What is Sucraid?
Sucraid is the only FDA-approved enzyme replacement therapy indicated for the treatment of genetically determined sucrase deficiency, which is a part of Congenital Sucrase-Isomaltase Deficiency (CSID).
In This Section
Sucraid is an enzyme replacement therapy that facilitates the breakdown of sucrose (sugar) into monosaccharides for absorption by the small intestine. It has been shown to help alleviate the gastrointestinal (GI) symptoms associated with CSID, and, as a result, patients can maintain a more normal diet that includes sucrose-containing foods.
- Sucraid is dispensed in 118-mL translucent plastic bottles, packaged with two bottles per box
- Each mL of solution contains 8,500 international units (IU) of sacrosidase
- A 1-mL measuring scoop is provided with each bottle
Congenital Sucrase-Isomaltase Deficiency is an autosomal recessive disease of the small intestine, also known as Genetic Sucrase-Isomaltase Deficiency (GSID), which was first discovered by Weijers and colleagues in 1960. When first detected nearly 60 years ago, the disease was originally characterized by undetectable sucrase activity, a decrease in maltase activity to nearly one third the normal level, and a varying degree of isomaltase activity.1
Figure 1. How Sucraid is dispensed
How Does Sucraid Work?
Sucraid has been shown in clinical trials to be effective in the treatment of patients with CSID. The active ingredient in Sucraid is sacrosidase, a sucrase enzyme replacement that catalyzes the hydrolysis of sucrose into glucose and fructose, thereby facilitating absorption from the small intestine into the bloodstream. Sacrosidase is a potent and robust enzyme; on a per milliliter basis, sacrosidase is approximately 100-fold more potent than endogenous sucrase.2 It has been shown to be stable when stored at 4°C.3
Although Sucraid provides replacement therapy for deficient sucrase, it does not provide specific replacement therapy for deficient isomaltase.4 Therefore, Sucraid does not metabolize dietary starches (for example, potato, bread, or pasta) and restricting starch in the diet may still be necessary to minimize symptoms in patients with CSID who are starch intolerant. When starting therapy with Sucraid, patients who still have symptoms are advised to restrict dietary starch for two weeks and then gradually reintroduce starch while monitoring for gastrointestinal symptoms. Keeping a dietary diary for the first few weeks of therapy is also recommended.
Figure 2. Role of Sucraid in the metabolism of sucrose and absorption of its metabolic products glucose and fructose across small intestine microvilli
- Weijers HA, van de Kamer JH, Mossel DA, Dicke WK. Diarrhoea caused by deficiency of sugar-splitting enzymes. Lancet. 1960;2(7145):296-7.
- Treem WR, McAdams L, Stanford L, Kastoff G, Justinich C, Hyams J. Sacrosidase therapy for Congenital Sucrase-Isomaltase Deficiency. J Pediatr Gatroenterol Nutr. 1999;28(2):137-142.
- Treem WR, Ahsan N, Sullivan B, et al. Evaluation of liquid yeast-derived sucrase enzyme replacement in patients with sucrase-isomaltase deficiency. Gatroenterology. 1993;105(4):1061-1068.
- Sucraid [package insert]. Vero Beach, FL: QOL Medical, LLC; 2017.