Endocinch therapy for gastro-oesophageal reflux disease: a one year prospective follow up.

BACKGROUND: Gastro-oesophageal reflux disease (GORD) is, in the main, treated with either proton pump inhibitor (PPI) drugs or a Nissen fundoplication operation. Recently, BARD developed Endocinch, a device used to place sutures just below the oesophagogastric junction (OGJ) to treat GORD. AIM: To evaluate the long term benefit of the Endocinch technique in patients seen up to 12 months post procedure. PATIENTS: Twenty six patients with symptoms of GORD were recruited and had the procedure performed. Four patients were lost to follow up. METHODS: Twenty two patients completed their one year follow up. Pre procedure and post procedure (up to 12 months) assessments included symptom scoring (DeMeester), upper intestinal endoscopy, oesophageal manometry and 24 hour oesophageal pH, and completion of quality of life (QOL) questionnaires. RESULTS: Mean age was 39 years (range 22-62). Heartburn symptom score was reduced from a mean value of 19.22 at baseline to 7.5 at 12 months (n=22) (p<0.0001). Regurgitation score reduced from a mean of 2.27 at baseline to 0.86 at 12 months (n=22) (p<0.001). Mean (SEM) pH DeMeester acid score was reduced from 44.1 (4.3) to 33.32 (4.73) (p=0.028) at three month post procedure. Percentage upright acid exposure and number of reflux episodes were also reduced significantly. Use of PPIs was reduced by 64% at 12 months post procedure. All QOL assessments showed significant improvement (p=0.01). All transient post procedure complaints resolved within 72 hours. CONCLUSION: The Endocinch procedure is an effective and safe outpatient procedure that offers GORD patients significant improvement in symptomatology, QOL, and reduced requirements for PPIs over at least a one year period.

The methylenetetrahydrofolate reductase (MTHFR) gene in colorectal cancer: role in tumor development and significance of allelic loss in tumor progression.

BACKGROUND AND AIM: Folate deficiency predisposes to sporadic colorectal cancer (CRC). Methylenetetrahydrofolate reductase (MTHFR) is a critical folate-metabolising enzyme and a polymorphism at position 677 (C677T), is associated with reduced enzyme activity. We investigated whether this functional polymorphism modulates the risk of developing CRC. METHODS: This was a retrospective case-control study. 136 unselected cases of sporadic CRC and 848 normal population controls were genotyped for the MTHFR C677T polymorphism. Tumor tissue was genotyped to assess loss of heterozygosity (LOH). RESULTS: MTHFR CT heterozygotes had a significantly increased risk of developing CRC (53.7% of CRC cases vs 38.4% of controls), odds ratio 1.86 (95% CI 1.3-2.7, p < 0.005). No increased cancer risk was observed in TT homozygotes. The MTHFR 'T' allele frequency was significantly higher in the cancer group (0.3713) as compared to controls (0.2900, p < 0.008). LOH at the MTHFR locus was observed in 18% of informative cancers, with exclusive loss of the variant 'T' allele, in all cases. CONCLUSION: In this study of a homogenous northern European population, MTHFR CT heterozygotes had an almost two-fold increased risk of developing sporadic CRC. The exclusive pattern of MTHFR allele loss in cases of LOH, suggest that functional MTHFR activity within a tumor might play an important role in the survival and progression of a colonic neoplasm.