Our final analysis shows that a single surgeon will not have a higher rate of either surgical-site infection or anastomotic failure if he/she routinely omits preoperative mechanical bowel preparation.

We report an interim analysis of a prospective single-blinded randomized trial designed to investigate whether preoperative mechanical bowel preparation influences the rate of surgical-site infection and anastomotic failure after elective colorectal surgery with primary intraperitoneal anastomosis performed by a single surgeon. Patients scheduled to undergo an elective colorectal procedure with a primary intraperitoneal anastomosis were randomized to receive either oral polyethylene glycol lavage solution and enemas (group A) or no preparation (group B). Surgical-site infection and anastomotic failure were investigated. Of 97 patients included, 48 were assigned to group A and 49 to group B. Twelve (12.4%) developed wound infections, six in each group (12.5 vs. 12.2%; NS). Intra-abdominal sepsis was only seen in group A (n = 3, 6.3%). Anastomotic failure occurred in four patients in group A (8.3%) vs. two patients in group B (4.1%) (NS). The overall complication rate in group A was 27.1%, vs. 16.3% in group B. The number needed to harm was 9.3. Our interim analysis of a prospective single-blinded randomized trial suggests that a surgeon may have the same or even worse outcomes when mechanical bowel preparation is routinely used for colorectal surgery with primary intraperitoneal anastomosis.

Several pieces of evidence suggest that female sex hormones may play a role in the regulation of electrolyte transport. We therefore hypothesized that female sex hormones might impair regulated transcellular chloride transport in human intestinal epithelial cells. The T84 cell line was used for electrophysiological studies. Changes in transepithelial resistance and short-circuit current (Isc) were measured via a dual voltage/current clamp in epithelial monolayers. Short-circuit current is equivalent to chloride secretion in T84 cells. Forskolin and 8-Br-cyclic adenosine monophosphate (cAMP) were used to activate cAMP-dependent Cl? transport. Ca2+-dependent secretion was stimulated by the receptor-mediated Ca2+ agonist carbachol. Acute exposure (30 minutes) to either progesterone or estradiol did not affect monolayer viability as reflected by transepithelial resistance. Moreover, the secretory response to both cAMP and Ca2+ agonists remained unaffected. In contrast, long-term exposure (24 hours) to physiological concentrations of progesterone (100 nM), but not estradiol, dose-dependently reduced the peak Isc induced by the cAMP-agonist forskolin from 125 +/- 2.7 mA. cm(2) in the control group to 96 +/- 2.5 mA. cm(2) in monolayers exposed to progesterone (n = 6 for each group; p <0.001). When the cAMP-analogue 8-Br-cAMP was used, the same behavior was observed (peak Isc = 112 +/- 1.6 mA. cm(2) vs 88 +/- 1.7 mA. cm(2) for control vs. progesterone-treated monolayers; n = 6 for each group; p <0.001). Taken together, our results suggest that progesterone but not estradiol inhibits cAMP-stimulated Cl- secretion in intestinal epithelial cells at a site distal to cyclic nucleotide generation.

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