Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Mycophenolate mofetil, an immunosuppressive agent, is frequently used following bone marrow and solid organ transplantation. Diarrhea is a commonly seen side effect of mycophenolate mofetil, which may necessitate colonic biopsy in some patients. The histologic changes found in this setting have been reported to mimic self-limited colitis, graft-vs-host disease or inflammatory bowel disease in isolated case reports, and could pose diagnostic and management difficulties. The goal of this study is to define the spectrum of histologic changes in colonic biopsies associated with mycophenolate mofetil usage. All solid organ transplant patients who received mycophenolate mofetil and underwent colonic biopsy for gastrointestinal symptoms from 1999 to 2007 were included in the study. Patients who did not receive mycophenolate mofetil were used as controls. Various histologic features including architectural distortion, apoptosis, inflammatory infiltrate, Paneth cell metaplasia and mucin depletion were subjectively evaluated and scored (scale: 0-3) by two independent reviewers in a blinded fashion. Forty solid organ transplant patients underwent colonic biopsy for gastrointestinal symptoms during the study period. Biopsies from 69% of patients on mycophenolate mofetil showed histologic changes. Apoptosis (41%) and architectural distortion (66%) were seen more frequently in patients receiving mycophenolate mofetil as compared to the control group (13%). The histologic changes in patients receiving mycophenolate mofetil were categorized as normal/near normal (31%), inflammatory bowel disease-like (28%), graft-vs-host disease-like (19%), ischemia-like (3%) and self-limited colitis-like (16%) changes. Of the controls, only one patient showed a graft-vs-host disease-like histologic pattern. In conclusion, histologic changes are frequently associated with mycophenolate mofetil use and can resemble self-limited colitis, graft-vs-host disease and inflammatory bowel disease leading to diagnostic difficulties. Increased awareness of the histologic spectrum of mycophenolate mofetil-induced changes is required by the pathologist to avoid diagnostic errors.
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PMID:Spectrum of histologic changes in colonic biopsies in patients treated with mycophenolate mofetil. 1932 37

Reflectance spectroscopy is an emerging technology which provides rapid and safe evaluation of tissue for dysplasia and ischemia. The probe-based devices can be passed through most endoscopes. Current applications include detection of dysplasia in Barrett's esophagus, colitis, and colon polyps.
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PMID:Fluorescence and Raman spectroscopy. 1942 20

Reflectance spectroscopy is an emerging technology which provides rapid and safe evaluation of tissue for dysplasia and ischemia. The probe-based devices can be passed through most endoscopes. Current applications include detection of dysplasia in Barrett's esophagus, colitis, and colon polyps.
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PMID:Reflectance spectroscopy. 1942 21

A(2B) adenosine receptors are increasingly recognized as important orchestrators of inflammation. A(2B) receptor activation promotes the inflammatory response of mast cells, epithelial cells, smooth muscle cells and fibroblasts, thereby contributing to the pathophysiology of asthma and colitis. A(2B) receptor stimulation limits endothelial cell inflammatory responses and permeability and suppresses macrophage activation thereby preventing tissue injury after episodes of hypoxia and ischemia. A(2B) receptor stimulation also promotes the production of angiogenic cytokines by endothelial cells, mast cells and dendritic cells, aiding granuloma tissue formation and inflammatory resolution, but can also contribute to tumor growth. A(2B) receptors are, thus, potentially important pharmacological targets in treating immune system dysfunction and inflammation.
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PMID:A(2B) adenosine receptors in immunity and inflammation. 1942 67

By its antioxidant effect, molecular hydrogen gas (H2) was reported to protect organs from tissue damage induced by ischemia reperfusion. To evaluate its anti-inflammatory effects, we established a mouse model of human inflammatory bowel disease (IBD) by supplying mice with water containing (1) dextran sodium sulfate (DSS) (5%), (2) DSS (5%) and H2, or (3) H2 only ad libitum up to 7 days. At day-7, DSS-induced pathogenic outcomes including, loss of body weight, increase of colitis score, pathogenic shortening of colon length, elevated level of IL-12, TNF-alpha and IL-1beta in colon lesion, were significantly suppressed by the addition of H2 to DSS solution. Histological analysis also revealed that the DSS-mediated colonic tissue destruction accompanied by macrophage infiltration was remarkably suppressed by H2. Therefore, the present study indicated that H2 can prevent the development of DSS-induced colitis in mice.
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PMID:Hydrogen mediates suppression of colon inflammation induced by dextran sodium sulfate. 1948 90

Colonic ulcerations can affect the entire colon and rectum, and have variable clinical presentation according to the anatomic location and underlying pathology. Diverse causes may lead to colonic ulceration, such as inflammatory bowel diseases, oral drugs (mostly nonsteroidal anti-inflammatory drugs), local or diffuse ischemia, and different intestinal microorganisms. An ulcer may also herald a concealed malignant disease. In most cases, colonic ulcerate is associated with diffuse colitis in the acute setup or with inflammatory bowel diseases, and to the lesser extent the ulceration is defined as solitary. This article focuses on two of the less commonly diagnosed diseases: solitary rectal ulcer syndrome and stercoral ulceration, both related to local tissue ischemia and often seen in the elderly population.
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PMID:Solitary rectal ulcer syndrome and stercoral ulcers. 1969 13

Extracellular adenosine functions as an endogenous distress signal via activation of four distinct adenosine receptors (A1, A2A, A2B and A3). Conditions of limited oxygen availability or acute inflammation lead to elevated levels of extracellular adenosine and enhanced signaling events. This relates to a combination of four mechanisms: i) increased production of adenosine via extracellular phosphohydrolysis of precursor molecules (particularly ATP and ADP); ii) increased expression and signaling via hypoxia-induced adenosine receptors, particularly the A2B adenosine receptor; iii) attenuated uptake from the extracellular towards the intracellular compartment; and iv) attenuated intracellular metabolism. Due to their large surface area, mucosal organs are particularly prone to hypoxia and ischemia associated inflammation. Therefore, it is not surprising that adenosine production and signaling plays a central role in attenuating tissue inflammation and injury during intestinal ischemia or inflammation. In fact, recent studies combining pharmacological and genetic approaches demonstrated that adenosine signaling via the A2B adenosine receptor dampens mucosal inflammation and tissue injury during intestinal ischemia or experimental colitis. This review outlines basic principles of extracellular adenosine production, signaling, uptake and metabolism. In addition, we discuss the role of this pathway in dampening hypoxia-elicited inflammation, specifically in the setting of intestinal ischemia and inflammation.
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PMID:Targeting the A2B adenosine receptor during gastrointestinal ischemia and inflammation. 1976 45

Lower gastrointestinal bleeding (LGIB) can present as an acute and life-threatening event or as chronic bleeding, which might manifest as iron-deficiency anemia, fecal occult blood or intermittent scant hematochezia. Bleeding from the small bowel has been shown to be a distinct entity, and LGIB is defined as bleeding from a colonic source. Acute bleeding from the colon is usually less dramatic than upper gastrointestinal hemorrhage and is self-limiting in most cases. Several factors might contribute to increased mortality, a severe course of bleeding and recurrent bleeding, including advanced age, comorbidity, intestinal ischemia, bleeding as a result of a separate process, and hemodynamic instability. Diverticula, angiodysplasias, neoplasms, colitis, ischemia, anorectal disorders and postpolypectomy bleeding are the most common causes of LGIB. Volume resuscitation should take place concurrently upon initial patient assessment. Colonoscopy is the diagnostic and therapeutic procedure of choice, for acute and chronic bleeding. Angiography is used if colonoscopy fails or cannot be performed. The use of radioisotope scans is reserved for cases of unexplained intermittent bleeding, when other methods have failed to detect the source. Embolization or modern endoscopy techniques, such as injection therapy, thermocoagulation and mechanical devices, effectively promote hemostasis. Surgery is the final approach for severe bleeding.
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PMID:Diagnosis and management of lower gastrointestinal bleeding. 1988 16

Ischemic colitis is the most common form of gastrointestinal ischemia. Patients present with either occlusive or nonocclusive vascular disease, although the latter is more common. Many causes of nonocclusive disease have been identified, but the exact pathophysiology remains unclear. Most commonly, patients develop abdominal discomfort and bloody diarrhea. Diagnosis is confirmed with colonoscopy. Treatment is contingent on the severity of disease: mucosal/nongangrenous ischemia requires only supportive measures and medical management, whereas transmural/gangrenous ischemia may require prompt surgical intervention. Ischemic colitis can also become a chronic process with persistent segmental colitis or colonic stricturing. The patient's outcome depends on the severity of disease, prompt recognition, and appropriate treatment.
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PMID:Ischemic colitis. 2001 55

The Digestive Disease Week 2010 conference, held in New Orleans, included topics covering new therapeutic developments in the field of gastroenterology, hepatology, endoscopy and gastrointestinal surgery. This conference report highlights selected presentations on the apolipoprotein E-mimetic peptide COG-112 (Cognosci Inc) for the potential treatment of Citrobacter rodentium-induced colitis; the inhibition of sphingosine kinase with ABC-294640 (Apogee Biotechnology Corp) to alleviate stress after hepatic ischemia-reperfusion injury; TLR4 targeting with NI-0101 (NovImmune SA) to prevent colitis-associated cancer; immunization against TNF with TNFalpha kinoid (Neovacs SA) for the treatment of patients with Crohn's disease; and preclinical studies with the anti-inflammatory agent minnelide (University of Minnesota) for the treatment of pancreatic cancer.
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PMID:Digestive Disease Week 2010. Turning Science into Medicine--part 2. 2058 61


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