Early metabolic improvement following bariatric surgery in morbidly obese adolescents.

Bariatric surgery results in durable weight loss and improved comorbidities. The objectives of this study were to examine the efficacy of gastric bypass in reducing comorbid burden and improving metabolic status among morbidly obese adolescents. The medical records of 15 gastric bypass patients were retrospectively reviewed. Changes in metabolic markers were determined at baseline, 1 and 2 years post-operatively. Comparative analysis demonstrated significant improvement in weight, BMI, insulin, HbA1C, C-peptide, %B, %S, IR, cholesterol, percentile cholesterol, TG, percentile TG, HDL, percentile HDL, LDL, percentile LDL, and VLDL. Results support bariatric surgery as a treatment for morbidly obese adolescents with comorbidities.

Streamlining the care of patients with hypertrophic pyloric stenosis: application of a clinical pathway.

PURPOSE: The purpose of this study was to evaluate the impact of a clinical pathway on infants admitted to a pediatric tertiary care center with the diagnosis of hypertrophic pyloric stenosis (HPS). METHODS: The records of 132 HPS patients were evaluated before and after implementation of a clinical pathway. Infants were excluded for prematurity, admission to nonsurgical services, or multiple diagnoses requiring prolonged hospitalization, resulting in 83 patients for analysis. Group I (prepathway, n = 40) and group II (postpathway, n = 43) infants were analyzed for time from admission to operation, operation to first feeding, operation to discharge, total length of stay, hospital charges, metabolic status at time of admission, and postoperative complications. The Mann-Whitney test was performed (statistical significance at P <.05). RESULTS: There was no significant difference between group I and group II patients in the length of preoperative hospitalization or metabolic status at the time of hospital admission. In comparison with group I patients, there was a significant reduction in time to resumption of oral feedings (4.6 +/- 1.9 hours v 7.5 +/- 3.2 hours; P <.001) for group II infants and a significantly earlier discharge (26.7 +/- 6.8 hours v 38.0 +/- 11.7 hours; P <.001). This resulted in a shortened length of stay (41.8 +/- 9.7 hours v 57.8 +/- 14.3 hours; P <.001) with an associated decrease in hospital charges ($4,555 +/- $464 v $5,400 +/- $1,017; P <.001). CONCLUSIONS: Elimination of practice variability by the use of a clinical pathway for HPS resulted in significant reduction of hospital stay and related charges. The impact of the pathway occurred in the postoperative period and is a consequence of a rapid and systematic return to oral feedings.

Heparin-binding EGF-like growth factor is present in human amniotic fluid and breast milk.

BACKGROUND/PURPOSE: Heparin-binding EGF-like growth factor (HB-EGF) is a member of the epidermal growth factor (EGF) family that has been implicated in the healing of various organ injuries. Endogenous HB-EGF production is upregulated in response to injury to the kidney, liver, brain, skin, and intestine. Exogenous administration of HB-EGF protects against intestinal epithelial cell apoptosis and necrosis and intestinal ischemia/reperfusion (I/R) injury. This study examines the presence of endogenous HB-EGF in human amniotic fluid and breast milk, fluids that are in intimate contact with the developing and neonatal gastrointestinal tract. METHODS: Breast milk samples were collected from lactating women and amniotic fluid was gathered from full-term uteri (cesarian sections) or preterm uteri (amniocentesis). Crude and partially purified breast milk and amniotic fluid samples were analyzed for HB-EGF levels using an HB-EGF-specific enzyme-linked immunosorbent assay (ELISA). RESULTS: Analysis results showed detectable HB-EGF levels in human amniotic fluid and breast milk, ranging from 0.2 to 230 pg/mL. Breast milk and amniotic fluid subjected to heparin affinity or HB-EGF-affinity column chromatography showed bioactivity eluting at positions consistent with those known for native HB-EGF. CONCLUSIONS: This study represents the first report of detectable HB-EGF in human amniotic fluid and breast milk. The presence of HB-EGF in these fluids may serve a role in the development of the gastrointestinal tract in utero, and in protection against gut mucosal injury after birth.

Heparin-binding EGF-like growth factor decreases apoptosis in intestinal epithelial cells in vitro.

BACKGROUND/PURPOSE: The production of heparin-binding EGF-like growth factor (HB-EGF) is upregulated during organ injury and has a cytoprotective effect during hypoxic stress in intestinal epithelial cells in vitro and intestinal ischemia-reperfusion injuries in vivo. The purpose of this study was to determine if HB-EGF-related cytoprotection is manifested through alterations in apoptosis. METHODS: Human intestinal epithelial cell monolayers (DLD-1 and Caco-2) were stimulated with interleukin (IL)-1 (20 ng/mL), tumor necrosis factor (TNF)-alpha (40 ng/mL), and interferon (IFN)-gamma (10 ng/mL) with or without HB-EGF (1, 10 or 100 ng/mL) and analyzed for rates of apoptosis utilizing a Cell Death Detection ELISA and flow cytometry. RESULTS: ELISA results showed a 3-fold increase in the level of apoptosis during stimulation with cytokines compared with nonstimulated cells (P <.05). Relative levels of cytokine induced apoptosis were reduced after 12 hours of HB-EGF exposure (P <.05) in a dose-dependent fashion. Results of flow cytometric analysis also showed a reduction in apoptosis at 6 hours when cell monolayers were stimulated with cytokines in conjunction with HB-EGF compared with cytokines alone (P <.05). CONCLUSIONS: HB-EGF downregulated apoptosis in intestinal epithelial cells exposed to proinflammatory cytokines in vitro. The results of this study suggest that alterations in apoptosis may represent a possible mechanism by which this growth factor exerts its cytoprotective effect at the mucosal level during the proinflammatory state.

Giant duodenal diverticulum: presentation by blunt trauma.

Most duodenal diverticula are asymptomatic, small (i.e., less than 5 cm in greatest dimension), acquired, extraluminal, and false. The only report of a massive or giant duodenal diverticulum (i.e., 10 cm or more), in the current literature, included severe nocturnal diarrhea. The present case report is the incidental finding of a massive duodenal diverticulum in a 34-year-old male trauma victim. The insidious nature of this case and the patient's age suggest a congenital etiology. We believe this is the first report of such a case.

Interleukin-6 and tumor necrosis factor production in an enterocyte cell model (Caco-2) during exposure to Escherichia coli.

Data linking interactions between bacteria and the intestine with elevated serum cytokine levels has led to the concept of the gut as a cytokine-producing organ. An in vitro cell culture model was used to investigate the potential role of intestinal mucosa within this paradigm. Polarized monolayers of human enterocytes (Caco-2) were grown in a two compartment system where the apical and basal aspects of the membrane could be studied. Supernatant was collected at 0, 1, 3, 6, and 24 h after the monolayer was exposed (apically or basally) to 10(2), 10(5), or 10(8) colony-forming units of Escherichia coli C25/mL and saved for interleukin (IL)-6 and tumor necrosis factor (TNF) bioassay analysis. Caco-2 cells (not bacterially challenged) secreted significant amounts of constitutive IL-6, but not TNF, into the apical and basal chambers. Both cytokines levels were increased in a dose-dependent fashion (p < .05) after the E. coli challenge. This stimulated cytokine response was polar, in that the highest cytokine levels were at the side of the bacterial challenge and were most notable at the highest dose (10(8) colony-forming units/mL) of E. coli C25 tested. Caco-2 cells produce IL-6 and TNF in a dose-dependent fashion in response to E. coli C25 and the magnitude of this response is maximal on the side of the bacterial challenge. This data supports the hypothesis that bacterially challenged human enterocytes may be important producers of cytokines.