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The pathogenesis of primary sclerosing cholangitis (PSC), a progressive biliary tract disease without approved medical therapy, is not well understood. The relationship between PSC and inflammatory bowel disease has inspired theories that intestinal factors may contribute to the development and progression of hepatobiliary fibrosis in PSC. There is evidence from both fecal and mucosa‐associated microbial studies that patients with PSC harbor an abnormal enteric microbiome. These organisms are thought to produce toxic byproducts that stimulate immune‐mediated damage of hepatocytes and the biliary tree. The link between these mechanisms may be related to altered intestinal permeability leading to migration of bacteria or associated toxins to the liver through the portal circulation. In support of these concepts, early trials have demonstrated improved biochemical parameters and symptoms of PSC with oral antibiotics, ostensibly through manipulation of the enteric microbiota. This article reviews the published literature for evidence as well as gaps in knowledge regarding these mechanisms by which intestinal aberrations might drive the development of PSC. We also identify areas of future research that are needed to link and verify these pathways to enhance diagnostic and therapeutic approaches.

Object Nerve transfers are an effective means of restoring control to paralyzed somatic muscle groups and, recently, even denervated detrusor muscle. The authors performed a cadaveric pilot project to examine the feasibility of restoring control to the urethral and anal sphincters using a femoral motor nerve branch to reinnervate the pudendal nerve through a perineal approach. Methods Eleven cadavers were dissected bilaterally to expose the pudendal and femoral nerve branches. Pertinent landmarks and distances that could be used to locate these nerves were assessed and measured, as were nerve cross-sectional areas. Results A long motor branch of the femoral nerve was followed into the distal vastus medialis muscle for a distance of 17.4 ± 0.8 cm, split off from the main femoral nerve trunk, and transferred medially and superiorly to the pudendal nerve in the Alcock canal, a distance of 13.7 ± 0.71 cm. This was performed via a perineal approach. The cross-sectional area of the pudendal nerve was 5.64 ± 0.49 mm2, and the femoral nerve motor branch at the suggested transection site was 4.40 ± 0.41 mm2. Conclusions The use of a femoral nerve motor branch to the vastus medialis muscle for heterotopic nerve transfer to the pudendal nerve is surgically feasible, based on anatomical location and cross-sectional areas.

Our retrospective study suggests that the male urethral sling may be an outpatient option for neurogenic incontinence secondary to sphincteric incompetence. Long-term followup in our initial 6 patients shows encouraging durability. Continued study is required to determine strategies that might decrease the complication rate of this approach.

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