Irritable Bowel Syndrome: Hanauer SB

Hanauer SB. · No affiliation provided · Nat Clin Pract Gastroenterol Hepatol. · Pubmed #18974750 No free full text.

This publication has no abstract.

Hanauer SB. · Section of Gastroenterology, Hepatology, and Nutrition, University of Chicago, Chicago, Illinois, USA. · Rev Gastroenterol Disord. · Pubmed #18477966 No free full text.

Abstract: Loperamide is an effective therapy for a variety of diarrheal syndromes, including acute, nonspecific (infectious) diarrhea; traveler's diarrhea; and chemotherapy-related and protease inhibitor?associated diarrhea. Loperamide is effective for the "gut-directed" symptom of diarrhea in patients with painless diarrhea or diarrhea-predominant irritable bowel syndrome. Loperamide and diphenoxylate are commonly used to treat diarrhea in numerous settings of inflammatory bowel disease. Loperamide has also been observed to increase anal sphincter tone, which may lead to improvement of fecal continence in patients with and without diarrhea. Loperamide is generally well tolerated at recommended nonprescription doses, with the most common side effects related to the impact on bowel motility (abdominal pain, distention, bloating, nausea, vomiting, and constipation).

Hanauer SB. · University of Chicago, IL 60637, USA. · Nat Clin Pract Gastroenterol Hepatol. · Pubmed #16265041 No free full text.

Abstract: Evidence is accumulating that both genetic and environmental factors contribute to ulcerative colitis. The most consistent genetic associations have been shown for the MHC locus HLA Class II alleles, but the interleukin-1 family of genes and the multidrug resistance gene MDR1 have also been implicated as genetic susceptibility factors for the development of disease. In addition, there is a relationship between ulcerative colitis and bacterial flora, with an increased number of adherent Bacteroides spp. and Enterobacteriaceae spp. present in inflamed bowel segments. Conversely, cigarette smoking and appendectomy have both been shown to protect against the development of ulcerative colitis. Despite our improved understanding of the genetics and inflammatory mechanisms that underpin this disease, however, the etiology and pathogenesis of ulcerative colitis remain undefined. The diagnosis of ulcerative colitis is being aided by recent advances in diagnostic strategies, including the detection of fecal and serologic markers and the use of wireless capsule endoscopy, but, in the absence of a pathognomonic marker, the definition of this disease remains based on well-established clinical, endoscopic and histologic criteria. In particular, it is difficult to discriminate ulcerative colitis from other forms of colitis, including Crohn's disease, and there seems to be a growing overlap of pathophysiologic processes between ulcerative colitis and post-infectious irritable bowel syndrome. Patients who remain indeterminate between ulcerative colitis and Crohn's disease also continue to be a diagnostic challenge.

Kane SV, Sandborn WJ, Rufo PA, Zholudev A, Boone J, Lyerly D, Camilleri M, Hanauer SB. · University of Chicago, Chicago, Illinois 60637, USA. · Am J Gastroenterol. · Pubmed #12818275 No free full text.

Abstract: OBJECTIVE: Lactoferrin is a glycoprotein expressed by activated neutrophils. The aim of this study was to determine the sensitivity and specificity of fecal lactoferrin concentrations for inflammatory bowel disease (IBD) or irritable bowel syndrome (IBS) versus healthy controls. METHODS: Fresh stool samples were collected from outpatients with ulcerative colitis (UC), Crohn's disease (CD), or IBS. Clinical disease activity for IBD was assessed using a modified Harvey-Bradshaw Activity Index. Fecal lactoferrin concentrations were determined using a polyclonal antibody-based enzyme linked immunoassay. Mean fecal lactoferrin concentrations for each group and sensitivity and specificity of the assay were determined. RESULTS: One hundred-four CD patients, 80 UC patients, 31 IBS patients, and 56 healthy controls were recruited. The mean +/- SE fecal lactoferrin concentration (microg/g fecal weight) was 440 +/- 128 for CD patients, 1125 +/- 498 for UC patients, 1.27 +/- 0.29 for IBS patients, and 1.45 +/- 0.4 for healthy controls. Fecal lactoferrin was 90% specific for identifying inflammation in patients with active IBD. Elevated fecal lactoferrin was 100% specific in ruling out IBS. CONCLUSIONS: Fecal lactoferrin is sensitive and specific for detecting inflammation in chronic IBD. This noninvasive test may prove useful in screening for inflammation in patients presenting with abdominal pain and diarrhea.

Hanauer SB. · Section of Gastroenterology, Hepatology, and Nutrition, Department of Medicine, University of Chicago, Chicago, Illinois, USA. · Rev Gastroenterol Disord. · Pubmed #18192960 No free full text.

This publication has no abstract.

Hanauer SB, Sandborn WJ, Vakil N, Katz PO, Talley NJ, Rex DK, Hawes RH, Guda NM, Freeman ML, Keeffe EB, Balart LA. · No affiliation provided · Rev Gastroenterol Disord. · Pubmed #16957658 No free full text.

Abstract: Highlights from the 2006 Digestive Disease Week May 20-25, 2006, Los Angeles, CA. In this meeting review, many of our editorial board members report on Digestive Disease Week 2006. They highlight the most noteworthy presentations in their respective areas of expertise, including the latest treatments, technologies, and diagnostic advances in ulcerative colitis, Crohn's disease, Helicobacter pylori infection, gastroesophageal reflux disease, irritable bowel syndrome, colorectal cancer, pancreatic and biliary disease, and liver disease.