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• W2077304479 endingPage "2028" @default.
• W2077304479 startingPage "2019" @default.
• W2077304479 abstract "S ecretory diarrhea is a common symptom associated with inflammation of the intestinal mucosa, regardless of the factor(s) responsible for initiation of the inflammation.* Reactive metabolites of oxygen and nitrogen, through oxidation and free radical reactions, are believed to contribute to the diarrhea by acting as secretagogues. 2 The purpose of this report is to succinctly review the evidence in support of the probability that highly reactive oxygenand nitrogen-containing molecules produced in the inflamed intestinal mucosa contribute to secretory diarrhea. Patients with ulcerative colitis can have fecal excretion weights of 234 to as much as 1500 g/day, 3-5 thus exceeding values that define diarrhea clinically. Harris and Shields 6 and Head et al. v reported that the colon of patients with proctocolitis and Crohn's disease, respectively, absorbed water and electrolytes at a reduced rate compared with healthy subjects. Similar findings were noted by other investigators in studies in vivo *-n and in vitro. 12'13 Impaired fluid absorption in the jejunum occurs in patients with ulcerative colitis, .4 and the coIonic mucosa from infants with colitis secretes NaC1 when studied in vitro. ~5 It is not possible from studies in patients with inflammatory bowel disease (IBD) to define with certainty the cause of the intraluminal fluid accumulation. There is little compelling evidence from human studies that active electrolyte secretion, rather than inhibition of absorption in the small bowel or colon, causes the diarrhea.16 The apparent reduction of sodium absorption may be due to electrolyte movement from the blood to the lumen. Studies in vivo, using 22Na and 36C1 or other suitable radiolabeled solutes, have not been performed in patients to confirm a mechanism of serosal-to-mucosal transport (i.e., active secretion). Activation of a secretory flux has been inferred, mostly from in vitro short-circuit current studies in which inflammatory mediators evoke secretion in normal mucosa. ~7'~8 However, in inflamed mucosa, the secretory response is less vigorous than in healthy tissue. 19 Thus, additional factors, such as increased mucosal permeability 2a6'2°-23 and interference with Na+,K+-adenosine triphosphatase and epithelial cell absorptive processes, 24 probably contribute to luminal fluid accumulation in IBD. As for potential secretagogues, a plethora of candidates is possible, including neuropeptides, 25 kinins, 26 C5a, 27'28 platelet activating factor, 29 biogenic amines, cytokines, eicosanoids, and reactive metabolites of oxygen and nitrogen. ~8'3°'31 Other inflammatory conditions of the gut are also associated with secretory diarrhea. For example, patients with food allergy often present with diarrhea, presumed to be primarily caused by intestinal secretion. 3° The mucosal response is associated with an eosinophilic enteritis. 3°'32 Rodent models have been developed based on immediate hypersensitivity reactions. 33 On challenge, sensitized animals show a mucosal inflammatory response characterized by increased permeability, 34 inhibition of electrolyte absorption, or stimulation of secretion. 3°'35-3v It is unlikely that a single mediator is responsible for these effects. There are a variety of factors associated with induction of an immune response by the intestinal mucosa. Most obvious among these are enteric infections. Salmonella, Shigella, and Escherichia coli (O157:H7) infections are especially associated with mucosal inflammation and secretory diarrhea. 38 E. coil O157:H7 reduces sodium absorption and stimulates secretion of chloride ions in the distal colon of rabbits, and these effects are related to infiltration of the tissue by neutrophils. 39 The parasite Trichinella spiralis also initiates an inflammatory response in the mucosa, which has been well characterized and serves as a model for investigating immune-mediated intestinal secretion in rats. 37 In rabbits infected with Yersinia entercolitica, inhibition of short-chain fatty acid absorption due to reduced Na + uptake (Na+/H + exchange) was sug-" @default.
• W2077304479 created "2016-06-24" @default.
• W2077304479 creator A5002619544 @default.
• W2077304479 creator A5005759765 @default.
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• W2077304479 date "1995-12-01" @default.
• W2077304479 modified "2023-09-29" @default.
• W2077304479 title "Reactive oxygen and nitrogen metabolites as mediators of secretory diarrhea" @default.
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