Transgastric endoscopic peritoneoscopy does not lead to increased risk of infectious complications.

BACKGROUND: It remains important to determine the risk of bacterial contamination and infectious complications of the peritoneal cavity as it pertains to transgastric natural orifice translumenal endoscopic surgery (NOTES) procedures. The infectious implications of such procedures have been quantified in animal models. This report discusses the infectious risks of transgastric endoscopic peritoneoscopy (TEP) in a human clinical trial. METHODS: Under institutional review board approval, 40 patients scheduled for laparoscopic Roux-en-Y gastric bypass (LRYGB) participated in this study. The TEP procedure was performed without preoperative gastric decontamination and without laparoscopic guidance. Preoperative intravenous antibiotics were given. Saline aspirates were taken from the gastric lumen before endoscopic gastrotomy creation and from the peritoneal cavity after transgastric access. Samples were sent for culture, identification, and bacterial counts. Subgroup analysis was performed on patients taking proton pump inhibitors (PPIs). These data were compared with data for "sterile" peritoneal aspirates from a historical cohort of 50 patients undergoing LRYGB. RESULTS: The median number of bacteria isolated from the gastric aspirates was 980 colony-forming units (CFU)/ml (n=40). The median number of bacteria isolated from the peritoneal aspirates was 323 CFU/ml. Cross-contamination from the stomach to the peritoneal cavity was documented in eight cases. No abscesses or anastomotic leaks were recorded. One port-site infection occurred. Subgroup analysis of 15 patients receiving PPIs showed elevated bacterial counts in gastric aspirates and the post-TEP peritoneal samples compared with patients not receiving PPIs (n=25). This subgroup on PPI's did not have an increase in infectious complications. CONCLUSIONS: Contamination of the peritoneal cavity does occur with TEP, but this does not lead to an increased risk of infectious complications. Similarly, patients receiving PPIs have an increased gastric bacterial load and increased contamination after TEP but not an increased risk of infectious complications.

Zinc finger transcription factor Egr-1 is involved in stimulation of NHE2 gene expression by phorbol 12-myristate 13-acetate.

The apical membrane Na(+)/H(+) exchanger isoforms NHE2 and NHE3 are involved in transepithelial Na(+) absorption in the intestine. However, they exhibit differences in their pattern of tissue expression and regulation of their activity by various molecular signals. To study the mechanisms involved in the transcriptional regulation of these genes, we characterized cis-acting elements within the human NHE2 promoter that regulate NHE2 promoter expression in C2BBe1 cells. A small DNA region (-85/+249) was involved in the regulation of basal transcriptional activity of the NHE2 promoter as determined by transient transfection assays. RT-PCR analysis showed that NHE2 mRNA was upregulated in response to phorbol 12-myristate 13-acetate (PMA). Results from actinomycin D-treated cells indicated that the regulation of the NHE2 gene by PMA occurs in part at the transcriptional level. Furthermore, PMA treatment led to a 100% increase in promoter activity through elements located on the -415/+249 DNA fragment. A PMA-induced nuclear factor that bound to the NHE2 promoter was identified as the transcription factor Egr-1. We identified two PMA response elements in the -415/+1 promoter region that bind to Sp1 and Sp3 in untreated nuclear extracts and to Egr-1 in PMA-treated nuclear extracts. In cotransfection experiments, Egr-1 was able to transactivate the NHE2 promoter. Our data indicate that Egr-1 may play a key role in regulated expression of the human NHE2 gene.