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Glucose-6-phosphate dehydrogenase deficiency disease, an inherited disorder, could mean trouble for patients infected with SARS-COV-2; we just don’t know yet.

2020-04-14

a photo of Grecian mountains and sea by MustangJoe via pixabay.com

A piece in the Medpage Today online paper from April 13 describes glucose-6-phosphate dehydrogenase (G6PD) deficiency disease as follows:

G6PD deficiency is a common, X-linked recessive genetic condition that affects some 400 million people worldwide. It is the most common human enzyme defect.

This means that G6PD deficiency is inherited (passed on from parents to children) and the gene for it is carried on the X-chromosome (the one that determines your gender, that is whether you are a boy or a girl biologically).  Mothers pass one X chromosome on to all of their children.  Fathers pass either an X or a Y chromosome on to their daughters and sons, respectively.  With only one X chromosome, sons are more likely to suffer from this disease than daughters (daughters will have roughly half of their body cells with one of the X’s and half with the other).  There are at least 186 known variations of this gene, each of which represents a certain degree of deficiency.  Genes for this disorder are particularly common in people from the Middle East, Mediterranean area, Africa, and Asia, and Mediterranean variants are some of the most dangerous.  The prevalence on Sardinia (an island between Italy and Spain) is particularly high, 7.5% overall, with some locales having much higher rates.  African-American males are said to have a prevalence of 10% for some variant of this genetic deficiency.

Deficiency of the G6PD enzyme results in a relative weakness in the cell’s ability to produce NADPH (just stick with the abbreviation, trust me on this).  Cells that do not have mitochondria, mainly red blood cells which carry oxygen from the lungs to the rest of the body, are particularly susceptible to this weakness.  The most important clinical effects of this deficiency are neonatal jaundice (excess bilirubin in newborn babies, who turn yellow, which can be very serious) and acute hemolytic anemia (a condition in which red blood cells break down after exposure to some drugs).  There are other manifestations (ways to appear): one problem is that patients with this condition are intolerant to fava beans (broad beans) and develop that acute hemolytic anemia after eating them.  Mostly the condition causes no symptoms and the patient is usually not aware that he (or she) has it.  It is most often discovered when a routine blood count is done and oddly shaped red blood cells are seen.  Men are mostly affected by this problem, but a few women also have it.

There is no definite connection established between G6PD deficiency and susceptibility to severe COVID-19 complications, but there are some suggestive links.  The fact that more men than women die of the new virus, the fact that black Americans seem to be dying in greater numbers (although there are several other possible reasons that this could be so), and the high death rates in Italy and Spain, are all possibly related.  There is a possible connection in that the enzyme deficiency makes people more susceptible to oxidative stress (damage due to “free-radical oxygen”), which is a feature of inflammation caused by certain viral infections.

Parents of children with this condition are petitioning NIH, WHO, and CDC for studies to be performed that could clear up this issue and establish whether there is a link between G6PD deficiency and severe COVID-19.  Further details are in the Medpage Today article.

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