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Several seminal studies published in Gut have demonstrated a strong association between dysfunctional sucrase-isomaltase (SI) gene variants and increased risk of diarrhoea-predominant irritable bowel syndrome (IBS-D).1–3 The common p.V15F variant has emerged as a key genetic hallmark of IBS. Notably, a multicentre study assessing the four major congenital sucrase-isomaltase deficiency (CSID) mutations, p.V557G, p.G1073D, p.R1124X and p.F1745C, found their frequency significantly higher in patients with IBS than in healthy controls when compared with the Exome-Aggregation-Consortium reference population (>30 000 Europeans; p=0.020, OR=1.57).4 These findings suggest that SI polymorphisms, whether in homozygous, heterozygous or compound heterozygous constellations, may play a pivotal role in predisposing individuals to IBS.