Celiac Disease Nutritional Status and Poor Adherence to Follow-up.

Introduction. Celiac disease, an autoimmune enteropathy, occurs in susceptible individuals and is treatable with a gluten-free diet. These may not be supplemented with vitamins. Objective. To assess the nutritional health of children who have biopsy-proven celiac disease. Methods. Charts were reviewed between July 1, 2007, and June 30, 2017. Results. A total of 252 children ages 0 to 21 years had biopsy-proven celiac disease, mean age 11 ± 4.1 years. Body mass index Z-score was 0.2 ± 1.2 at diagnosis. Except for vitamin D, few had deficiencies at diagnosis. At 1-year follow-up, there was no significant change in anthropomorphics or vitamin status. Adherence to follow-up was poor; at 5 years after diagnosis, 39% adhered to follow-up. Conclusion. Despite a rigorous, proactive protocol for contacting and following children with celiac disease, adherence to follow-up was poor. New strategies, such as follow-up through the primary care provider, are needed.

Suppressed hepatic bile acid signalling despite elevated production of primary and secondary bile acids in NAFLD.

OBJECTIVE: Bile acids are regulators of lipid and glucose metabolism, and modulate inflammation in the liver and other tissues. Primary bile acids such as cholic acid and chenodeoxycholic acid (CDCA) are produced in the liver, and converted into secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid by gut microbiota. Here we investigated the possible roles of bile acids in non-alcoholic fatty liver disease (NAFLD) pathogenesis and the impact of the gut microbiome on bile acid signalling in NAFLD. DESIGN: Serum bile acid levels and fibroblast growth factor 19 (FGF19), liver gene expression profiles and gut microbiome compositions were determined in patients with NAFLD, high-fat diet-fed rats and their controls. RESULTS: Serum concentrations of primary and secondary bile acids were increased in patients with NAFLD. In per cent, the farnesoid X receptor (FXR) antagonistic DCA was increased, while the agonistic CDCA was decreased in NAFLD. Increased mRNA expression for cytochrome P450 7A1, Na+-taurocholate cotransporting polypeptide and paraoxonase 1, no change in mRNA expression for small heterodimer partner and bile salt export pump, and reduced serum FGF19 were evidence of impaired FXR and fibroblast growth factor receptor 4 (FGFR4)-mediated signalling in NAFLD. Taurine and glycine metabolising bacteria were increased in the gut of patients with NAFLD, reflecting increased secondary bile acid production. Similar changes in liver gene expression and the gut microbiome were observed in high-fat diet-fed rats. CONCLUSIONS: The serum bile acid profile, the hepatic gene expression pattern and the gut microbiome composition consistently support an elevated bile acid production in NAFLD. The increased proportion of FXR antagonistic bile acid explains, at least in part, the suppression of hepatic FXR-mediated and FGFR4-mediated signalling. Our study suggests that future NAFLD intervention may target the components of FXR signalling, including the bile acid converting gut microbiome.

Images in Clinical Medicine: Oral Manifestation of Crohn's Disease.

A 13-year-old boy presented with a 9-month history of episodic unilateral swelling of the face and oral pain. He reported having loose, nonbloody stools. Granulomatous inflammation consistent with Crohn's disease was found on histopathological examination.

Increased apolipoprotein A5 expression in human and rat non-alcoholic fatty livers.

Apolipoprotein A5 (apoA5) is a potent regulator of triglyceride (TG) metabolism and therefore may contribute to the pathogenesis of non-alcoholic fatty liver disease (NAFLD), a disease characterised by excessive TG-rich lipid droplets in hepatocytes. To test this hypothesis, we examined the mRNA expression of apoA5 in paediatric NAFLD livers in comparison to healthy controls. According to microarray and quantitative real-time PCR, human NAFLD livers exhibited elevated apoA5 expression compared to healthy controls. The apoA5 expression levels were positively correlated with hepatic TG storage and a marker for lipid droplets (perilipin), but were not correlated with plasma TG levels. These observations were confirmed with a NAFLD rat model. Interestingly, apoA5 expression was not altered in cultured fat-laden HepG2 cells, demonstrating that fat storage does not induce apoA5 in NAFLD livers. Therefore, the correlation between apoA5 and intracellular fat storage is likely explained by the potent effect of apoA5 in promoting intracellular fat storage. Our NAFLD patients and rats had elevated insulin resistance, which may have a role in elevating apoA5 expression in NAFLD livers. Our data support the hypothesis that apoA5 promotes hepatic TG storage and therefore contributes to the pathogenesis of NAFLD, and may represent a potential target for therapeutic intervention.