Laparoscopic cecostomy button placement for the management of fecal incontinence in children with Hirschsprung's disease and anorectal anomalies.

BACKGROUND: Antegrade colonic enemas offer a surgical solution for many children with chronic constipation and encopresis associated with Hirschsprung's disease and anorectal malformations. This study demonstrated the feasibility of a new laparoscopic technique for cecostomy button placement (LCBP) to allow antegrade enema treatment. METHODS: Charts of children with encopresis who underwent LCBP between 1999 and 2001 were reviewed. The age, weight, primary diagnosis, operative time, hospital stay, associated complications, follow-up duration, and outcome of the patients were recorded. The surgical technique used a "U-stitch" method and a chait tube or a standard gastrostomy button. A follow-up telephone survey was conducted to assess parental satisfaction and overall success in continence. RESULTS: Seven patients ages 4 to 12 years (mean, 7.3 +/- 1.3 years) and weighing 15 to 44 kg (mean, 24.5 +/- 4 kg) underwent LCBP over a 2-year period. The mean follow-up period was 15 +/- 4 months (range, 6-33 months). Four patients had anorectal malformations, and three patients had Hirschsprung's disease. For all the patients, LCBP was accomplished without any intraoperative complications. The mean operative time was 33 +/- 2 min, and the hospital stay was 2 to 5 days (mean, 3.8 +/- 0.5 days). The patients received one or two daily antegrade enemas, and none had accidental bowel movements. Episodes of soiling at night once or twice a week were observed with two children. Two patients had hypertrophic granulation tissue formation, which responded to topical therapy. The button was uneventfully changed twice in one patient because of mechanical malfunction. CONCLUSION: To manage overflow incontinence of children with anorectal malformations and Hirschsprung's disease, LCBP is a technically straightforward, effective, and reversible method for the placement of a cecostomy button.

Recent developments in our understanding of melanocortin system in the regulation of food intake.

Obesity has become one of the most significant public health problems facing the world today. However, the pathogenesis of obesity is multifactorial and involves the interaction of genetic and environmental factors. There is a pressing need to better understand the biochemical pathways that control energy intake and expenditure. In the last few years, a number of important signalling molecules have been identified that play important roles in obesity. One family of these molecules is the melanocortin system, which consists of several components: (1) melanocortin peptides; (2) the five seven-transmembrane G-protein coupled melanocortin receptors (MCRs); (3) the endogenous MCR antagonists, agouti and agouti-related protein; (4) the endogenous melanocortin mediators, mahogany, and syndecan. This system plays a key role in the central nervous system control of feeding behaviour and energy expenditure. This article will provide an overview of the anatomy, physiology, and molecular biology of the melanocortin system, and recent developments in our understanding of this system in obesity.

Effect of secretory immunoglobulin A on bacterial translocation in an enterocyte-lymphocyte co-culture model.

Intestinal secretory immunoglobulin A (sIgA) plays an important role in gut mucosal immunity in vivo; however, in-vitro enterocyte models for studying the mechanisms of these effects are lacking. This study utilizes a cell-culture model to investigate the effect of sIgA on bacterial translocation (BT) across human enterocytes co-cultured with human lymphoid cells (Raji cells). This model is intended to mimic in-vivo enterocyte/lymphocyte interactions found in intestinal follicle-associated epithelia. Human Caco-2 enterocytes were grown to confluence on porous filters in the apical chamber of a two-chamber cell-culture system. After differentiation, human B lymphoid cells (Raji cells) were added to the basolateral surface of Caco-2 monolayers for 3 days' co-culture, followed by washing away of unincorporated Raji cells. Transepithelial electrical resistance (TEER) was used to measure tight-junction permeability. Monolayers were treated with or without sIgA, IgG (negative control), or mannose (positive control). BT across the cell monolayer was determined 1.5 h after addition of Escherichia coli. Statistical analysis was by the Kruskal-Wallis test, P below 0.05 considered significant. In co-culture monolayers treated with sIgA, IgG, or mannose, there was no significant effect on TEER; however, the magnitude of BT across cells treated with sIgA (1.3 +/- 0.4 log10CFU/ml) and mannose (1.6 +/- 1.1 log10CFU/ml) was significantly decreased compared to PBS (3.9 +/- 0.4 log10CFU/ml) and IgG (2.9 +/- 0.6 log10CFU/ml) controls (P < 0.05). sIgA BT inhibition was dose-dependent. BT inhibition by sIgA and mannose was additive (0.5 +/- 1 log10CFU/ml). Inhibition of BT was negated when sIgA and mannose were removed by washing prior to E. Coli addition (3.6 +/- 0.5 log10CFU/ml), suggesting that both inhibitors act through bacterial binding.