bromochloroacetic-acid and Peptic-Ulcer-Perforation

bromochloroacetic-acid has been researched along with Peptic-Ulcer-Perforation* in 2 studies

Reviews

1 review(s) available for bromochloroacetic-acid and Peptic-Ulcer-Perforation

ArticleYear
Liver penetration by a duodenal ulcer in a young woman.
    Journal of clinical gastroenterology, 2001, Volume: 33, Issue:1

    Liver penetration is a rare but serious complication of peptic ulcer disease. We report a case of a 33-year-old woman who took large doses of nonsteroidal antiinflammatory drugs and developed a giant duodenal ulcer that penetrated into her liver. The diagnosis was based on histologic examination of endoscopic biopsies. She was initially treated with a proton pump inhibitor, but, within 5 weeks, she developed a symptomatic postbulbar stricture that required surgical correction. We also review 11 other reported cases of endoscopically and histologically diagnosed peptic ulcer penetration into the liver.

    Topics: Adult; Anti-Inflammatory Agents, Non-Steroidal; Chemical and Drug Induced Liver Injury; Diclofenac; Duodenal Ulcer; Duodenoscopy; Duodenum; Female; Humans; Immunoenzyme Techniques; Intervertebral Disc Displacement; Keratins; Liver; Liver Diseases; Liver Function Tests; Peptic Ulcer Hemorrhage; Peptic Ulcer Perforation

2001

Other Studies

1 other study(ies) available for bromochloroacetic-acid and Peptic-Ulcer-Perforation

ArticleYear
Cytokeratin-positive subserosal myofibroblasts in gastroduodenal ulcer; another type of myofibroblasts.
    Histology and histopathology, 2006, Volume: 21, Issue:7

    To investigate the distribution and origin of alpha-smooth muscle actin (ASMA)-positive stromal cells in the perforation of human gastroduodenal ulcers. Perforative lesions of 24 surgically resected gastroduodenal ulcers were examined immunohistochemically for ASMA, HCD, CD34, CD31, CAM5.2 and HMW-CK, and double staining of ASMA and CAM5.2 was also performed. In addition, to determine the cell source of collagen, in situ hybridization of collagen I mRNA was performed. In the normal gastroduodenal wall, the reticular network of CD34-positive stromal cells was identified in the muscularis mucosa, submucosa, muscular propria, and subserosa. In the subepithelial area, many myofibroblasts were observed, whereas no CD34-positive stromal cells were seen. In areas neighboring ulcerative lesions, no CD34-positive stromal cells were observed, but a significant number of myofibroblasts were present there. In the deep layer of ulceration, numerous fusiform or stellate stromal cells strongly positive for ASMA and CAM5.2 were observed in the subserosal area around the perforation. In the same site, many cells co-expressing ASMA and CAM5.2 were identified by double staining. In contrast, in the surface layer of ulceration, stromal cells expressing only ASMA were observed. The cytokeratin-positive subserosal myofibroblastic cell in human gastroduodenal ulcer is a novel type of myofibroblast.

    Topics: Actins; Antigens, CD34; Biomarkers; Collagen Type I; Fibroblasts; Humans; Immunoenzyme Techniques; In Situ Hybridization; Keratins; Myocytes, Smooth Muscle; Peptic Ulcer; Peptic Ulcer Perforation; RNA, Messenger; Serous Membrane; Stromal Cells

2006