Double balloon enteroscopy: effective and minimally invasive method for removal of retained video capsules.

BACKGROUND AND AIM: Prior case series document removal of retained video capsules predominantly via surgical intervention. Data on endoscopic removal of retained capsules are limited. Our aim was to describe an endoscopic method of retrieval using double balloon enteroscopy (DBE). METHODS: A retrospective case series examination found 10 patients who underwent DBE for retrieval of a retained video capsule at two large tertiary referral academic centers from May 2007 to June 2013. RESULTS: Mean age of patients was 64.9 ± 18.1 years (four females, six males). Five patients failed to pass the capsule as a result of an ileal or jejunal stricture (one patient with ulcerative colitis; four patients with Crohn's disease); two patients had a small bowel stricture as a result of non-steroidal anti-inflammatory drug enteropathy; one patient had intermittent partial small bowel obstruction without evidence of a stricture; one patient had an obstructing malignant jejunal mass and one patient had a small bowel stricture as a result of radiation enteritis. Endoscopic removal via DBE was successful in eight of 10 patients (80%). The remaining two patients underwent surgical removal of the retained capsule. The two failed cases of capsule retrieval were both patients with suspected ileal disease. CONCLUSIONS: The most common cause of capsule retention was underlying Crohn's disease. DBE is an effective and minimally invasive method of capsule retrieval, including those patients with ileal disease, which has not been previously described. DBE can prevent unnecessary surgery while providing endoscopic therapy of inflammatory strictures by dilation.

Embryonic development in the reduced folate carrier knockout mouse is modulated by maternal folate supplementation.

BACKGROUND: The reduced folate carrier (RFC1) is a ubiquitously expressed integral membrane protein that mediates delivery of 5-methyltetrahydrofolate into mammalian cells. In this study, embryonic/fetal development is characterized in an RFC1 knockout mouse model in which pregnant dams receive different levels of folate supplementation. METHODS: RFC1(+/-) males were mated to RFC1(+/-) females, and pregnant dams were treated with vehicle (control) or folic acid (25 or 50 mg/kg) by daily subcutaneous injection (0.1 mL/10 g bwt), beginning on E0.5 and continuing throughout gestation until the time of sacrifice. RESULTS: Without maternal folate supplementation, RFC1 nullizygous embryos die shortly postimplantation. Supplementation of pregnant dams with 25 mg/kg/day folic acid prolongs survival of mutant embryos until E9.5-E10.5, but they are developmentally delayed relative to wild-type littermates, display a marked absence of erythropoiesis, severe neural tube and limb bud defects, and failure of chorioallantoic fusion. Fgfr2 protein levels are significantly reduced or absent in the extraembryonic membranes of RFC1 nullizygous embryos. Maternal folate supplementation with 50 mg/kg/day results in survival of 22% of RFC1 mutants to E18.5, but they develop with multiple malformations of the eyelids, lungs, heart, and skin. CONCLUSIONS: High doses of daily maternal folate supplementation during embryonic/fetal development are necessary for early postimplantation embryonic viability of RFC1 nullizygous embryos, and play a critical role in chorioallantoic fusion, erythropoiesis, and proper development of the neural tube, limbs, lungs, heart, and skin.