Video
The microbiome – a new target for IBD therapy
Video report of the presentation given by Prof. Jonathan Rhodes, University of Liverpool, United Kingdom, at the Falk Symposium 192 ” IBD 2014: Thinking out of the Box” in Paris, May 30 – 31, 2014.
© Falk Foundation e.V., Freiburg. All rights reserved.
Summary
There is no doubt whatsoever that changes to intestinal microbiota play a fundamental role in inflammatory bowel disease. This is supported by numerous studies showing altered fecal and mucosa-associated microbiota and also by case histories such as that of a 14-year-old patient with Crohn’s disease whose microbiome profile normalised after reaching clinical remission by enteral nutrition.
The pathological mechanisms of Crohn’s disease and ulcerative colitis are probably different. It seems, for example, that in the case of Crohn’s disease, genetic (or environmental) changes may cause a defect in the innate immune system which allows bacteria, and E. coli in particular, to invade the intestinal wall more easily. In ulcerative colitis, however, environmental factors seem to play an even greater role, modulating interactions between bacterial components and the colonic surface epithelium.
In theory there are several approaches we can take to normalising disturbed gut microbiota. However, treatment trials involving prebiotics, plant fibres that promote the growth of probiotic bacteria in the bowel, have so far been disappointing. Results achieved using genetically modified bacteria as probiotics may hold more promise, and they may also prove to be of value for maintaining remission in ulcerative colitis patients. “Contrabiotics”, i.e. soluble plant fibres that prevent interaction between bacteria and the intestinal wall, are virtually untested in humans to date. A diet high in fruit fibre does, however, appear to halve the risk of developing Crohn’s disease. Finally, the precise mechanism of action of enteral nutrition is still unclear and needs further study
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Link to Falk Mediacenter:
http://media.falkfoundation.de/index.php?id=102&L=1
Link to the video directly:
http://media.drfalkpharma.de/fileadmin/media/Rhodes_ENG_FINAL_03_mittel.mp4
Bowel
Text:
Mouli VP et al, Aliment Pharmacol Ther. 2014;39(2):125–36
There is growing epidemiological evidence for a role of vitamin D deficiency in the development of inflammatory bowel diseases and also its influence on disease severity.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26500
Text:
Ban L et al, Gastroenterology. 2014;146(1):76–84
No evidence was found that inflammatory bowel disease during pregnancy or medical therapy for inflammatory bowel disease during pregnancy increases the risk of a major congenital anomaly in children.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26501
Text:
Singh S et al, Clin Gastroenterol Hepatol. 2014;12(2):210–8
Based on a meta-analysis, inflammatory bowel disease has been associated with an increased risk of melanoma, independent of the use of biologic therapy.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26502
Liver
Biliary Tracts
Text:
Kowdley KV et al, N Engl J Med. 2014;370(3):222–32
In this phase 2b study, all-oral regimens of antiviral agents (the protease inhibitor ABT-450/ritonavir + the non-nucleoside polymerase inhibitor ABT-333) and ribavirin were effective both in patients with hepatitis C virus genotype 1 infection who had not received therapy previously and in those who had not had a response to prior therapy.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26503
Text:
Pearlman BL et al, Hepatology. 2014;59(1):71–7
Protease inhibitor therapy could be obviated in genotype 1-infected treatment-naive patients with low viral load at baseline who achieve undetectable viremia after 4 weeks of peginterferon/ribavirin.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26504
Text:
Bravi F et al, Clin Gastroenterol Hepatol. 2013;11(11):1413–21
Coffee reduces risk for hepatocellular carcinoma by 40%: An updated meta-analysis.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26507
Oesophagus
Stomach
Duodenum
Text:
Anaparthy R et al, Clin Gastroenterol Hepatol. 2013;11(11):1430–6
In patients with Barrett’s esophagus without dysplasia, length of Barrett’s esophagus was associated with progression to high-grade dysplasia or esophageal adenocarcinoma.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26508
Text:
Li X et al, Aliment Pharmacol Ther. 2014;39(3):270–81
Human papillomavirus infection was observed to be associated with an increased risk of esophageal squamous cell carcinoma in this meta-analysis.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26509
Text:
Matos JI et al, Eur J Gastroenterol Hepatol. 2013;25(12):1431–41
Individuals infected with CagA+ Helicobacter pylori strains and those infected with VacA s1 and m1 strains have an increased risk for gastric cancer.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26506
Pancreas
Text:
Akshintala VS et al, Aliment Pharmacol Ther. 2013;38(11–12):1325–37
Topical epinephrine and rectal NSAIDs are the most efficacious agents for preventing post-ERCP pancreatitis, based on existing randomized controlled trials.
Link:
http://www.drfalkpharma.de/index.php?L=1&id=18861#c26505
Current Falk literature:
Sonographic Gallstone Diagnosis
Authors: M. Sackmann und W.G. Zoller
(38 pages)
Revised edition 2014
U45e
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