Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0740441 (acute diarrhea)
 2,275 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Clostridium difficile is well known for causing pseudomembranous colitis. Most cases are associated with the use of antimicrobial agents. Non-antibiotic associated colitis has rarely been reported. The causes of colitis are related to dietary changes, anesthesia, uremia, and various non-antibiotics medications, especially antineoplastic agents. Most responsible antineoplastics in previous reports are methotrexate and 5FU. From July 1993 to August 1994, 34 cancer patients developed acute diarrhea after chemotherapy. Six cases hd chemotherapy-associated colitis. All patients presented with moderate to severe diarrhea and demonstrable C.difficile toxin in fecal specimens and did not receive any antibiotics before the onset of diarrhea. Premier enzyme immunoassay (EIA) was used for toxin A assay because it is easy to perform and needs no special tissue culture laboratory facility. Data from multicenters studies have shown good sensitivity and specificity of the test. We found documented antineoplastics associated colitis, 7 episodes from 35 episodes of diarrhea (20.0%) that had been tested with EIA for toxin A. Five of 6 episodes were 5FU related. One patient had 2 episodes of antineoplastic associated colitis with the same chemotherapy regimen. The underlying malignancies were GI malignancies in 3 of 6 patients. In conclusion, moderate to severe diarrhea in cancer patients after chemotherapy should alert the physician to be aware of a potential fatal complication caused by C.difficile infection. True incidence has been undoubtedly masked by concomitant antimicrobial treatment and physician unawareness. Early recognition, discontinuation of chemotherapy and prompt treatment should be done to reduce morbidity and mortality of this disease.
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PMID:Antineoplastic-associated colitis in Chulalongkorn University Hospital. 756 66

Zinc has been recognized as an antioxidant with potential for chronic and acute effects. Oxidative damage produced by free radicals, including nitric oxide (NO), is responsible for certain types of intestinal malabsorption syndromes and diarrhea. Under physiologic or mildly stimulatory conditions for NO synthesis, the small intestine characteristically is in a proabsorptive state; however, an excessive production of NO triggers formation of cyclic nucleotides, which cause secretion and malabsorption. In this study, we hypothesized that low-molecular-weight, soluble zinc chelates could modulate the effects of induced NO excess on the small intestine. In vitro experiments demonstrated that zinc-citrate or zinc-histidine at > or =0.66 mM, as well as a known NO scavenger, 2-[carboxyphenyl]-4,4,4,4-tetramethylimidazoline-1-oxyl-3-oxide, at 2 microM, were effective at removing chemically generated NO. In vivo jejunal perfusions, conducted in healthy rats under anesthesia, showed that c-PTIO reduced the proabsorptive effects produced by 1 mM L-arginine, the precursor of NO. In a standard oral rehydration solution, 1 mM zinc-citrate partially reversed the antiabsorptive effects on potassium caused by an excess of NO generated from 20 mM L-arginine but did not alter sodium or water absorption. The data are consistent with the view that soluble zinc compounds incorporated into an oral rehydration solution may deserve further attention as a means to scavenge NO with fluids used for the treatment of chronic or acute diarrhea, especially in malnourished children who are often zinc deficient.
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PMID:Zinc as a potential enteroprotector in oral rehydration solutions: its role in nitric oxide metabolism. 1259 91