.
