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)

A total of 512 colectomy and endoscopic biopsy specimens were reviewed to define the prevalence and possibly the significance of dystrophic goblet cells (DGCs) in neoplastic and nonneoplastic colonic diseases. As compared with an incidence of 1% in disease-free specimens, DGCs were observed in 38% of cases of inflammatory bowel disease, 23% of colonic malignancies, 30% of nonneoplastic polyps, 22% of adenomas, and 8% of cases showing acute self-limited colitis. In contrast, no dystrophic cells were seen in a group of miscellaneous diseases including diverticulitis, diverticulosis, abscesses, fistulas, ischemia, pseudomembranous colitis, melanosis coli, amyloidosis, shock, and mechanical trauma. Although dystrophic cells occur in association with dysplasia and carcinoma, their presence in nonpremalignant lesions, including acute self-limited colitis, raises doubt as to their diagnostic significance. Histochemical studies of the mucin composition in DGCs were unrevealing, failing to show any differences between DGCs and their morphologically normal counterparts in the same region of the colon.
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PMID:The incidence and carbohydrate histochemistry of dystrophic goblet cells in colon. 323 12

Fiberoptic colonoscopy is 25 years old this year. Improvement in instruments led rapidly to wide acceptance of colonoscopy in diagnosis and therapy of colorectal diseases. The diagnosis of benign and malignant neoplasms was revolutionized by colonoscopy. The differential diagnosis of inflammatory bowel disease, assessment of its extent and severity, response to treatment, and potential for development of cancer are all made easier by colonoscopy. Colonoscopy has improved the diagnosis of diverticular disease, rectal bleeding, identification of ischemia, and other problems. Therapeutic colonoscopy has radically changed the management of colonic polyps, and colonoscopic polypectomy is now the standard form of treatment for most of these lesions. Treatment of bleeding lesions, decompression of obstruction, and removal of foreign bodies are other examples of therapeutic colonoscopic procedures.
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PMID:Conceptual developments through colonoscopy. 324 46

The hospital and office records of 86 patients who underwent proctectomy for cancer of inflammatory bowel disease with primary closure of the perineal wound were reviewed. Almost one fourth of all patients suffered a significant perineal wound complication, the majority of which were infections. The incidence of postoperative perineal wound complications was comparable in both groups of patients. Urinary retention occurred in 24 percent of patients who underwent abdominoperineal resection or rectal cancer, and half of these patients required transurethral resection which indicates the need for more thorough preoperative assessment of bladder function, especially in older men. The development of leg ischemia that resulted in amputation in two elderly patients who had preoperative evidence of obstructive peripheral vascular disease suggests that a synchronous two-team abdominoperineal resection with the patient in the modified lithotomy position for a prolonged period should be avoided. One third of all patients were discharged less than 10 days after surgery and two thirds within 2 weeks. Prolonged stays were more frequent in cancer patients and appeared to be related to age rather than to the development of postoperative complications. The perineal wound after abdominoperineal resection for cancer healed more rapidly and more completely than did the wound after proctectomy for inflammatory bowel disease. Fourteen percent of the inflammatory bowel disease patients did not have a healed wound 1 year after surgery. The extent of rectal cancer as determined by Duke's classification played no role in healing of the perineal wound, but women with rectal cancer healed at a slower rate than did men. The location of the exit site for wound catheters and the use of cautery and preoperative steroid therapy appeared too have no effect on the healing of the perineal wound.
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PMID:Factors influencing perineal wound healing after proctectomy. 684 90

Amyloidosis not infrequently involves the gastrointestinal tract and may result in a variety of symptoms, including those related to impaired motility, malabsorption, and ulceration due to ischemia. This report describes the case of a 74-year-old man with systemic amyloidosis secondary to multiple myeloma, with striking gross morphologic findings involving the colon, seen at autopsy, resembling severe inflammatory bowel disease. Microscopically, the small arterioles of the lamina propria were markedly narrowed or occluded by massive deposition of amyloid, presumably leading to diffuse ischemia and mucosal necrosis. Although the radiologic appearance of this condition has been well recognized, and ischemia due to amyloidosis has been described, this case is presented to demonstrate the gross anatomic changes not illustrated in previous reviews of the subject.
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PMID:Amyloid colitis. 712 79

The records of 81 patients with colitis whose symptoms began after the age of 50 years were analyzed to determine the importance of ischemia as a cause of colitis in this age group and to evaluate the accuracy of previous diagnoses. Patients were classified by clinical, roentgenological and pathologic criteria. A retrospective diagnosis of ischemic colitis was made in three-fourths of the patients, one-half of whom had original discharge diagnoses of ulcerative, Crohn's or nonspecific colitis. This study supports our belief that ischemia is the most common cause of colitis beginning in patients older than 50 years of age. Moreover, the incorrect diagnosis of idiopathic inflammatory bowel disease in a large proportion of these patients may explain why colitis has been reported to behave differently in the elderly than in the young.
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PMID:Colitis in the elderly. A reappraisal. 731 20

Nitric oxide (NO.) plays a central role in the physiology of the gastrointestinal tract and its response to critical illness. Potential sources of NO. in the gut include: intrinsic intestinal tissue (mast cells, epithelium, smooth muscle, neural plexus), resident and/or infiltrating leukocytes (neutrophils, monocytes), reduction of luminal gastric nitrate, and denitrification by commensal anaerobes. The brain and endothelial isoforms of nitric oxide synthase are expressed under resting conditions, whereas inflammatory stimuli are required for the induction of the inducible type. Under resting conditions, mucosal perfusion is regulated by NO. derived from the vascular endothelium of the mesenteric bed. During inflammation, excessive NO. production from the inducible synthase may contribute to mucosal hyperemia. Coordination of peristalsis and sphincteric action is mediated by the release of NO., which acts as the principal neurotransmitter of the nonadrenergic, noncholinergic enteric nervous system. Alterations in bowel motility, such as ileus, result from excessive concentrations of NO. generated during endotoxicosis and inflammatory bowel disease. The role of NO. in the regulation of salt and water secretion is poorly understood. Endotoxin-induced inhibition of gastric acid secretion appears to be mediated by the action of NO. on parietal cells. NO. may protect the gastrointestinal mucosa from a variety of stimuli (caustic ingestion, ischemia, ischemia/reperfusion injury, early endotoxic shock) by maintaining mucosal perfusion, inhibiting neutrophil adhesion to mesenteric endothelium, blocking platelet adhesion, and preventing mast cell activation. Excessive NO., however, may directly injure the mucosa. Barrier function of the intestinal mucosa is protected by NO. in the early stages of injury, when neutrophil adhesion, ischemia, and mast cell activation are relevant. Inhibition of NO. synthesis ameliorates barrier dysfunction during more advanced stages of inflammation, when activation of inducible NOS yields toxic concentrations of NO.. At high concentrations, NO. disrupts the actin cytoskeleton, inhibits ATP formation, dilates cellular tight junctions, and produces a hyperpermeable state. Selective inhibition of the inducible isoform of NOS and maintenance of the constitutive types may be therapeutic.
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PMID:Nitric oxide in the gut. 758 76

Nitric oxide (NO.) plays a central role in the Physioliology of the gastrointestinal tract and its response to critical illness. Potential sources of NO. in the gut include: intrinsic intestinal tissue (mast cells, epithelium, smooth muscle, neural plexus), resident and/or infiltrating leukocytes (neutrophils, monocytes), reduction of luminal gastric nitrate, and denitrification by commensal anaerobes. The brain and endothelial isoforms of nitric oxide synthase are expressed under resting conditions, whereas inflammatory stimuli are required for the induction of the inducible type. Under resting conditions, mucosal perfusion is regulated by NO. derived from the vascular endothelium of the mesenteric bed. During inflammation, excessive NO. production from the inducible synthase may contribute to mucosal hyperemia. Coordination of peristalsis and sphincteric action is mediated by the release of NO., which acts as the principal neurotransmitter of the nonadrenergic, noncholinergic enteric nervous system. Alterations in bowel motility, such as ileus, result from excessive concentrations of NO. generated during endotoxicosis and inflammatory bowel disease. The role of NO. in the regulation of salt and water secretion is poorly understood. Endotoxin-induced inhibition of gastric acid secretion appears to be mediated by the action of NO. on parietal cells. NO. may protect the gastrointestinal mucosa from a variety of stimuli (caustic ingestion, ischemia, ischemia/reperfusion injury, early endotoxic shock) by maintaining mucosal perfusion, inhibiting neutrophil adhesion to mesenteric endothelium, blocking platelet adhesion, and preventing mast cell activation. Excessive NO., however, may directly injure the mucosa. Barrier function of the intestinal mucosa is protected by NO. in the early stages of injury, when neutrophil adhesion, ischemia, and mast cell activation are relevant. Inhibition of NO. synthesis ameliorates barrier dysfunction during more advanced stages of inflammation, when activation of inducible NOS yields toxic concentrations of NO.. At high concentrations, NO. disrupts the actin cytoskeleton, inhibits ATP formation, dilates cellular tight junctions, and produces a hyperpermeable state. Selective inhibition of the inducible isoform of NOS and maintenance of the constitutive types may be therapeutic.
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PMID:Nitric oxide in the gut. 770 93

Reactive oxygen metabolites are implicated in gastrointestinal disease and enterocyte injury associated with ischemia-reperfusion, bacterial translocation, inflammatory bowel disease, and necrotizing enterocolitis. The ileal-like, human colon carcinoma cell line, Caco-2, was used to investigate oxidative damage. After challenging Caco-2 cells with reactive oxygen metabolites, the permeability, viability, and energy charge of Caco-2 cells were assessed. Permeability was determined by transepithelial electrical potential and flux of small molecules. Viability was determined by release of 51Cr. Cell energy was evaluated by determining adenylate energy charge. The source of reactive oxygen metabolites, with the exception of menadione, did not affect viability of Caco-2 cells; cell permeability was increased. The increased varied with the source and location of the reactive oxygen metabolite. There was no change in energy charge. This study suggests that reactive oxygen metabolites could cause enterocyte damage and that the source of the reactive oxygen metabolite is an important variable in determining the extent of damage. Antioxidants might prevent injury.
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PMID:Polarized Caco-2 cells. Effect of reactive oxygen metabolites on enterocyte barrier function. 789 34

Eicosanoids were discovered as "prostaglandins" in the mid-1930s. The discovery that eicosanoids were ubiquitous in mammalian cells and that nonsteroidal anti-inflammatory drugs worked by inhibiting enzymes that synthesized these chemicals heralded their extensive investigation in all fields of biology. Precursor fatty acids (arachidonic acids) are stored in cell phospholipids, acted on by two enzymes (cyclooxygenase and lipooxygenase) that yield prostaglandins, thromboxane, prostacyclin, and leukotrienes. Knowledge of their biochemical processes continue to unfold, but it is now believed that eicosanoids are part of a larger group of agents termed phospholipid mediators. Eicosanoids are intimately involved with cardiovascular function as well as central and peripheral vascular disease processes and ischemia. In the gastrointestinal tract, these potent lipids not only participate in many normal functions (eg, acid secretion and motility) but also in disease states (eg, inflammatory bowel disease and peptic ulcer disease). In shocklike states of sepsis and/or endotoxemia, eicosanoids have assumed a major role in many events that occur. Recently, discoveries have demonstrated that platelet-activating and tumor necrosis factors exert their effects in part through eicosanoids. The future will demonstrate these compounds to be critical not only in intracellular (molecular) events but also in the effects they produce that are far from the source of origin.
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PMID:Eicosanoids. Critical agents in the physiological process and cellular injury. 823 81

The patient with acute abdominal pain presents the attending physician with a wide and varied gamut of diagnostic possibilities. Prompt and accurate diagnosis is essential for the proper care and management of these acutely ill patients. Diagnostic radiology is often an integral part of the emergent evaluation of these patients. This article focuses on some of the key plain-film findings in the patients suffering from acute abdominal pain of intestinal causes and reviews the radiologic evaluation of several major abdominal conditions such as acute appendicitis, diverticulitis, inflammatory bowel disease, bowel ischemia, and infarction.
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PMID:The radiologic evaluation of acute abdominal pain of intestinal origin. A clinical approach. 837 22


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