![]() NCG/WS seems to be triggered by activation of the innate immune system rather than the adaptive immune system. Several components of wheat have been postulated as key for symptom generation in NCG/WS, including gluten, fructans (a FODMAP), wheat germ agglutinins, alpha-amylase trypsin inhibitors, and potentially a nocebo response. Although wheat has been postulated as being the key trigger for symptoms, the component of wheat that triggers symptoms in individuals currently seems to be unclear. The pathophysiology of NCG/WS is still not fully understood. If these patients are on a GFD, they should be encouraged to ensure that they do not have celiac disease by undergoing a gluten challenge along with appropriate diagnostic testing ( 10). ![]() This means that some patients with self-reported NCG/WS may have undiagnosed celiac disease. The controversy is that currently systematic review and meta-analysis suggest that the worldwide prevalence of celiac disease is around 1% ( 9), and most cases remain unrecognized. A more pragmatic approach of assessing symptoms on a gluten-containing diet vs a GFD has been suggested for diagnosis ( 8). However, it is worth noting that this is rarely applied outside research settings, with many patients already on a GFD and unwilling to reintroduce gluten at time of diagnosis ( 6). Formalized criteria for its diagnosis, using the Salerno's experts criteria, have been developed, involving assessing response to a gluten-free diet (GFD) and measuring the effect of reintroduction of gluten after a period of being on a GFD ( 6). The variable prevalence rate is in part due to NCG/WS being self-reported, differing population groups, and there being a lack of diagnostic biomarkers for its diagnosis. The reported prevalence of NCG/WS ranges between 0.49% and 14.9% in the published literature ( 7). NCG/WS was first coined in the late 1970s ( 5) and is characterized by symptoms triggered by the ingestion of gluten or wheat products, with individuals presenting with intestinal and extraintestinal manifestations, in the context of celiac disease and wheat allergy being excluded ( 6). There have been significant clinical advances in dietary interventions related to the small bowel, but this area is currently a novel and advancing field for both patients and clinicians. Currently, antimicrobials are the established management option. However, the diagnosis of small intestinal bacterial overgrowth is limited by a lack of sensitive and specific tests, with significant knowledge gaps in relation to therapeutic measures to manage and cure small intestinal bacterial overgrowth. Small intestinal bacterial overgrowth is an example of microbial dysbiosis, with renewed interest in diet being postulated to cause an adaptive change of the microbes colonizing the small intestine. Diet seems to be an important driver of disease pathogenesis in eosinophilic gastroenteritis, with elimination and elemental diets showing promise in management, with further robust trials required. Several primary gastrointestinal disorders are associated with an increase in inflammatory cells including eosinophils. A gluten-free diet that excludes the abovementioned triggers is the cornerstone of treatment however, unlike celiac disease, there is uncertainty about the level of adherence or whether the gluten-free diet is a lifelong intervention. ![]() The diagnosis can be challenging, given the lack of validated biomarkers. Although gluten is believed to be a potential trigger for symptoms, other components of wheat may also be triggers, including fructans, alpha-amylase trypsin inhibitors, and wheat germ agglutinins. Self-reported nonceliac gluten/wheat sensitivity is prevalent. There are predominantly 3 small bowel conditions that have potential dietary interventions. Diet plays a key role in the manifestation and severity of gastrointestinal symptoms, with increasing research interest on the role of diet in small bowel disorders. ![]()
0 Comments
Leave a Reply. |