In normal individuals, the epithelium of the colon absorbs 1.5–2 l of water a day to generate dehydrated feces. However, in the condition of bile acid malabsorption (BAM), an excess of bile acids in the colon results in diarrhea. Several studies have attempted to address the mechanisms contributing to BAM induced by various bile acids. However, none have addressed a potential dysregulation of aquaporin (AQP) water channels, which are responsible for the majority of transcellular water transport in epithelial cells, as a contributing factor to the onset of diarrhea and the pathogenesis of BAM. In this study, we aimed to systematically analyze the expression of AQPs in colonic epithelia from rat, mouse, and human and determine whether their expression is altered in a rat model of BAM. Mass spectrometry-based proteomics, RT-PCR, and western blotting identified various AQPs in isolated colonic epithelial cells from rats (AQP1, 3, 4, 7, 8) and mice (AQP1, 4, 8). Several AQPs were also detected in human colon (AQP1, 3, 4, 7–9). Immunohistochemistry localized AQP1 to the apical plasma membrane of epithelial cells in the bottom of the crypts, whereas AQP3 (rat, human) and AQP4 (mice, human) were localized predominantly in the basolateral plasma membrane. AQP8 was localized intracellularly and at the apical plasma membrane of epithelial cells. Rats fed sodium cholate for 72 h had significantly increased fecal water content, suggesting development of BAM-associated diarrhea. Colonic epithelial cells isolated from this model had significantly altered levels of AQP3, 7, and 8, suggesting that these AQPs may be involved in the pathogenesis of bile acid-induced diarrhea.

Aim Our aim was to study the implementation of the low anterior resection syndrome (LARS) score in a clinical setting and to evaluate a nurse‐led standardized intervention for bowel dysfunction following rectal cancer surgery. Method All patients who underwent curatively intended, restorative rectal cancer resection in a single centre between 2012 and 2016 were screened using the LARS score. At clinical follow‐up, patients with major LARS were offered treatment in a nurse‐led clinic. Data were retrospectively collected from patients' electronic medical records. Results In total, 190 out of 286 (66%) patients were screened with the LARS score of whom 89 had major LARS. A total of 86 patients requested treatment for their bowel dysfunction and the majority obtained acceptable function after nurse‐led optimized conservative treatment. Seventeen patients went on to transanal irrigation, and seven patients were treated with biofeedback. Five patients were referred for surgery, three for gastroenterological evaluation. After treatment in the clinic, patients achieved a statistically significant decrease in median LARS score from 37 (interquartile range 34–39) to 31 (interquartile range 23–34) (P < 0.001), and the prevalence of major LARS fell from 95% to 53% (P < 0.001). Conclusion Screening for LARS was not optimal as one‐third of patients were not screened. The majority of patients with major LARS requested treatment for their symptoms and could be successfully treated with standardized interventions managed in a nurse‐led setting.

Only minor AVN of clinical importance was seen after Ludloff's procedure.