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The term recurrent abdominal pain (RAP), based on the pioneering work of Apley and Naish, describes children who have chronic abdominal pain without an identifiable organic basis (1). Community-based studies worldwide show that 10% to 46% of children 4 to 16 years old meet the criteria for RAP (2–5). Based on other reports and data from our institution, RAP accounts for approximately 25% of visits to a pediatric gastroenterologist/nurse practitioner (4,6,7). The pediatric Rome III committee introduced the term abdominal pain–related functional gastrointestinal disorders (APFGIDs) to supersede the term RAP (8). APFGIDs include 4 phenotypic subtypes: functional abdominal pain (FAP), irritable bowel syndrome (IBS, essentially, FAP with changes in stooling pattern), functional dyspepsia, pain in the upper abdomen), and the relatively rare disorder, abdominal migraine (8). APFGIDs are associated with variable levels of symptoms and distress, ranging from episodic mild to severe abdominal pain, often disruptive to school and other activities. Evidence demonstrates that 30% to 66% of children with RAP experience pain similar to that of adults and meet the adult Rome criteria for IBS (9–12).
Although the etiology of APFGIDs is likely multifactorial, in some patients diet may play a critical role. This is an important area for study because the symptoms of APFGIDs (eg, abdominal pain, diarrhea, constipation) also can be caused by nutrient malabsorption (eg, lactose intolerance) or inadequate intake (eg, lack of dietary fiber leading to constipation). There are, however, a limited number of large, well-controlled studies of the role of diet in children and adults with APFGIDs. Because of space limitations, only FAP and IBS are discussed in this brief review.
Three pediatric studies prospectively evaluated the role of fiber in the pathogenesis of pain in APFGIDs. Christensen reported no benefit of psyllium in a randomized trial, but critical information from the report is missing (eg, P values, standard deviations), making interpretation of the results difficult (13). Corn fiber was suggested to be beneficial in a study by Feldman et al, but as in the Christensen article, critical information is lacking, limiting interpretation (14). In a study by Humphreys and Gevirtz, benefit was found for increasing dietary fiber (>10 g/day), but the type of fiber used was not described (15). Retrospective studies suggest a benefit of increased fiber intake in reducing the risk of abdominal pain in children (16,17). Even in adult studies of IBS, there is controversy regarding the effectiveness of psyllium fiber supplementation in patients with IBS (18,19).
Fructose may cause osmotic diarrhea and be a substrate for colonic bacterial fermentation and gas production, resulting in abdominal pain; however, given a large enough dose, even healthy individuals will malabsorb fructose and develop symptoms (20,21). That said, studies in adults suggest that poorly absorbed, fermentable oligo-, di-, and monosaccharides and polyols contribute to gastrointestinal symptoms in some patients with IBS but not in controls (22). An open-label trial in children presented as an abstract suggests that approximately 20% of children with APF-GIDs may respond to a low fermentable oligo-, di-, and monosaccharides and polyols diet (23). A randomized, double-blind trial in children is under way.
The contribution of lactose malabsorption to APFGIDs was evaluated in 2 small (n = 21 and n = 38) prospective placebo-controlled trials in children (24,25). Although interpretation is limited by their study design, these investigations suggest that lactose malabsorption (ie, lactase deficiency) may play a role in some but not most children with APFGIDs.
The potential role of other carbohydrate digestive enzyme deficiencies, besides lactase, in the production of gastrointestinal symptoms in APFGIDs remains underexplored. Preliminary data in a small number of subjects (n = 10) suggest that starch maldigestion as measured by breath testing is more frequent in children with APFGIDs as compared with adult controls (26). Potentially supporting, in part, this observation, a small pilot trial (n = 49) of pancreatic enzyme supplementation in adults with diarrhea-predominant IBS suggested benefit (27). Children undergoing upper gastrointestinal endoscopy for the evaluation of abdominal pain, vomiting, or gastroesophageal reflux (n = 44) were evaluated for lactase, sucrase, and glucoamylase activities (28). Low enzyme activities were found in 32%, 34%, and 28% of children, respectively, with some children having a combination of enzyme deficiencies (28). There was no correlation, however, of abdominal pain symptoms or diarrhea with enzyme activities and no controls were evaluated (28). These results fit with another preliminary report (abstract) from the same group, suggesting that in children with APFGIDs (n = 32) mucosal maltase activity does not correlate with abdominal pain symptoms, diarrhea, or constipation (29).
Food allergies/intolerances may be a cause of FAP and IBS; however, the frequency with which they are to blame is somewhat obscure. A retrospective study suggests that they are infrequent etiologies (30). Milk allergy/intolerance specifically appears to be an infrequent cause (2% of cases) (31). Among other diagnostic considerations, lymphonodular hyperplasia on upper or lower gastrointestinal endoscopy has been reported to be suggestive of food hypersensitivity (32). Patients with celiac disease may have symptoms that suggest FAP or IBS (33). Appropriate testing should be carried out to exclude this disorder (33).
Given the ubiquity of APFGIDs and their associated emotional and economic costs, greater insight into the contribution of diet to these disorders is urgently needed. We await the results of large, prospective, well-controlled studies to clarify how diet may influence the expression of abdominal pain and stooling symptoms in children (and adults) with APFGIDs.
The author receives support from R01 NR05337, R34 AT006986, and UH3 DK083990 from the National Institutes of Health, Daffy’s Foundation, the US Department of Agriculture/Agricultural Research Service under Cooperative Agreement No. 6250–51000–043, and P30 DK56338, which funds the Texas Medical Center Digestive Disease Center.
The content of this manuscript is solely the responsibility of the author and does not necessarily represent the official views or policies of the National Institutes of Health or the US Department of Agriculture, nor does mention of trade names, commercial products, or organizations imply endorsement by the US government.
The authors report no conflicts of interest.