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Guideline [Surgery -- fistulas] 2003
Buhr HJ, Kroesen AJ, Stange EF, Anonymous00109. · Chirurgische Klinik I, Universitätsklinikum Benjamin Franklin, Berlin. · Z Gastroenterol. · Pubmed #12541173 No free full text.
This publication has no abstract.
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Review [Diagnostics and treatment of Crohn's disease -- results of an evidence-based consensus conference of the German Society for Digestive and Metabolic Diseases] 2003
Stange EF, Schreiber S, Fölsch UR, von Herbay A, Schölmerich J, Hoffmann J, Zeitz M, Fleig WE, Buhr HJ, Kroesen AJ, Moser G, Matthes H, Adler G, Reinshagen M, Stein J, Anonymous00103. · Abteilung Innere Medizin 1, Robert-Bosch-Krankenhaus, Stuttgart. · Z Gastroenterol. · Pubmed #12541167 No free full text.
This publication has no abstract.
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Review New aspects of surgical therapy of recurrent Crohn's disease. free! 2000
Kroesen AJ, Buhr HJ. · Department of Surgery, University Hospital Benjamin Franklin, Freie Universität, Berlin, Germany. · Yonsei Med J. · Pubmed #10731912 links to free full text
Abstract: Crohn's disease can neither be cured by surgery nor by medical therapy. Surgical therapy of recurrent Crohn's disease requires special precautions. The recurrence rate is 60% after 15 years. There are no certain data of the risk factors influencing the recurrence rate. The only clear facts are that wide resection out of the resection margins and smoking negatively influence recurrence. Hence, the major principles of therapy is a minimally-resected surgery. This mainly concerns strictures and stenosis. Strictures should be treated by stricturoplasty and stenosis by limited resection with Crohn-free resection margins. Just in case of interenteric and enterocutanous with a concomitant short bowel syndrome, in blind-ending fistulas with an abscess or in enterovesical fistulas, we recommend immediate operation. The therapy of recurrent anorectal Crohn's disease underlies the same rules as primary therapy. If necessary, proctectomy remains the last option. Also, emergency surgery in recurrent Crohn's disease follows the same rules as in elective surgery.
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Review [Anorectal fistulas in Crohn disease] 1999
Kroesen AJ, Buhr HJ. · Chirurgische Klinik I, Universitätsklinikum Benjamin Franklin der FU Berlin. · Zentralbl Chir. · Pubmed #10544473 No free full text.
Abstract: Anorectal fistulas don't follow the same rules as idiopathic anorectal fistulas do. Their cause and treatment is completely different. Almost 40% of all patients suffering from Crohn's disease show anorectal manifestations. In 10-15% of the cases the anorectal manifestation is the first sign of Crohn's disease at all. 30% of all fistulas heal at least for a while spontaneously. The diagnostic procedures include nowadays anal endosonography and MRI as most sensitive ones and should be added for every work-up of anorectal Crohn. We differ a conservative from a radical therapy. To our opinion every therapy should be adopted to the individual needs of each patient. The most important principle in anorectal Crohn's disease is laying open of the fistula tract and excision of all the diseased tissue. This should be followed either by a drainage seton or by a definitive plastic closure of the fistula (mucosa-muscle flap). For a mucosa-muscle-flap there is only in otherwise disease-free patients and there only for high transsphincteric fistulas an indication. In our own series we treated of 69 patients 59 with a drainage seton and 10 with a mucosa-muscle flap. Recurrence occurred in 6/59 respectively 2/10 of the treated patients. Anovaginal fistulas should due to the high recurrence rate of surgically closed fistulas (> 50%) only be operated if there are serious symptoms such as recurrent vaginal infection, vaginal flatus and permanent vaginal defecations.
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Article Through the endoscope balloon dilation of ileocolonic strictures: prognostic factors, complications, and effectiveness. 2008
Hoffmann JC, Heller F, Faiss S, von Lampe B, Kroesen AJ, Wahnschaffe U, Schulzke JD, Zeitz M, Bojarski C. · Medizinische Klinik I mit Schwerpunkt Gastroenterologie, Infektiologie, Rheumatologie, Charité, Campus Benjamin Franklin, 12200 Berlin, Germany. · Int J Colorectal Dis. · Pubmed #18338175 No free full text.
Abstract: BACKGROUND/AIMS: About half of all Crohn's disease (CD) patients undergo surgery at some point, many because of strictures. An alternative possibility is to dilate strictures endoscopically. However, little is known about prognostic factors. PATIENTS AND METHODS: Thirty-two patients with primary CD (n=2), radiogenic strictures (n=1), or postoperative strictures (27 because of CD; 2 after resection because of cancer), were planned to undergo colonoscopic dilatation of which 25 patients were dilated (10 men; 15 women; median age 48). Length of stenosis, diameter of stricture, balloon size, smoking status, ulcer in the stricture, passage postdilatation, hemoglobin level, complications, redilatation, and subsequent surgery were recorded. Only patients with at least 6 months follow up were included. RESULTS: Five out of 32 patients had no stenosis, marked inflammation, or fistulas adjacent to the stricture. One patient each had a long stricture (8 cm) or a filiform stenosis ruling out dilatation [technical success, 25/27 (92.6%)]. Among these 25 patients, 39 colonoscopies with 51 dilatations were performed. After a single dilatation, 52% were asymptomatic while 48% needed another intervention, half of them surgery. Bleeding without need for transfusion occurred in 3 out of 39 colonoscopies and one perforation required surgery. Significant prognostic factors were smoking and ulcers in the stricture (P<0.05 each). Some ulcers led to intussusception requiring surgery in spite of good dilatation results. CONCLUSION: Through the endoscope balloon stricture dilatation is a relatively safe and often effective treatment modality in ileocolonic strictures. The presence of ulcers in the stricture have a worse outcome as do smokers.
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Article Changes in expression and distribution of claudin 2, 5 and 8 lead to discontinuous tight junctions and barrier dysfunction in active Crohn's disease. 2007
Zeissig S, Bürgel N, Günzel D, Richter J, Mankertz J, Wahnschaffe U, Kroesen AJ, Zeitz M, Fromm M, Schulzke JD. · Department of Gastroenterology, Charité, Campus Benjamin Franklin, Hindenburgdamm 30, 12200 Berlin, Germany. · Gut. · Pubmed #16822808 No free full text.
Abstract: BACKGROUND: Epithelial barrier function is impaired in Crohn's disease. AIM: To define the underlying cellular mechanisms with special attention to tight junctions. METHODS: Biopsy specimens from the sigmoid colon of patients with mild to moderately active or inactive Crohn's disease were studied in Ussing chambers, and barrier function was determined by impedance analysis and conductance scanning. Tight junction structure was analysed by freeze fracture electron microscopy, and tight junction proteins were investigated immunohistochemically by confocal laser scanning microscopy and quantified in immunoblots. Epithelial apoptosis was analysed in terminal deoxynucleotidyl transferase-mediated deoxyuridine triphosphate nick-end labelling and 4',6-diamidino-2-phenylindole staining. RESULTS: Patients with active Crohn's disease showed an impaired intestinal barrier function as indicated by a distinct reduction in epithelial resistance. As distribution of conductivity was even, focal epithelial lesions (eg, microerosions) did not contribute to barrier dysfunction. Instead, freeze fracture electron microscopy analysis showed reduced and discontinuous tight junction strands. Occludin and the sealing tight junction proteins claudin 5 and claudin 8 were downregulated and redistributed off the tight junction, whereas the pore-forming tight junctions protein claudin 2 was strongly upregulated, which constitute the molecular basis of tight junction changes. Other claudins were unchanged (claudins 1, 4 and 7) or not detectable in sigmoid colon (claudins 11, 12, 14, 15 and 16). Claudin 2 upregulation was less pronounced in active Crohn's disease compared with active ulcerative colitis and was inducible by tumour necrosis factor alpha. As a second source of impaired barrier function, epithelial apoptosis was distinctly increased in active Crohn's disease (mean (SD) 5.2 (0.5)% v 1.9 (0.2)% in control). By contrast, barrier function, tight junction proteins and apoptosis were unaffected in Crohn's disease in remission. CONCLUSION: Upregulation of pore-forming claudin 2 and downregulation and redistribution of sealing claudins 5 and 8 lead to altered tight junction structure and pronounced barrier dysfunction already in mild to moderately active Crohn's disease.
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Article [Continence preserving surgery in inflammatory bowel disease -- possibilities and limitations] 2002
Buhr HJ, Kroesen AJ. · Chirurgische Klinik I: Visceral- Gefäss- und Thoraxchirurgie; Universitätsklinikum Benjamin Franklin, FU Berlin. · Z Gastroenterol. · Pubmed #12467017 No free full text.
This publication has no abstract.
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Article Mucosal and invading bacteria in patients with inflammatory bowel disease compared with controls. 2002
Kleessen B, Kroesen AJ, Buhr HJ, Blaut M. · German Institute of Human Nutrition (DIFE) Potsdam-Rehbrücke, Dept of Gastrointestinal Microbiology, Bergholz-Rehbrücke. · Scand J Gastroenterol. · Pubmed #12374228 No free full text.
Abstract: BACKGROUND: Endogenous intestinal bacteria and/or specific bacterial pathogens are suspected of being involved in the pathogenesis of inflammatory bowel diseases (IBD). The aim of this study was to investigate IBD tissues for different bacterial population groups harbouring the mucosal surface and/or invading the mucosa. METHODS: Tissue sections from surgical resections from the terminal ileum and/or the colon from 24 IBD patients (12 active ulcerative colitis (UC), 12 active Crohn disease (CD)) and 14 non-IBD controls were studied by fluorescent in situ hybridization on a quantifiable basis. RESULTS: More bacteria were detected on the mucosal surface of IBD patients than on those of non-IBD controls (P < 0.05). Bacterial invasion of the mucosa was evident in 83.3% of colonic specimens from the UC patients, in 55.6% of the ileal and in 25% of the colonic specimens from the CD patients, but no bacteria were detected in the tissues of the controls. Colonic UC specimens were colonized by a variety of organisms, such as bacteria belonging to the gamma subdivision of Proteobacteria, the Enterobacteriaceae, the Bacteroides/Prevotella cluster, the Clostridium histolyticum/Clostridium lituseburense group, the Clostridium coccoides/Eubacterium rectale group, high G + C Gram-positive bacteria, or sulphate-reducing bacteria, while CD samples harboured mainly bacteria belonging to the former three groups. CONCLUSION: Pathogenic events in CD and UC may be associated with different alterations in the mucosal flora of the ileum and colon.
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