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)

Pathologic increases in intestinal permeability to hydrophilic macromolecules has been identified in a number of clinical conditions. The significance of gut barrier dysfunction as a clinical issue remains to be delineated, although it seems likely that alterations in intestinal epithelial permeability play a causative role in a number of conditions ranging from inflammatory bowel disease to the development of complications after cardiopulmonary bypass. It is unlikely that any one mechanism can account for all cases of intestinal hyperpermeability. Rather, it is more probable that myriad factors or combinations of factors, including mesenteric ischemia and cytokine-induced phenomena, lead to alterations in permeability in different clinical entities. Nevertheless, from a purely mechanistic standpoint, some common themes, notably the role of ATP depletion, increases in [Ca2+]i, and cytoskeletal derangements in enterocytes, have emerged as being particularly important.
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PMID:Intestinal epithelial hyperpermeability. Mechanisms and relevance to disease. 965 18

Oxidative stress appears to play a role in the pathogenesis of a number of gastrointestinal disease states, including pancreatitis; gastric and duodenal ulcer disease; IBD; gastric, esophageal, and colon cancers; and hepatic injury secondary to alcohol, metal storage disorders, hepatitis, and ischemia/reperfusion injury. The nutritional antioxidants are attractive potential therapeutic and chemopreventive agents because they are inexpensive and have a relatively low toxicity profile. A word of caution should be noted: Some antioxidants, such as vitamin C, can be prooxidant under certain conditions, and systemically altering the redox state may have untoward effects on the inflammatory response in certain disease states. Thus, at the current time, antioxidant therapy should be restricted to randomized, controlled clinical trials, in which treatment effects can be closely monitored, and therapeutic efficacy can be determined with scientific accuracy.
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PMID:Nutrient antioxidants in gastrointestinal diseases. 965 24

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

Colon perforation can be caused by a variety of entities, including iatrogenic trauma, tumors, ischemia, inflammatory bowel disease, and steroid use. Parasitic infection rarely leads to colon perforation. Secondary peritonitis results from mixed microorganism infection, including enterococci, enteric bacilli, and anaerobes. A combination of an optimal antibiotic regimen and surgical intervention is of paramount importance. Nevertheless, intra-abdominal infections usually have a high mortality rate. Schistosomiasis occurs worldwide. S. japonicum infection is endemic in Asia. The most common complications of gastrointestinal schistosomiasis are periportal fibrosis, intestinal polyposis, and bowel stricture. Rarely, schistosomiasis results in colon perforation. The diagnosis of schistosome infections is based on ova in stool or tissue specimens, and/or immunologic diagnostic tests. The most effective anti-schistosomiasis agent is praziquantel. Herein, we describe an unusual case of colon perforation associated with Schistosoma japonicum infection, which resulted in severe peritonitis and led to the patient's death.
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PMID:Schistosoma japonicum infection presenting with colon perforation: case report. 1069 21

The loss of small intestinal mucosal surface area is a relatively common clinical situation seen in both the pediatric and adult population. The most frequent causes include mesenteric ischemia, trauma, inflammatory bowel disease, necrotizing enterocolitis, and volvulus. Following surgical resection, the remnant intestine compensates or adapts to the loss of native bowel by increasing its absorptive surface area and functional capacity. Unfortunately, many patients fail to adapt adequately, and are relegated to lifelong intravenous nutrition. Research into intestinal adaptation following small bowel resection (SBR) has evolved only recently from the gross and microscopic level to the biochemical and genetic level. As understanding of this process has increased, numerous therapeutic strategies to augment adaptation have been proposed. Epidermal growth factor (EGF) is an endogenous peptide that is secreted into the gastrointestinal tract and able to influence gut ontogeny, as well as mucosal healing. Early studies have demonstrated its ability to augment the adaptive process. Focusing on a murine model of massive intestinal loss, the morphological, structural, biochemical, and genetic changes that occur during the intestinal adaptive process will be reviewed. The role of EGF and its receptor as critical mediators of the adaptive process will be discussed. Additionally, the ability of EGF to augment intestinal proliferation and diminish programmed cell death (apoptosis) following SBR will be examined. Enhancing adaptation in a controlled manner may allow patients to transition off parenteral nutrition to enteral feeding and, thereby, normalize their lifestyle.
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PMID:Epidermal growth factor is critical for intestinal adaptation following small bowel resection. 1105 64

Oxidation of biological membranes has been suggested as a major pathological process in a variety of disease states including intestinal ischemia and inflammatory bowel disease. Previous studies on the small intestinal brush border membrane have shown that part of the decrease in the activity of the Na(+)-dependent glucose transporter (SGLT1) observed after oxidation could be secondary to the derangement in membrane fluidity that accompanied oxidative damage. The present study examined the relationship between oxidative-induced hemileaflet fluidity alterations and the resultant change in Na(+)-dependent glucose transport activity. To address this issue, in vitro oxidation of guinea pig brush border membrane vesicles was induced by incubation of the vesicles with ferrous sulfate and ascorbate. We found that oxidation decreased the fluidity of both the outer and inner hemileaflets, the decrease being greater in the outer leaflet. Moreover, the preferential alteration in hemileaflet fluidity was accompanied by a decrease in glucose transport. However, when membrane perturbing agents such as hexanol and A(2)C were used to restore membrane fluidity to levels comparable to controls, rates of glucose transport could not be interpreted in terms of variation of bulk membrane fluidity or variation in fluidity of any specific membrane leaflet. On the basis of these experiments, we propose that previous studies that reported coincidental alteration in membrane fluidity and glucose transport cannot be interpreted on the basis of bulk fluidity or hemileaflet fluidity.
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PMID:Oxidative and drug-induced alterations in brush border membrane hemileaflet fluidity, functional consequences for glucose transport. 1134 71

Multi-detector row computed tomography (CT) offers important advantages over more conventional imaging methods in the evaluation of the mesenteric vasculature. It allows faster scanning, which practically eliminates motion and breathing artifacts, as well as thinner collimation. These advances, coupled with rapid intravenous administration of contrast material, allow excellent opacification of the mesenteric arteries and veins. This improves the quality of the three-dimensional (3D) data sets, which in turn leads to improved 3D vascular maps and more accurate assessment of various conditions such as arterial or venous encasement in patients with pancreatic cancer, mesenteric ischemia, or inflammatory bowel disease. Three-dimensional multi-detector row CT also allows better visualization of arterial and venous branching, thereby improving detection of more distal vascular involvement. In addition, 3D multi-detector row CT may help detect hemodynamic changes in patients with active inflammation and hyperemia of a bowel segment because it can be used to measure bowel wall enhancement over time. Carcinoid tumors that have infiltrated the mesentery have a characteristic CT appearance, and other conditions such as lymphoma or sclerosing mesenteritis can also manifest as an infiltrating mass that envelops mesenteric vessels. Three-dimensional multi-detector row CT represents a significant advance in CT technology and can help ensure prompt, accurate evaluation of the mesenteric vasculature.
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PMID:Volume-rendered 3D CT of the mesenteric vasculature: normal anatomy, anatomic variants, and pathologic conditions. 1179 5

Distinctive arthritic patterns, some of which may parallel or even precede intestinal disease activity, are seen in inflammatory bowel disease. Some spondyloarthropathies are associated with transient ileocolic inflammation. Vasculitis frequently affects the gastrointestinal tract, predominantly manifesting with abdominal pain. In severe cases, intestinal ischemia and perforation may occur. Various arthritides are thought to be associated with other gastrointestinal diseases, such as celiac disease and hepatitis. The association between intestinal disease and arthritis is still being investigated. Interactions between the inflammatory intestinal cells and inflamed synovial cells have been demonstrated. Certain intestinal bacteria such as Klebsiella pneumoniae are suspected to play a role as triggers for the development of arthropathies. Genetic factors, especially human leukocyte antigen associations, are also being increasingly investigated for better characterization of the types of arthritis and possible prognostic implications. Various therapies, including nonsteroidal anti-inflammatory drugs, used to treat rheumatologic diseases have the potential to cause gastrointestinal complications.
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PMID:Gastrointestinal issues in children with rheumatologic disease. 1242 59

During inflammatory bowel disease and intestinal ischemia, epithelial cells of the gut mucosa produce various inflammatory mediators, including the chemokine interleukin (IL-8). This IL-8 produced by intestinal epithelial cells has recently been implicated as a contributory factor to the deleterious inflammatory process resulting in colitis during inflammatory bowel disease or multiple organ failure following shock and trauma. Recent evidence suggests that the transcription factor nuclear factor kappaB (NF-kappaB) is a central regulator of IL-8 gene expression. In the present paper we investigated the effect of pharmacological inhibition of NF-kappaB with pyrrolidinedithiocarbamate (PDTC) on IL-1beta-induced IL-8 production by the human intestinal epithelial cell line HT-29. Pretreatment of cells with PDTC (3-1000 microM) dose-dependently attenuated IL-8 production. Furthermore, PDTC (100 microM) suppressed the accumulation of IL-8 mRNA. PDTC inhibited the activation of NF-kappaB, because PDTC suppressed both NF-kappaB DNA binding and NF-kappaB-dependent transcriptional activity. Taken together, our data demonstrate that NF-kappaB inhibition with PDTC decreases IL-8 production by intestinal epithelial cells.
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PMID:Pyrrolidinedithiocarbamate inhibits NF-kappaB activation and IL-8 production in intestinal epithelial cells. 1250 95

New-onset idiopathic inflammatory bowel disease (IBD) is not uncommon among the elderly, although more common are colonic infection, ischemia, or neoplasia, all of which may mimic IBD. Although the clinical presentation of IBD in the elderly often resembles that of younger subjects, atypical manifestations are common and may lead to difficulty in diagnosis. Much progress has been made in both medical and surgical therapy for IBD, but such therapy poses additional challenges in the elderly, who are more likely to experience adverse effects of medications or complications of surgery. The elderly generally have a favorable outcome to both medical and surgical therapy for IBD. Although concern about possible untoward effects of therapy is warranted, treatment should not be withheld because of fear of complications.
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PMID:Inflammatory Bowel Disease After Age 60. 1274 21


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