Lack of Follow-up of Pediatric Patients With Celiac Disease.

Celiac disease (CD) is often diagnosed in childhood, and the treatment is a lifelong gluten-free diet (GFD).1,2 It may take several years to gain competence in the skills required to follow a GFD successfully. Inadequately treated CD is associated with bone fractures, nutritional deficiencies, and lymphoma.3,4 Healthcare providers are key resources for patients with CD. Consultation with a dietitian with GFD expertise at diagnosis and annual disease-specific follow-up care are recommended.2,5 The primary objective of this study was to evaluate adherence to guidelines for dietitian consultation and follow-up for children with CD. A secondary objective was to identify factors associated with loss to follow-up.

Red Spot Lesions in the Duodenal Bulb Are a Highly Specific Endoscopic Sign of Celiac Disease: A Prospective Study.

We have recognized red spot lesions (RSLs) in the duodenal bulb in children with celiac disease (CD) and believe they may represent an underappreciated and distinct endoscopic sign of CD. A total of 171 pediatric patients undergoing esophagogastroduodenoscopy with duodenal biopsy for symptoms consistent with CD were prospectively recruited. There were 75 patients who met criteria for CD and the remaining 96 patients served as symptomatic controls. As compared to endoscopic markers frequently mentioned in literature, RSLs had comparable sensitivity, specificity, positive predictive value, and negative predictive value of 31%, 94%, 80%, and 64%, respectively. If RSLs are noted during endoscopy in a patient with gastrointestinal symptoms that might be the result of CD, then sufficient duodenal biopsies to make the diagnosis of CD should be obtained.

Low Levels of Detectable Urine and Stool GIPs in Children with Celiac Disease on a Gluten-Free Diet.

Objectives: This study examines the prevalence of detectable gluten immunogenic peptides (GIPs) as a proxy for gluten exposure in children with celiac disease on a gluten-free diet in the United States, as estimated by gluten breakdown products excreted in urine and stool. Methods: Urine and stool samples were collected in 3 settings (home, gastroenterology clinic, and endoscopy) for pediatric participants (ages 6-21 years old) across 2 medical centers. Commercial ELISA assays were used to quantify the GIPs in each sample. Results: GIPs were detected in 4 out of 44 (9.1%) of stool samples and 6 out of 125 (4.8%) of urine samples provided by 84 children. These samples were collected across all settings, and most participants (70%) were asymptomatic at the time of sample collection. For the urine samples collected at the time of endoscopy, all subjects found to have persistent enteropathy had no detectable GIPs (0/12). Discussion: GIPs provide an additional method for screening for gluten exposures in individuals with celiac disease on a gluten-free diet, and may be used across multiple settings. We found a low detection rate of GIPs in children. Our finding of undetectable GIPs in individuals with persistent enteropathy may be expected of a single determination under close observation or represent a lack of gluten exposure within the detection window. More research is needed to understand the dynamics of gluten absorption and excretion in the US pediatric population.

Nuclear degradation dynamics in a nonapoptotic programmed cell death.

Nuclear degradation is a major event during programmed cell death (PCD). The breakdown of nuclear components has been well characterized during apoptosis, one form of PCD. Many nonapoptotic forms of PCD have been identified, but our understanding of nuclear degradation during those events is limited. Here, we take advantage of Drosophila oogenesis to investigate nuclear degeneration during stress-induced apoptotic and developmental nonapoptotic cell death in the same cell type in vivo. We find that nuclear Lamin, a caspase substrate, dissociates from the nucleus as an early event during apoptosis, but remains associated with nuclei during nonapoptotic cell death. Lamin reveals a series of changes in nuclear architecture during nonapoptotic death, including nuclear crenellations and involutions. Stretch follicle cells contribute to these architecture changes, and phagocytic and lysosome-associated machinery in stretch follicle cells promote Lamin degradation. More specifically, we find that the lysosomal cathepsin CP1 facilitates Lamin degradation.