Comparison of transesophageal endoscopic plication (TEP) with laparoscopic Nissen fundoplication (LNF) in the treatment of uncomplicated reflux disease.

BACKGROUND: Transesophageal endoscopic plication (TEP) is a novel endotherapeutic approach in the management of gastroesophageal reflux disease (GERD). This non-randomized prospective study compares TEP with laparoscopic Nissen fundoplication (LNF). METHODS: Twenty-four consecutive patients treated with LNF, and 27 managed by TEP were studied. Symptom severity scores, endoscopy, 24 h esophageal pH and esophageal manometry and quality-of-life assessments were obtained pre- and posttreatment. RESULTS: In the LNF group the mean age was 36 yr (17-68) compared with 39 yr (22-62) in the TEP group. Symptom scoring, acid regurgitation score, reduction in the requirements of proton pump inhibitors (PPIs), and quality of life remained significantly improved in both groups at a median of 1 yr [10-18 months] follow-up post procedure. However, the improvement was significantly better in symptom score (p= 0.0383) and the control of acid reflux in the LNF group (p= 0.0007). Post-procedure dysphagia was more common in the LNF group. CONCLUSION: Both techniques improved symptom score, acid regurgitation, quality of life, and reduced the requirements for PPIs. The control of heartburn and acid reflux was better for LNF. TEP, like LNF, is a safe and effective method of management of symptomatic GERD but further developments are necessary to ensure control of esophageal acid reflux.

Ursodeoxycholic acid inhibits interleukin 1 beta [corrected] and deoxycholic acid-induced activation of NF-kappaB and AP-1 in human colon cancer cells.

Deoxycholic acid (DCA) has been implicated in colorectal carcinogenesis in humans with effects on proliferation and apoptosis, mediated at least in part by activation of transcription factors nuclear factor kappa B (NF-kappaB), activator protein 1 (AP-1) and protein kinase C (PKC) enzymes. Ursodeoxycholic acid (UDCA) is reported to reduce the frequency of colonic carcinogenesis in ulcerative colitis patients. Hence, we postulated that it might differ from DCA in its regulation of these transcription factors. The aim of the study was to determine effects of DCA and UDCA on NF-kappaB and AP-1 activation and explore its relationship to PKC. Human colonic tumour cell lines HCT116 were treated with DCA, UDCA, alone or pretreated with UDCA followed by DCA or IL-1beta. In other experiments, cells were pretreated with PKC inhibitors and then stimulated with DCA and IL-1beta or PMA. Gel shift assays were performed on nuclear extracts of the cells for NF-kappaB and AP-1 analysis. Western blot analyses and immunofluorescence were performed for Rel A (p65) and IkappaB-alpha levels on the treated cells. DCA increased NF-kappaB and AP-1 DNA binding. UDCA did not increase DNA binding of NF-kappaB and AP-1 and UDCA pretreatment inhibited DCA-induced NF-kappaB and AP-1 DNA binding. PKC inhibitors blocked DCA-induced NF-kappaB and AP-1 activation. These results were validated by Western blot analysis for RelA and IkappaB-alpha. In conclusion, UDCA did not induce NF-kappaB and AP-1 DNA binding but also blocked DCA-induced NF-kappaB and AP-1 activation. These findings suggest a possible mechanistic role for UDCA in blocking pathways thought to be involved in colon carcinogenesis.