Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0022116 (ischemia)
 91,303 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To clarify the mode of action of aminosalicylates, which are generally used as therapeutic agents for ulcerative colitis, we investigated the effect of some of the aminosalicylates on lipid peroxidation in the large intestinal mucosa after mesenteric ischemia/reperfusion in the rat. Lipid peroxidation was assessed by measuring the level of thiobarbituric-acid-reactive substances. It was found that aminosalicylates dose-dependently inhibited the elevation of the level of thiobarbituric-acid-reactive substances in the large intestinal mucosa after ischemia/reperfusion. This effect may partly contribute to the therapeutic actions of aminosalicylates in ulcerative colitis.
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PMID:Inhibition by aminosalicylates of lipid peroxidation in large intestinal mucosa after mesenteric ischemia/reperfusion in the rat. 941 34

Microcirculation and molecular biology are the hottest topics in modern surgical research. In familial adenomatous polyposis the incidence of carcinoma can be assessed by the localisation of the PAC-gene mutation. Restorative proctocolectomy with ileoanal pouch represents the procedure of choice. The optimal age for the operation varies between 20 and 35 years according to the localisation of the mutation. RT-PCR directed to recently defined surface antigens allows for the sensitive detection of intraoperative tumor cell liberation. Due to tumor cell detection in the systemic circulation the perioperative administration of monoclonal antibodies must be advocated. A preciser definition of lymphogenic tumor spread underlines the importance of systematic lymphadenectomy in resection of the colon. The understanding of microcirculatory disorders has optimized surgical decision-making intra- and perioperatively: function of renal and hepatic microcirculation is a reliable parameter to predict graft quality already intraoperatively and to monitor therapeutic approaches to ischemia/reperfusion injury. Results in the therapy of acute pancreatitis could be improved by operating less and later. Analysis of pancreatic microcirculation resulted in an improvement of ICU-therapy in the early stages of the disease. Transplantation of the liver is limited to hepatocellular carcinoma when its localisation or the residual hepatic function after resection preclude curative excision. In addition liver transplantation should not be carried out in tumors larger than 5 cm or in patients with more than 3 tumor nodules. Liver resection for colorectal metastases is a standard procedure. A second resection of recurrent metastases is advocated since an identical median survival can be achieved compared to the primary resection (32 mo). The surgical treatment of non-colorectal liver metastases is under evaluation and should be restricted to oncological centers. Special aspects of backwashileitis in ulcerative colitis will be outlined concerning timing of colectomy, pouch construction, and follow-up.
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PMID:[State of the art: gastroenterologic surgery]. 1006 3

A staging classification is proposed by CT findings in 27 patients with acute abdomen, caused by inflammatory colonic non-parasitic pathology. Of the 17 patients with diverticular disease, 4 were stage A (edema/ischemia on thickness of the abdominal wall), 2 were stage B (partial intramural infarction on the abdominal wall) and 3 were stage C (abscess/peritonitis and obstruction/vascular strangulation). None of the patients in the series were stage D (ischemia/infarction of the colonic wall with dilatation). Of the 4 patients with ulcerative colitis, 3 were stage A and 1 in stage C. Of the 3 patients with Crohn's disease, 2 were stage A and 1 was in stage C. Classified as stage D were 1 pseudomembranous colitis, 1 volvulus and 1 idiopathic megacolon. Clinical severity was in parallel with CT stages that gave better information on the progression of the pathology. Staging by CT in acute abdomen caused by inflammatory colonic non-parasitic pathology could be useful in therapeutics.
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PMID:Acute abdomen caused by inflammatory colonic non-parasitic pathology: staging by CT. 1042 Oct 16

The concordance rate of monozygotic twins showed that the occurrence of ulcerative colitis required both internal and environmental conditions. Genetic studies revealed that IBD1 locus on chromosome 16 and IBD2 locus on chromosome 12 showed highly suspicious susceptibility for inflammatory bowel disease. The other possible internal factors include antineutrophil cytoplasmic antibodies and mucin abnormality. Many environmental factors have been reported to cause relapse. These are viral and bacterial infection, medicine such as antibiotics, non-steroidal anti-inflammatory drugs and aminosalicylates, colonic ischemia, post-examination state, psychological stress, winter season, travel and overwork.
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PMID:[Influencing factors on occurrence and relapse in ulcerative colitis]. 1057 4

Monosaccaride transporter proteins are responsible for transmembrane transport of monosaccarides into cells. Glucose transporter protein 1 (Glut-1) is most prevalent in the cell membranes of erythrocytes and facilitates transport of glucose in tissues with barrier functions, i.e. blood brain barrier. Expression of Glut-1 in malignant tumors is increased due to increased metabolic need of the proliferating cell populations. In colorectal adenomas and carcinomas, membranous expression of Glut-1 has been associated with higher grade of tumors and decreased survival time. We studied the expression of Glut-1 in dysplastic proliferations of the colon which included sporadic adenomas and dysplasia associated lesions (DALM) in patients with ulcerative colitis and reactive/regenerative proliferations of the colon, including non-dysplastic chronic colitis, acute colitis and ischemia. Two patterns of Glut-1 expression were detected. Most adenomas and DALMs showed at least focal membranous expression of Glut-1. In addition a second staining pattern was recognized which consisted of prominent supranuclear dots. This pattern of staining was not only seen in adenomas and DALM but also in non-dysplastic areas immediately surrounding sporadic adenomas, in regenerative chronic colitis and in areas surrounding acute inflammation. Areas away from dysplasia did not show any positive staining for Glut-1. We conclude that two distinct patterns of Glut-1 expression may be found in colonic epithelial proliferation: membranous staining, associated with dysplasia, and, heretofore not described, supranuclear staining which may be related to Glut-1 expression secondary to expression of specific growth factors and not necessarily related to dysplasia.
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PMID:Glut-1 expression in dysplastic and regenerative lesions of the colon. 1135 Dec 74

Nitration of tyrosine residues in proteins has been observed in many inflammatory tissues of arthritis, ulcerative colitis, septic shock and ischemia-reperfusion injury. Although several studies have been carried out, it is still unclear what type of protein is nitrated and whether tyrosine nitration interferes with protein function. Peroxisome proliferator-activated receptor gamma (PPARgamma) is a nuclear receptor whose activation is linked to several physiological pathways including regulation of insulin sensitivity and control of inflammation. PPARgamma possesses several tyrosine residues, which might be potential targets for nitration by peroxynitrite during inflammatory responses. Here we have investigated whether PPARgamma is nitrated in macrophage-like RAW 264 cells and the effect of nitration on the translocation of PPARgamma into the nucleus. Western blot analysis showed that tumor necrosis factor-alpha, lipopolysaccharide or peroxynitrite treatment significantly increases the nitration of PPARgamma. Cell fractionation analysis and immunofluorescence coupled with confocal laser microscopy revealed that nitration of PPARgamma inhibits its ligand-dependent translocation from the cytosol into the nucleus. Together, these results indicate that nitration of PPARgamma during inflammation may be involved in a reduction in the control of inflammatory responses and also in the development of resistance to PPARgamma ligand-based therapies against inflammation.
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PMID:Nitration of PPARgamma inhibits ligand-dependent translocation into the nucleus in a macrophage-like cell line, RAW 264. 1216 59

Within a framework of dual involvement of mucosa and submucosa on the one hand, and of the muscularis propria of the bowel wall on the other, it might be valid to consider involvement of the vascular supply as the essential means in itself of not only causing the morphologic lesions in inflammatory bowel disease, but also especially in accounting for persisting patterns of inflammatory response both in ulcerative colitis and in Crohn's disease. Inflammatory bowel disease as a group constitutes a spectrum of biologic and pathobiologic manifestations in terms not only of inflammatory involvement of the bowel wall but also in terms of how the bowel in its turn deals with inflammation as a pathologic lesion in its own right. Parameters of inflammatory bowel activity transcend simple concepts of etiology and pathogenesis as applicable to category disorders such as infections or bowel ischemia. Indeed, the strictly characterized initiation of the inflammatory bowel response as a function of defective regulation of the antigenicity of the luminal contents on the one hand, and on interactions between nitric oxide and free oxygen radicals on the other, might help determine a persistence of tissue damage in inflammatory bowel disease that is either relapsing/remitting or chronic in progression. In a final analysis, perhaps, there might be involved a single central form of pathway induction of dysregulated immune reactivity arising from an early disturbance in activation patterns as induced by the onset of luminal antigenicity at an early or specific-stage, further characterized perhaps by specific forms of intestinal epithelial defects of the bowel mucosa in patients subsequently developing inflammatory bowel disease. Specific genetic markers for disease susceptibility and for therapeutic responsiveness are particularly of interest. The Nucleotide binding oligomerization Domain 2 (NOD2) would recognize microbial lipopolysaccharide or else mark systemic responses to pathogens that are pathogenic to evolving inflammatory bowel disease.
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PMID:A primary dysregulation in the immunoregulatory role of the intestinal mucosal epithelial cell in inflammatory bowel disease pathogenesis? Biology of inflammatory response as tissue pattern entities in Crohn's versus ulcerative colitis. 1499 Mar 86

The ileal pouch anal anastomosis (IPAA) procedure has become the preferred surgical option for most patients with ulcerative colitis who require surgical removal of the colorectum. The vast majority of patients with this new anatomy will either not develop pouchitis or develop a few discrete episodes of acute pouchitis. However approximately one fourth of patients will develop recurrent pouchitis, with 5% being categorized as chronic pouchitis requiring maintenance therapy or, on rare occasion, pouch excision. Factors that are associated with an increased risk of pouchitis include primary sclerosing cholangitis, extraintestinal manifestations, and nonsmokers. Controversy surrounds other risk factors such as extent of colitis, backwash ileitis, preoperative pANCA levels, and carrying a specific allele for IL-1 receptor antagonist. The etiology of pouchitis is unknown, but theories range from genetic susceptibility, bacterial overgrowth, ischemia, and fecal stasis, to a recurrence of ulcerative colitis in the pouch, a missed diagnosis of Crohn's disease, or possibly a novel third form of inflammatory bowel disease. Some patients with symptoms of pouchitis will not have inflammation of the pouch, but rather, irritable pouch syndrome. Thus, endoscopic investigation with biopsy is important for declaring whether a patient has pouchitis. Indeed, the more commonly used scores, such as the pouch disease activity index, incorporate both endoscopic and histologic criteria. Not surprisingly, treatment options for patients with pouchitis resemble that of regular inflammatory bowel disease, although there have only been a few controlled trials. Antibiotics are the mainstay of therapy, with metronidazole and ciprofloxacin demonstrating benefit in controlled trials. Probiotics are effective for maintaining remission of pouchitis. Mesalamine, corticosteroids, and immunomodulators have been used with some success. Occasionally, patients with well-documented ulcerative colitis as the indication for IPAA will develop what appears to be Crohn's disease of the pouch, on the basis of granulomatous inflammation, pre-pouch ileitis, or fistulae. The treatment is similar to Crohn's disease, including the use of infliximab. Dysplasia within the pouch mucosa itself is quite rare. Reports of dysplasia occurring in patients with IPAA are usually due to neoplastic change within the residual cuff of rectal or transition zone mucosa just below the pouch, rather than in the ileal mucosa of the pouch. With further elucidation of the genetic basis for inflammatory bowel disease, we should be able to more accurately classify patients with ulcerative colitis and Crohn's disease genotypically. Hopefully, this will also bring more clarity to the heterogeneous population of patients with pouchitis and allow for more focused therapeutic strategies.
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PMID:The diagnosis and treatment of pouchitis in inflammatory bowel disease. 1511 32

Proctitis refers to inflammation of the rectum, a diagnosis made by endoscopic evaluation. Symptoms of proctitis include rectal bleeding, urgency, tenesmus, diarrhea or constipation, and occasionally rectal pain. The causes of proctitis include infection, medication, ischemia, radiation, and ulcerative proctitis. Ulcerative proctitis is an important and increasingly common subcategory of ulcerative colitis (UC) in which inflammation is limited to the rectum. Historically, oral aminosalicylates have been the mainstay of acute and maintenance therapy. A growing body of data, however, indicates that topical aminosalicylates are effective first line agents in ulcerative proctitis and distal UC. Topical aminosalicylates act more effectively and rapidly to induce and maintain remission compared with their oral counterparts or topical steroids. Rarely ulcerative proctitis is refractory to topical therapy and in these instances systemic corticosteroids, antibiotics, immunomodulators, or surgery is required. This review highlights the pathogenesis, diagnosis, and treatment of ulcerative proctitis.
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PMID:Diagnosis and treatment of ulcerative proctitis. 1536 96

We report on a 33-year-old women with ulcerative colitis, who presented with inspiratory thoracic pain due to perimyocarditis. Furthermore, postprandial abdominal pain associated with diarrhea and different blood pressure values on both arms were recorded. Computed tomography revealed embolism of the pulmonal arteries and angiography demonstrated stenoses of the subclavian and renal arteries and the celiac trunc suggesting the diagnosis of Takayasu's arteritis. A coronary or infectious etiology could be excluded. Since a coincidence of Takayasu's arteritis and ulcerative colitis has been reported in the literature, abdominal pain and diarrhea can either be explained by the inflammatory bowel disease or by chronic ischemia due to intestinal vasculitis. Differential diagnosis will be facilitated by the future course of the disease.
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PMID:[33-year old patient with thoraco-abdominal pain and differences of blood pressure]. 1537 64


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