Fecal calprotectin (FC) is a marker of intestinal inflammation. Data are limited on utility of routine FC testing in pediatric primary care. Participants 0 to 18 years old who had an FC test in the years 2010-2014 were retrospectively identified. Those with less than a year of follow-up or a prior diagnosis of inflammatory bowel disease (IBD) were excluded. In all, 84% (689/822) had normal FC; no participant with normal FC was diagnosed with IBD in the subsequent 12 months. Also, 16% (133/822) had elevated FC, and 31% of those (42/133) were diagnosed with IBD. FC values for IBD and non-IBD groups were 1084 µg/g (interquartile range [IQR] = 514.4-2000) and 27.05 µg/g (IQR = 15.6-62.6; P < .001), respectively. Abdominal pain was the primary indication. In this cohort, sensitivity of FC for IBD is 100%, and specificity is 88%. The FC test can be an excellent tool in the primary care setting to exclude IBD and avoid unnecessary referrals and colonoscopies.

Effective therapies are limited for patients with parenteral nutrition-dependent short bowel syndrome. We previously showed that intestinal expression of the transcriptional coregulator tetradecanoyl phorbol acetate-induced sequence 7 ( tis7) is markedly increased during the adaptive response following massive small bowel resection and tis7 plays a role in normal gut lipid metabolism. Here, we further explore the functional implications of tis7 deletion in intestinal lipid metabolism and the adaptive response following small bowel resection. Intestinal tis7 transgenic ( tis7tg), tis7−/−, and wild-type (WT) littermates were subjected to 50% small bowel resection. Mice were fed a control or a high-saturated-fat (42% energy) diet for 21 days. Survival, body weight recovery, lipid absorption, mucosal lipid analysis, and the morphometric adaptive response were analyzed. Quantitative real-time PCR was performed to identify tis7 downstream gene targets. Postresection survival was markedly reduced in high-fat, but not control, diet-fed tis7−/− mice. Decreased survival was associated with anastomotic inflammation and intestinal obstruction postresection. High-fat, but not control, diet-fed tis7−/− mice had increased intestinal IL-6 expression. Intestinal lipid trafficking was altered in tis7−/− compared with WT mice postresection. In contrast, high-fat diet-fed tis7tg mice had improved survival postresection compared with WT littermates. High-fat diet feeding in the setting of tis7 deletion resulted in postresection anastomotic inflammation and small bowel obstruction. Tolerance of a calorie-rich, high-fat diet postresection may require tis7 and its target genes. The presence of luminal fat in the setting of tis7 deletion promotes an intestinal inflammatory response postresection.

No abstract

No abstract

No abstract