Sacrosidase 8,500units/ml oral solution

An uncommon hereditary condition known as CSID affects around 0.05%–0.2% non-HispanicWhites; meanwhile, AfricanAmericans and White Hispanics exhibit a lower prevalence. As many as 5 in 100 people may be affected by this disorder in the native communities of Canada, Alaska, andGreenland. CSID is characterized by a lack of the sucrase-isomaltase (SI) enzyme complex, usually present in the brush border of the small intestine, which is necessary for the dissociation of α-glycosidic bonds in sucrose and maltose. At the molecular level, homozygous or heterozygous mutations on chromosome 3q25-q26 lead to improper synthesis and transportation of the SI gene. Ouwendijk et al were the first to describe a mutation in the SI gene linked to CSID. Suchmutations have also been demonstrated to increase the incidence of irritable bowel syndrome (IBS), which shares symptoms and clinical characteristics with CSID. Over 40 known mutations in the SI gene cause CSID. Sucrase activity is typically decreased in CSID patients, but the activity of isomaltase varies from nonexistent to fairly normal, due to which nutrients from ingested starch and sucrose cannot be adequately absorbed when this enzyme complex is insufficient.

Abstract licence: CC BY-NC-ND 4.0

Abstract Introduction: Abdominal pain, nausea, and diarrhea are common symptoms in individuals with congenital sucrase-isomaltase deficiency (CSID) and are often misdiagnosed as irritable bowel syndrome (IBS). While research on CSID prevalence is limited, there is even less data available specifically concerning children diagnosed with IBS. This study aims to explore the prevalence and clinical characteristics of CSID in patients diagnosed with IBS. Methods Patients diagnosed with IBS according to the Rome IV criteria were included in the study. Genetic analysis was performed to identify CSID-related gene mutations in all enrolled patients. Nutritional guidance based on the FODMAP diet was provided to all participants. Results A total of 70 patients (33 females, 37 males) diagnosed with IBS, with a mean age of 9.8 ± 4.6 years, were included in the study. Among these patients, 87.1% reported recurrent abdominal pain, and 54.3% experienced diarrhea. The average duration of symptoms before seeking medical attention was 54.3 ± 53.1 months. Approximately 50% of the patients were following a diet that included processed convenience foods. Notably, 30% of the patients experienced symptom improvement through dietary interventions. Three patients were identified with CSID gene mutations. The strict sucrose-isomaltase restriction for all three patients was alleviated by adding sacrosidase to their meals. Conclusions The prevalence of CSID in patients diagnosed with IBS was found to be 4.28%, consistent with existing literature. These findings highlight the importance of considering CSID in cases of IBS that do not respond to conventional treatment methods and lifestyle modifications.

Abstract licence: CC BY

SSDXA-14 is a Phase 2 (feasibility/pilot) double-blind, placebo-controlled, crossover study to evaluate the efficacy and safety of sacrosidase and placebo in 25 subjects objectively diagnosed with fructan intolerance. Conditions: Fructan Intolerance. Interventions: Sacrosidase Oral Solution, Placebo.

Source: ClinicalTrials.gov (public domain)

S09A is a Phase 4, multicenter, randomized, double-blind, placebo-controlled, parallel study examining the efficacy and safety of a Sucraid (sacrosidase) Oral Solution in comparison to a placebo in 150-200 subjects with chronic diarrhea possibly attributable to sucrase deficiency. Conditions: Genetic Sucrase-Isomaltase Deficiency. Interventions: Sucraid, Placebo.

Source: ClinicalTrials.gov (public domain)

This is a Phase 4, U.S. only, multi-center study using a 7-day therapeutic response dose (TRD) of commercial Sucraid® to assess the response of treatment in 1100 symptomatic pediatric (6 months to 17 years old) subjects with low, moderate, and normal sucrase activity determined by a disaccharidase assay via EGD within 1 year of the Screening Visit. This study will also explore the relationship between known genetic CSID mutations and sucrase activities via (EGD) disaccharidase assay (low, moderate, and normal). Conditions: Congenital Sucrase-Isomaltase Deficiency, CSID, Sucrase Isomaltase Deficiency. Interventions: Sucraid (sacrosidase) Oral Solution 8500 IU/mL.

Source: ClinicalTrials.gov (public domain)