Markers of Hypoxia Correlate with Histologic and Endoscopic Severity of Colitis in Inflammatory Bowel Disease.

BACKGROUND: Inflammation results in significant shifts in tissue metabolism. Recent studies indicate that inflammation and hypoxia occur concomitantly. We examined whether circulating and tissue markers of hypoxia could serve as surrogate indicators of disease severity in adult and pediatric patients with inflammatory bowel disease (IBD). METHODS: Serum and colonic biopsies were obtained from pediatric subjects with active IBD colitis and adult subjects with active and inactive ulcerative colitis, along with healthy non-colitis controls of all ages. Disease activity was evaluated by endoscopy and histopathology. Levels of serum hypoxia markers (macrophage inflammatory protein-3α [MIP-3α], vascular endothelial growth factor [VEGF], and erythropoietin [EPO]) were measured. RESULTS: Children with active IBD colitis had higher levels of serum MIP-3α and VEGF compared to non-colitis controls (p<0.01 and p<0.05, respectively). In adult subjects with endoscopically active ulcerative colitis, serum MIP-3α and EPO were significantly elevated compared to non-colitis controls (both p<0.01). In parallel, analysis of colon tissue MIP-3α mRNA and protein in pediatric subjects revealed increased expression in those with IBD colitis compared to controls (p<0.05 and p<0.01 for mRNA and protein, respectively). Serum MIP-3α and VEGF significantly increased with histology grade. CONCLUSION: Peripheral blood hypoxia markers may be useful indicators of disease activity for pediatric and adult IBD patients.

Management of button battery-induced hemorrhage in children.

OBJECTIVES: Button battery ingestions are potentially life threatening for children. Catastrophic and fatal injuries can occur when the battery becomes lodged in the esophagus, where battery-induced injury can extend beyond the esophagus to the trachea or aorta. Increased production of larger, more powerful button batteries has coincided with more frequent reporting of fatal hemorrhage secondary to esophageal battery impaction, but no recommendations exist for the management of button battery-induced hemorrhage in children. MATERIALS AND METHODS: We reviewed all of the reported pediatric fatalities due to button battery-associated hemorrhage. Our institution engaged subspecialists from a wide range of disciplines to develop an institutional plan for the management of complicated button battery ingestions. RESULTS: Ten fatal cases of button battery-associated hemorrhage were identified. Seven of the 10 cases have occurred since 2004. Seventy percent of cases presented with a sentinel bleeding event. Fatal hemorrhage can occur up to 18 days after endoscopic removal of the battery. Guidelines for the management of button battery-associated hemorrhage were developed. CONCLUSIONS: Pediatric care facilities must be prepared to act quickly and concertedly in the case of button battery-associated esophageal hemorrhage, which is most likely to present as a "sentinel bleed" in a toddler.