title: Pathophysiology of increased intestinal permeability in obstructive jaundice.
abstract: Despite advances in preoperative evaluation and postoperative care, intervention, especially surgery, for relief of obstructive jaundice still carries high morbidity and mortality rates, mainly due to sepsis and renal dysfunction. The key event in the pathophysiology of obstructive jaundice-associated complications is endotoxemia of gut origin because of intestinal barrier failure. This breakage of the gut barrier in obstructive jaundice is multi-factorial, involving disruption of the immunologic, biological and mechanical barrier. Experimental and clinical studies have shown that obstructive jaundice results in increased intestinal permeability. The mechanisms implicated in this phenomenon remain unresolved, but growing research interest during the last decade has shed light in our knowledge in the field. This review summarizes the current concepts in the pathophysiology of obstructive jaundice-induced gut barrier dysfunction, analyzing pivotal factors, such as altered intestinal tight junctions expression, oxidative stress and imbalance of enterocyte proliferation and apoptosis. Clinicians handling patients with obstructive jaundice should not neglect protecting the intestinal barrier function before, during and after intervention for the relief of this condition, which may improve their patients' outcome.
authors.affiliation: Department of Internal Medicine, School of Medicine, University of Patras, Vironos 18, Patras 26224, Greece. sassim@upatras.gr
authors.forename: Stelios F
authors.initials: SF
authors.lastname: Assimakopoulos
authors.forename: Chrisoula D
authors.initials: CD
authors.lastname: Scopa
authors.forename: Constantine E
authors.initials: CE
authors.lastname: Vagianos
mesh_terms: D001646:Bile / Q000502:physiology; D049109:Cell Proliferation; D020895:Enterocytes / Q000502:physiology; D006801:Humans; D007408:Intestinal Absorption / Q000502:physiology*; D041781:Jaundice, Obstructive / Q000473:pathology / Q000503:physiopathology*; D018384:Oxidative Stress / Q000502:physiology; D019108:Tight Junctions / Q000502:physiology