The AFD Full Form in medical term is Anderson-Fabry disease. The lysosomal storage disorder Anderson-Fabry disease (AFD) is brought on by an abnormal accumulation of globotriaosylceramide in tissues due to a lack of the enzyme -galactosidase A (-Gal A). The most frequent cause of death in AFD patients is now Anderson-Fabry cardiomyopathy, characterized by structural, valvular, vascular, and conduction anomalies.
These enzymes prevent Sphingolipids, a molecule resembling fat, from accumulating in blood vessels and tissue. Sphingolipids accumulate in dangerous amounts in blood vessels and tissues without active alpha-GAL enzymes. The heart, brain, kidneys, spine, central nervous system, as well as skin are all impacted by Fabry disease. It is an inherited disorder that parents pass on to their offspring. The condition is also known as Anderson-Fabry disease.
AFD patients lack the enzymes needed to break down lipids or fats. The chance of stroke, heart attack, and renal failure is increased when these fats accumulate in blood arteries and tissue. Parents pass on this hereditary issue to their offspring. Serious problems can be avoided with oral chaperone therapy plus enzyme replacement.
A parent passes on a mutation (change) to their offspring, as in the X chromosome’s galactosidase alpha (GLA) gene.
Fabry disease has no known treatment. Painkillers and gastrointestinal medications can help with symptoms. To prevent health problems, two treatments could reduce the accumulation of fatty substances. They are oral chaperone therapy and enzyme replacement therapy.