- Medical benefits
Nowadays, medicine has managed to advance tremendously. Hence, research scientists have finally understood the link between the digestive system and genetics. Chronic diarrhea left untreated might have severe side effects later on in the future. Throughout life, the digestive imbalance might worsen and thus people might experience serious gut abnormalities. People who lack enzymes cannot break down properly disaccharide sucrose. Several research studies have shown that fungal derived maltase has amazing clinical improvement in kids and adults with challenging digestive problems. Read what is bookkeeping and what does a bookkeeper do.
- Infantile, or type A acid maltase deficiency normally starts showing symptoms at the ages of 5 months until 2 years old.
- Childhood or type B acid maltase deficiency normally starts showing visible symptoms in early childhood at the age of 7-8 years old.
- The last type of deficiency is type C or adult and it highlights side effects around the age of 30-40.
AMD or acid maltase deficiency is additionally known as pompe disease which is a genetic condition that can affect proper muscle function. Passed from parents to their kids, the mutation is called acid alph-glucosidae and can cause a certain substance known as glycogen to boost within the muscles of AMD patients. The chemical substance known as acid maltase regulates glycogen stored within muscle cells. The moment the muscle cell accumulates too much glycogen, acid maltase is being released to break down the surplus. AMD is thought to affect around 40,000 births and the sooner is spotted the better for the child. In general, more severe symptoms appear after 10-20 years. As of April 2006, the Food and Drug Administration in the US approved Myozyme as an enzyme therapy replacement for patients with lack of maltase in their bodies. Results were quite positive and the condition of most patients was really improved.
While maltase is the enzyme that can easily break down disaccharide maltose, maltase deficiency is an actual disease that forms because of excessive buildup of glycogen within the lysosome-derived vacuoles. Described for the first time by JC Pompe in 1932, the scientist brought to light the special case of a 7 month girl who was believed to have pneumonia when in fact she had maltase deficiency.