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Query: UMLS:C0009319 (colitis)
 19,384 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To investigate three possible causes of the acute hemolysis in the hemolytic-uremic syndrome, we studied prospectively 207 children and 34 adults with shigellosis in Bangladesh. Nineteen children showed acute hemolytic anemia, a leukemoid reaction, thrombocytopenia and oliguria; nine other had, in addition, a serum urea nitrogen level of over 100 mg per diciliter. Eight of the nine had pseudomembranous colitis, and six of the nine died. The frequency of bacteremia was similar in all grades of shigellosis. Circulating immune complexes were found in 10 of 20 patients with uncomplicated shigellosis and in four of six with severe hemolytic-uremic syndrome. Limulus assay for endotoxemia was positive in nine of 18 patients with hemolysis (50 per cent) and three of 61 with uncomplicated shigellosis (5 per cent) (P less than 0.001). These data support the hypothesis that severe colitis in shigellosis is associated with circulating endotoxin from the colon producing coagulopathy, renal microangiopathy and hemolytic anemia.
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PMID:Hemolytic-uremic syndrome after shigellosis. Relation to endotoxemia and circulating immune complexes. 64 73

Recent studies have shown that intrarectal administration of 2,4,6-trinitrobenzene sulfonic acid (TNBS) in ethanol or intramural injection of TNBS in saline produces an acute and possibly chronic colitis in rats. It has been assumed that interstitial TNBS initiates the inflammatory response via macrophage-mediated recognition and degradation of TNBS-modified mucosal cells and proteins. However, it is known that certain flavoproteins and/or reductants interact with compounds containing the nitro functional group to generate pro-inflammatory, nitrogen-centered free radicals and reactive oxygen metabolites. The objective of this study was to assess the ability of the rat colon, using either colon homogenates, isolated colonocytes, or intestinal interstitial fluid, to produce reactive oxygen species via enzymatic and/or nonenzymatic metabolism of TNBS. It was found that the addition of TNBS (1 mmol/L) to the 10,000 x g supernatant of rat colon homogenates increased the rate of superoxide production from normally undetectable levels to 2.6 +/- 0.23 nmol.min-1.mg protein-1. Addition of nicotinamide adenine dinucleotide, reduced form (NADH; 1 mmol/L) to colon homogenates containing TNBS significantly enhanced superoxide production to 10.4 +/- 0.9 nmol.min-1.mg-1. Similarly, addition of nicotinamide adenine dinucleotide phosphate, reduced form (NADPH; 1 mmol/L) to colon extracts containing TNBS produced an even further increase in the rate of superoxide formation to 25.2 +/- 1.1 nmol.min-1.mg-1. Addition of NADH or NADPH to the colon homogenate in the absence of TNBS produced no detectable superoxide formation, suggesting that TNBS was required for the enhanced oxidative metabolism. In a separate series of experiments, it was found that isolated colonocytes produced small but significant amounts of superoxide (3.15 +/- 0.6 nmol/2 x 10(6) cells) that were significantly increased in the presence of ethanol to 6.55 +/- 1.14 nmol/2 x 10(6) cells. Using purified preparations of two flavoproteins found in the rat colon, it was shown that the addition of TNBS (1 mmol/L) to purified NADH dehydrogenase or glutathione reductase increased the rate of superoxide formation by these enzymes from normally undetectable levels to 1.6 nmol/min and 1.2 nmol/min, respectively. In addition, it was found that intestinal interstitial fluid (lymph) initiated redox cycling of TNBS such that 28.1 +/- 1.6 nmol of oxygen was consumed per minute per milliliter of lymph. This increase in oxygen consumption was inhibited by the addition of superoxide dismutase and catalase. One possible metabolite involved in both mucosal and lymph-mediated metabolism of TNBS is ascorbic acid.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Metabolism of trinitrobenzene sulfonic acid by the rat colon produces reactive oxygen species. 164 28

A previous article (Part I) described the patient population and operative management of 666 patients who had surgery for nonruptured abdominal aortic aneurysms. This article details the perioperative complications and, by chi-square and logistic regression analysis, identifies the variables that are associated with each complication. In summarizing the results (below) the incidence of each complication is listed, along with the predictive risk factors in parentheses that have significance levels less than 0.05. Vascular morbidity data are as follows: intraoperative bleeding, 4.8%; postoperative bleeding requiring transfusion, 2.3% or repeat operation, 1.4% (large volume of blood transfusion and/or use of an autotransfusion device); intraoperative limb ischemia, 3.5%; graft thrombosis, 0.9% (femoropopliteal disease and/or distal anastomosis at the femoral level); distal thromboembolism, 3.3% (male sex, femoral popliteal disease, and/or intraoperative graft thrombosis); amputation, 1.2%; graft infection, 1 case. General morbidity data are as follows: cerebrovascular event, 0.6%; paraplegia, 1 case; cardiac event, 15.1% (age, previous episode of congestive heart failure, and/or electrocardiogram [ECG] evidence of a previous myocardial infarction); myocardial infarction, 5.2% (advancing age, angina, and/or prolonged aortic cross-clamp time); congestive heart failure, 8.9% (previous history of congestive heart failure, ECG evidence of ischemia, and/or chronic obstructive lung disease); arrhythmia requiring treatment, 10.5% (preoperative ventricular premature beats and/or respiratory failure requiring ventilation for more than 48 hours); new arrhythmia, 8.4% (angina and/or chronic obstructive lung disease); respiratory failure, 8.4% (chronic obstructive lung disease, large volume of blood transfused, and/or occurrence of postoperative bleeding, cerebrovascular accident, congestive heart failure, or myocardial infarction); renal damage with rise in creatinine or blood urea nitrogen, 5.4% and/or renal failure requiring dialysis, 0.6% (elevated preoperative creatinine, suprarenal aortic cross-clamping, and/or renal vein ligation); diarrhea without evidence of ischemia colitis, 7.1% and ischemic colitis, 0.6% (pelvic flow interrupted); prolonged ileus, 11.0% (aortoiliac occlusive disease, deterioration of renal function, prolonged ventilation, and/or preoperative history of angina); superficial wound infection, 1.5% and deep infection, 0.5% (femoral anastomosis and/or female sex); coagulopathy, 1.1% (large volume of blood transfused).(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Multicenter prospective study of nonruptured abdominal aortic aneurysm. Part II. Variables predicting morbidity and mortality. 264 60

The annual incidence of the hemolytic-uremic syndrome was determined for the well-defined population of King County, Washington, between 1971 and 1986, inclusive, to ascertain temporal trends in the epidemiology of this disease. The average annual incidence rose from 0.69 cases per 100,000 children under age 15 years between 1971 and 1975 to 1.77 cases between 1976 and 1980 and 1.74 cases between 1981 and 1986. The mean hematocrits, platelet counts, and blood urea nitrogen and creatinine concentrations on admission were similar in all periods, as were the mean length of hospital stay and the proportions of patients requiring erythrocyte and/or platelet transfusions and dialysis. These results indicate that the increased incidence of hemolytic-uremic syndrome in childhood has been sustained in King County, Washington, and that this increase is not due to ascertainment bias caused by the diagnosis of less severely ill cases. Further investigations are needed to determine whether this increased incidence is being experienced in other populations and to assess strategies for the prevention of microangiopathic sequelae to hemorrhagic colitis.
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PMID:The increasing incidence of the hemolytic-uremic syndrome in King County, Washington: lack of evidence for ascertainment bias. 291 51

The effect of a pectin-supplemented enteral diet on experimental colitis was compared with parenteral nutrition and with a pectin-free enteral diet. Forty-five rats had feeding catheters placed into either the stomach (IG, n = 31) or the superior vena cava (IV, n = 14) and then received acetic acid (colitis) or saline (control) enemas. After the enema, all rats received the same diet, either IG or IV, for 6 d except for 15 rats (IGP, 9 colitis and 6 controls), which had 1% pectin added to the diet. At the end of the feeding period the IGP group had significantly less colonic inflammation and/or necrosis than either IV (p less than 0.03) or IG (p less than 0.04) groups. Nitrogen balance, serum albumin, total iron-binding capacity and body weight did not differ significantly among dietary regimens. Thus, the degree of bowel injury in experimental colitis was decreased when animals were fed a pectin-supplemented enteral diet and this effect was independent of nutritional status.
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PMID:Comparison of parenteral nutrition and enteral feeding with pectin in experimental colitis in the rat. 312 1

36 patients with severe neurological diseases (craniocerebral trauma, cerebrovascular insufficiency, meningo-encephalitis, polyneuropathy, paraplegia, intoxication etc.) received for more than 3 months monosaccharides and polyols (Triofusin E 1000) and a 10-%-concentration of crystalline amino acids (Aminofusin L10% kohlenhydratfrei) via the parenteral route in combination with / or exclusively a nutrient-defined diet (Biosorb). Exclusive enteral nutrition was given preference if possible. Numerous laboratory parameters, as for example blood counts, "hepatic enzymes", electrolytes, trace elements, plasma proteins, lipids, urea and creatinine were determined once a week. Substitutions and secondary complications were registered in addition. Iron and plasma proteins had to be substituted most frequently. It could be proved that hypoferremia was caused by insufficient iron supply in case of exclusive/prevailing parenteral nutrition, incorrect application of the iron preparations, inflammatory complications with iron moving into the R.E.S., as well as malabsorption syndromes probably induced by bacteria. Inflammatory complications were also the major cause of protein deficiency syndromes (hypoalbuminemia). In case of relatibely often occurring diarrhea, however, it could clearly be proved that it was not induced by nutrition but was produced by a broad-spectrum antibiosis. Chronically persistent diarrhea with colitis-like colonic changes required enteral feeding with an oligopeptide diet (z.B. Peptisorb) via jejunal feeding tube. Nitrogen balances which were determined after more than 3 months of artificial nutrition formed the basis of a nutritional plan differentiated according to diagnostic groups and stages of disease.
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PMID:[Artificial nutrition in neurology--indications and problems]. 640 43

In a double blind study, 40 infants with cows' milk intolerance of various causes were randomised to receive a nutritionally complete formula in which nitrogen was supplied either as whey hydrolysate or amino acids. The median age of infants was 10 weeks (range 36 weeks' gestation to 108 weeks' postnatal age). After a median follow up period of 25 weeks there was no significant difference in dietary intake between the formulas. Twenty four weeks after entry, weight and weight for length improved equally on both formulas. Plasma albumin improved significantly on the hydrolysed whey formula but not in the amino acid group. Both milks were palatable and normal intakes of formula were maintained. Biochemical and haematological indices remained within normal limits. There was no difference in stool frequency and vomiting between the two formulas. Two infants developed a probable allergic colitis while receiving hydrolysed whey. Amino acid formula may have a role in the management of atopic infants with severe cows' milk intolerance who have already reacted to whey or casein hydrolysate formula.
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PMID:Comparison of an elemental with a hydrolysed whey formula in intolerance to cows' milk. 749 57

Ten infants with colitis due to milk protein allergy, presenting as hematochezia, whose symptoms did not resolve with the use of hydrolyzed cow-milk-based formulas, were treated with a modular lamb-meat-based formula (LOP). The patients were followed up for 3 months to 5 years. Prompt resolution of symptoms was achieved. In three patients, increased levels of creatinine and blood urea nitrogen and mild metabolic acidosis were noted, all returning to normal after the protein intake was lowered. All patients had normal growth. Seven patients were able to tolerate cow milk protein or soy at age 9-15 months. The LOP formula is well tolerated and is a safe alternative formula for infants allergic to cow milk hydrolysate formula.
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PMID:A lamb-meat-based formula for infants allergic to casein hydrolysate formulas. 890 26

Reactive oxygen and nitrogen species have been implicated in the inflammation of the gastrointestinal tract. The objective of this study was to investigate mechanisms of free radical formation from the colitis inducer 2,4,6-trinitrobenzene sulfonic acid (TNBS). We showed that TNBS was rapidly metabolized to TNBS nitro radical anion via metabolic reduction by flavinmononucleotide/NADPH, xanthine/xanthine oxidase as well as the rat small intestine and colon. TNBS nitro radical anion was directly detected with electron paramagnetic resonance (EPR) spectroscopy. EPR spectra of TNBS nitro radical anion showed hyperfine coupling constants from the proximal nitrogen, two hydrogens and the two distal nitrogens with respective magnitudes of a(N)(4) = 9.7 G; a(H)(3,5) = 3.2 G (2); and a(N)(2,6) = 0.25 G. EPR spin trapping using 5.5-dimethyl-1-pyrroline N-oxide in aerobic incubations of isolated enterocytes (or colonocytes, or red blood cells) and TNBS, in the presence or absence of NADPH, produced radical adducts characteristic of superoxide and hydroxyl radicals. Our EPR data showing generation of TNBS nitro and superoxide radical anions demonstrate that one-electron reduction of TNBS may be an initial step in the cascade of the in vivo inflammatory events in TNBS-induced colitis.
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PMID:Generation of nitro and superoxide radical anions from 2,4,6-trinitrobenzenesulfonic acid by rat gastrointestinal cells. 927 Dec 52

Reactive oxygen and nitrogen species have been implicated as mediators of mucosal injury in inflammatory bowel disease. This study investigated hydroxyl radical (.OH) generation in the inflamed colon of dextran sulfate sodium (DSS)-induced colitis by measuring the .OH-specific product of salicylate hydroxylation, 2,3-dihydroxybenzoic acid (DHB). Colitis was induced in 6-7 week old CBA/H male mice by supplementing the drinking water with 5% DSS for 7 days. On the last day of dextran exposure, mice were injected with salicylate (SAL) (100 mg/kg i.p.) 60 min before sacrifice, and mucosal homogenates were assayed for SAL and 2,3-DHB by HPLC with fluorescence and electrochemical detection. Mucosal 2,3-DHB levels in mice exposed to 5% DSS were increased by 83% (p < .005); however, SAL levels were also elevated by 182% (p < .001). This translated to a 34% decrease in the ratio 2,3-DHB:SAL in inflamed mucosa, possibly indicating greater catabolism or decreased production of 2,3-DHB. In vitro investigation of the stability of DHBs and SAL in the presence of oxidants of inflammatory lesions revealed that 2,3-DHB and 2,5-DHB were rapidly degraded by hypochlorous acid (HOCl), with initial decomposition rates of 190 and 281 nmol/min, respectively (100microM DHB with 200microM HOCl). Methionine prevented decomposition of DHBs in vitro; however, in mice with 5% DSS-induced colitis, where mucosal myeloperoxidase activity was ten-fold control levels (p < .001), administration of methionine (up to 200 mg/kg i.p.) with SAL was ineffective at increasing the ratio 2,3-DHB:SAL. SAL was also degraded in vitro by HOCl (4.7 nmol/min) resulting in the formation of new fluorescent species which may be useful as indicators of HOCl-mediated injury. Salicylate hydroxylation was unable to provide conclusive evidence supporting a role for .OH in the tissue injury of DSS-induced colitis, as metabolic disturbances in the diseased animals other than changes in .OH generation may have altered 2,3-DHB levels. This problem is relevant to any study involving the in vivo use of trapping molecules. In particular, the susceptibility of 2,3-DHB to degradation by HOCl brings into question the usefulness of salicylate hydroxylation for measurement of .OH-generation in any neutrophilic inflammatory lesion.
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PMID:Salicylate hydroxylation as an indicator of hydroxyl radical generation in dextran sulfate-induced colitis. 968 Jan 76


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