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

Whole colon perfusion studies and measurements of luminal prostaglandin E2 were carried out in a 41-year-old female with collagenous colitis to investigate pathophysiological mechanisms for the diarrhea. Biopsies of the colorectal mucosa had revealed a continuous 25- to 60-micron subepithelial collagenous layer, but normal junctional complexes and capillaries. When the patient fasted, the diarrhea persisted and fecal electrolytes, as estimated from the concentration of sodium, potassium, and their anions, accounted for all the osmolality (284 mosm/kg) of stool water, the pH of which was above 8.0. The lumen-negative electrical potential difference in the rectum was -64 mV vs -45 +/- 2 mV (mean +/- SEM) in healthy controls. Profuse secretion of fluid and electrolytes occurred during colonic perfusion with saline. Transport of sodium appeared to be passive with flux ratios equal to those predicted for passive sodium movements, while chloride transport against a steep electrical gradient indicated active secretion. Perfusion with an "ileal output"-like solution decreased fluid and electrolyte secretion, suggesting that bicarbonate, in addition to chloride, may be a major determinant of secretion rates. Since immunoreactive prostaglandin E2 levels following in vivo equilibrium dialysis of feces ranged from 555 to 650 pg/ml vs 55 to 235 pg/ml (99% confidence limits) in healthy controls, it is speculated that prostaglandins synthesized locally in response to mucosal hypoxia might be the mediators of anion secretion.
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PMID:Colonic transport of water and electrolytes in a patient with secretory diarrhea due to collagenous colitis. 658 Oct 38

Five cases of Campylobacter fetus bacteremia are reported. This germ, found in blood cultures, induces high fever and is accompanied by either gastroenteritis with colitis or thrombophlebitis. Other, but much rarer septic sites are the meninges and endocardium. Patients already debilitated by chronic disease are more susceptible to bacteremia with Campylobacter fetus, which worsens the prognosis of the infection. Although non-debilitated patients can contract this infection, the prognosis here is more favourable. Antibiotic treatment is indicated in all cases. Campylobacter fetus bacteremias are rare and their pathogenesis still little understood. This "microaerophil" germ does not survive in air which makes culturing difficult under ordinary conditions. On the other hand, Campylobacter jejuni induces gastrocolitis with spontaneous recovery. It is found in feces and thrives in contaminated water and milk.
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PMID:[Campylobacter fetus bacteremia]. 683 51

Anaerobic bacteria constitute more than 90% of the bacteria in the colon. An anaerobic environment is needed to maintain their growth and the production of short-chain fatty acids by these bacteria from carbohydrates. Short-chain fatty acids are rapidly absorbed and essential for metabolic as well as functional welfare of the colonic mucosa. The importance of these acids in water absorption and in the patogenesis of colitis is discussed in relation to the concept of "energy deficiency diseases" of the colonic mucosa.
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PMID:Anaerobic bacteria, the colon and colitis. 692 66

Many antibiotics, particularly the lincomycins, may cause diarrhoea with or without enterocolitis. The pathogenesis of antibiotic-associated diarrhoea without colitis is uncertain; colloidosmotic water binding in the colon by endogenous glycoproteins undegraded by colonic bacteria is considered. Antibiotic-associated enterocolitis is now known to be due to toxin-producing clostridia, proven for Cl. difficile. Improved methods for the detection of toxin and clostridia are presently being studied. Endoscopically, pseudomembranes are characteristic but not antibiotic-specific, they may be absent or missed diagnostically. A possible role of asymptomatic clostridia-carriers in enterocolitis clustering remains to be determined. The potentially lethal course of the disease requires rapid diagnosis and therapy, with discontinuation of the antibiotic, intensive supportive measures and, at least in severe disease, oral vancomycin.
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PMID:[Antibiotic-associated diarrhoea and enterocolitis (author's transl)]. 699 76

We report four patients with bloody diarrhea and colitis from Campylobacter fetus subspecies jejuni. Two patients had dogs with Campylobacter fetus in their stools. All patients responded rapidly and completely to erythromycin therapy. Campylobacter fetus subspecies jejuni is now a relatively common cause of enterocolitis, more common than salmonella or shigella. When the organism causes short-lived water diarrhea, a definitive diagnosis is not necessary. In a patient with bloody diarrhea and acute colitis, the clinician should pursue Campylobacter fetus as a potential offender, recognizing that acute colitis from Campylobacter fetus is clinically and and pathologically indistinguishable from any other acute colitis.
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PMID:Campylobacter enterocolitis. 724 Jun 91

A case of thermal burn and stricture of the colon following colostomy irrigation with hot water is described. The initial radiographic features on barium enema simulated nonspecific segmental colitis. Colonic stricture and enterolith formation developed subsequently. This case emphasizes that care should be taken in preparing irrigating and barium enema solutions.
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PMID:Thermal injury of the colon due to colostomy irrigation. 730 96

Severe intracellular potassium depletion was found with maldigestion (short bowel, high output fistula, M. Crohn, colitis ulcerativa) when total body potassium and water measurement were taken. Serum potassium levels were misleading. These methods are of particular value in planning and conducting a preoperative infusion therapy to correct the documented deficit.
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PMID:[Assessment of total body potassium and water for therapeutic control of maldigestion syndromes (author's transl)]. 738 86

A case study is presented of a 47-year old, white female with a 1-year progressive history of diarrhea up to 20 liquid stools per day, accompanied by an 18-pound weight loss. She had presented with previous workup of gastroscopy revealing two stomach ulcers; colonoscopy revealing nonspecific colitis and one polyp that was subsequently removed and found to be benign; and a negative abdominal ultrasound. She was Helicobacter pylori negative and HIV negative. Her stools had been negative for blood, ova and parasites, and culture. She had been using well water from a new well for 2 years. String test was negative for Giardia. She had no diarrhea during a day of fasting. Carbon 14 D-xylose breath test was positive. She was discharged on a 14-day course of 500 mg. Augmentin (amoxicillin 500 mg. with clavulanate potassium 125 mg.) by mouth every 8 hours. Seven weeks later, she was having four to five formed stools per day and had gained 16 pounds.
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PMID:Bacterial overgrowth in a patient with chronic diarrhea. 750 17

The objective of this study was to assess the role that nitric oxide (NO) may play in mediating the colonic inflammation observed in a model of chronic granulomatous colitis using two pharmacologically different inhibitors of nitric oxide synthase (NOS). The NOS inhibitors NG-nitro-L-arginine methyl ester (L-NAME; 15 mumol/kg/day) and aminoguanidine (AG; 15 mumol/kg/day) were administered to rats in their drinking water, beginning 3 days before the induction of colitis and continuing for the entire 3-week period. We found that chronic NOS inhibition by L-NAME or AG significantly attenuated the peptidoglycan/polysacchride (PG/PS)-induced increases in macroscopic colonic inflammation scores and colonic MPO activity. Only AG, and not L-NAME, attenuated the PG/PS-induced increases in colon dry weight. Both L-NAME and AG significantly attenuated the PG/PS-induced increases in spleen inflammation, whereas neither drug significantly attenuated the PG/PS-induced liver inflammation. Although both L-NAME and AG inhibited NO production in vivo, as measured by decreases in plasma nitrite and nitrate levels, only AG was found to attenuate these values significantly (38 +/- 3 vs. 83 +/- 8 microM, respectively; P < .05). Finally, administration of L-NAME, but not of AG, significantly increased mean arterial pressure from 83 mm Hg in colitic animals to 105 mm Hg in the PG/PS+L-NAME-treated animals (P < .05). We conclude that NO may play an important role in mediating some of the pathophysiology associated with this model of chronic granulomatous colitis.
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PMID:Effects of nitric oxide synthase inhibition on the pathophysiology observed in a model of chronic granulomatous colitis. 752 37

We investigated the involvement of nitric oxide in trinitrobenzene-sulfonic acid (TNB) colitis. Every 24 h after TNB, rats were orally dosed with NG-nitro-L-arginine methyl ester (L-NAME; 30 mg/kg), NG-nitro-D-arginine methyl ester (D-NAME), or water, and food intake, body weight, and plasma nitrite levels were measured. On day 6, colonic nitric oxide synthase and myeloperoxidase (MPO) activity, histology, intestinal muscle growth, NADPH-diaphorase, and myenteric nerve function were assessed. Food intake and body weight were reduced during the first 72 h of colitis. On day 6 post-TNB, a fourfold increase in mucosal nitric oxide synthase, a 30-fold increase in MPO, and a fivefold elevation in plasma nitrite were measured. Smooth muscle hyperplasia and hypertrophy in both colonic muscle layers, numerous diaphorase-positive macrophages in the myenteric plexus, and a suppression of myenteric nerve function were also observed. Unlike D-NAME, oral L-NAME reduced MPO and intestinal muscle hyperplasia by > 90%. Likewise, plasma nitrite and colonic nitric oxide synthase were reduced by > 70%. L-NAME completely prevented macrophage infiltration into the muscle. Conversely, it had no effect on anorexia or intestinal smooth muscle hypertrophy, nor did it affect suppressed myenteric nerve neurotransmitter release. These results demonstrate the selective transmural protective effects of L-NAME in the inflamed colon, implicating nitric oxide as a mediator.
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PMID:The selective beneficial effects of nitric oxide inhibition in experimental colitis. 753 57


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