Disease relevance of Enterocolitis, Pseudomembranous

• Toxin A, an enterotoxin from Clostridium difficile, mediates pseudomembranous colitis in humans [1].
• Used of clindamycin was nearing a level similar to that of cephalosporin use until 1975, when its risk of precipitating severe colitis, including pseudomembranous colitis, became well-known [2].
• These observations indicate that IFN-gamma is the crucial mediator of toxin A-induced acute enteritis and suggest that IFN-gamma is an important molecular target for the control of C. difficile-associated pseudomembranous colitis [3].
• Adverse events included neutropenia (TMP-SMX: two; placebo: three), pseudomembranous colitis (TMP-SMX: one), severe skin rash (TMP-SMX: two; placebo: one), and drug fever (TMP-SMX: one) [4].
• Clindamycin-induced enterocolitis in hamsters as a model of pseudomembranous colitis in patients [5].

High impact information on Enterocolitis, Pseudomembranous

• Pseudomembranous colitis associated with single-dose cephalosporin prophylaxis [6].
• Intermittent therapy with metronidazole for relapse of pseudomembranous colitis [7].
• Pseudomembranous colitis. A fatal case following prophylactic cephaloridine therapy [8].
• Pseudomembranous enterocolitis resulting from therapy with antibiotics such as clindamycin and lincomycin hydrochloride monohydrate does not always respond to drug and vigorous medical support [9].
• Gallium citrate Ga 67 accumulation in pseudomembranous colitis [10].

Chemical compound and disease context of Enterocolitis, Pseudomembranous

• Two patients with diarrhea and pseudomembranous colitis associated with lincomycin hydrochloride monohydrate and clindamycin phosphate therapy were treated with cholestyramine resin, with prompt remission of symptoms [11].
• Cephalosporin-associated pseudomembranous colitis [12].
• Pseudomembranous colitis associated with ciprofloxacin [13].
• In view of its low cost, bacitracin is a reasonable first-line alternative to vancomycin in the treatment of antibiotic-associated colitis [14].
• Clarithromycin and pseudomembranous enterocolitis [15].

Biological context of Enterocolitis, Pseudomembranous

• An increased serum creatinine level was observed in 0.8 percent of ceftazidime-treated patients, an increased blood urea nitrogen level in 1.6 percent, hepatic abnormalities in approximately 6 percent, diarrhea in 1.3 percent, pseudomembranous colitis in 0.12 percent, increased prothrombin time in 0.5 percent, and clinical bleeding in none [16].
• Apart from the retinoids, which can be associated with the risk of embryotoxicity/teratogenicity, and clindamycin, which might cause pseudomembranous colitis, information on the systemic pharmacokinetics of other topical agents is not readily available [17].
• In addition, the results obtained here indicate that C. difficile toxins are a useful tool for researching the regulation of the Rho family protein-mediated PLD activation and also provide a clue toward understanding the pathogenic background of pseudomembranous colitis from the viewpoint of signal transduction [18].
• TcdB from Clostridium difficile glucosylates small GTPases (Rho, Rac, and Cdc42) and is an important virulence factor in the human disease pseudomembranous colitis [19].

Anatomical context of Enterocolitis, Pseudomembranous

• BACKGROUND & AIMS: Antibiotic-associated pseudomembranous colitis in humans is caused by proliferation of Clostridium difficile, which elaborates an enterotoxin toxin A that causes epithelial damage and altered motility in rabbit small intestine [20].
• His course was complicated by central line infection, jugular and subclavian vein thrombosis, pseudomembranous colitis, recurrent bacteremia, cholestasis on total parenteral nutrition and cytomegalovirus infection [21].
• Trimethoprim-sulfamethoxazole, pseudomembranous colitis, and spinal cord injury [22].

Gene context of Enterocolitis, Pseudomembranous

• The Clostridium difficile toxA and toxB genes, encoding cytotoxic and enterotoxic proteins responsible for antibiotic-associated colitis and pseudomembranous colitis, were shown to be transcribed both from gene-specific promoters and from promoters of upstream genes [23].
• Anion-exchange resins in pseudomembranous colitis [24].
• Clostridium difficile toxin B (269 kDa), which is one of the causative agents of antibiotic-associated diarrhea and pseudomembranous colitis, inactivates Rho GTPases by glucosylation [25].
• The Premier Clostridium difficile toxin A enzyme immunoassay (PTA EIA) (Meridian Diagnostics, Inc., Cincinnati, Ohio) for rapid diagnosis of antibiotic-associated colitis (AAC) was evaluated in a multicenter study [26].
• To determine if SP plays a role in the pathogenesis of human pseudomembranous colitis, SP receptor distribution was examined in a toxin A-positive specimen of bowel [27].

Analytical, diagnostic and therapeutic context of Enterocolitis, Pseudomembranous

• Numerous antibiotics are associated with pseudomembranous colitis; ampicillin is associated with hemorrhagic colitis; chemotherapy is associated with neutropenic colitis; and deferoxamine is associated with Yersinia enterocolitis [28].
• We describe a 25-year-old male with juvenile onset diabetes mellitus who developed severe pseudomembranous enterocolitis with intractable diarrhea for which he was maintained on total parenteral nutrition [29].
• An existing intensive drug monitoring system was used to study the occurrence of pseudomembranous colitis and diarrhoea in 100 patients treated with lincomycin and clindamycin [30].
• Two patients on antibiotic prophylaxis with cephradine after orthopaedic implant surgery developed pseudomembranous colitis [31].

References