Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011991 (diarrhea)
 57,543 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

We report the development of ulcerative colitis (UC) and Crohn's disease (CD) Health Status Scales that improve on existing inflammatory bowel disease (IBD) activity measures by their added association with health status. We surveyed 991 members of the Crohn's and Colitis Foundation of America (CCFA) and analyzed the half with greater disease activity (114 UC, 330 CD, ostomies excluded). Our analysis strategy involved (a) identification of items that discriminated active from inactive disease, (b) factor analysis to reduce the items to clusters sharing common symptom relationships, and (c) regression analysis to select those variables best associated with a composite measure of health status (health care use, daily function, psychologic distress). The factor analyses yielded two indexes for UC and CD: "Diarrhea," and "Other GI symptoms" (Cronbach's alpha 0.59-0.84). The regression analyses for both diseases showed that poorer well-being, the Diarrhea index, and dependence on medication for pain were associated with poorer health status. For UC, lower educational attainment and lower steroid dose, and for CD, the Other GI symptoms index and eye disease, also correlated with poorer health status. By design, the UC and CD Scales are better predictors of health status than the survey version of the CD Activity Index (CDAI), explaining 17 and 21% more of the variance of the health status measure. The final UC and CD Health Status Scales can be used in research and clinical care. They contain symptom items used to assess disease activity and also correlate with health status. Prospective assessment is needed to confirm their accuracy in assessing prognosis and treatment response.
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PMID:Ulcerative colitis and Crohn's disease health status scales for research and clinical practice. 140 20

Extracolonic manifestations of inflammatory bowel disease are common and diverse. Cardiac complications, however, are rare and of these pericarditis is the most frequently described association. A 57 year old man with a 20 year history of ulcerative colitis presented with a four day history of retrosternal chest pain and exertional dyspnoea. Electrocardiogram showed Wenckebach atrioventricular block. Three days later he developed bloody diarrhoea and sigmoidoscopy showed active proctocolitis. He was treated with oral prednisolone after which the chest pain and diarrhoea settled within 48 hours. At outpatient review two weeks later he was completely well and the electrocardiogram had returned to normal.
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PMID:Ulcerative colitis complicated by Wenckebach atrioventricular block. 144 75

In the presence of halides, granulocytes generate hypochlorous acid and, subsequently, chlorinated amines (chloramines). These lipophilic, potent reactive oxygen metabolites may contribute to the mucosal pathophysiology associated with inflammatory bowel disease. A common symptom of inflammatory bowel disease is mucosal secretion of fluid and electrolytes, leading to diarrhea. Because acetylcholine (Ach) can stimulate colonic fluid secretion, we determined the effect of monochloramine (NH2Cl) on Ach release by mucosal/submucosal nerves. Mucosa from the rat colon was separated from outer muscle layers and minced before incubation with [14C]choline to label stores of Ach in cholinergic neurons. Release of [14C]Ach was evoked with NH2Cl in the absence and presence of 5-aminosalicylic acid, glutathione, nordihydroguaiarectic acid or the cyclooxygenase inhibitor piroxicam. NH2Cl produced concentration-related increases in [14C] Ach release into the medium; greater than 100% over base line was observed at 0.5 mM. Glutathione inhibited the NH2Cl-evoked release in a concentration-dependent fashion. Release induced by 0.1 mM NH2Cl was abolished by 5-aminosalicylic acid and significantly inhibited by nordihydroguaiarectic acid. Piroxicam also prevented the effect of NH2Cl on release of [14C] Ach. None of these agents alone had any effect on base line [14C]Ach release. Tetrodotoxin (5 microM) did not significantly inhibit the NH2Cl-evoked transmitter release. We conclude that NH2Cl, at concentrations believed to exist in inflamed tissue, causes the release of Ach from mucosal/submucosal nerves primarily through nonspecific neural membrane injury. Endogenous prostaglandins, possibly liberated as a consequence of the injury, may be involved in the Ach release process.
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PMID:Oxidant-evoked release of acetylcholine from enteric neurons of the rat colon. 146 20

Crohn's disease is a rare cause of gastrocolic and duodenocolic fistulas. Only 83 examples (27 gastric, 52 duodenal, four both) have been described. Weight loss, abdominal pain, and diarrhea are common features but fail to distinguish a fistula from active inflammatory bowel disease. Fecal vomiting is pathognomic but is present in one third of gastrocolic and only 2% of duodenocolic fistulas. Diagnosis is most readily made by contrast radiography, with barium enema being more sensitive than barium meal. Although several gastrocolic fistulas have been successfully treated with long-term 6-mercaptopurine, surgery is the mainstay of therapy. An isolated duodenocolic fistula should not be regarded as the primary indication for operation because most are asymptomatic. Ileocolonic resection with simple gastric or duodenal repair is safe and effective in most cases. An ileocolonic anastomosis should be positioned away from the stomach or duodenum or protected with omentum to prevent recurrent fistulization. A number of fistulas appear to have arisen from gastric or duodenal Crohn's, but the vast majority originate from diseased colon.
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PMID:Gastrocolic and duodenocolic fistulas in Crohn's disease. 147 63

Diarrhoea is defined as the frequent passage of loose or watery stools. Most patients can easily recognise and accurately define acute diarrhoea as an abrupt change in their bowel habits. Chronic or recurrent diarrhoea is more difficult for the patient to define, since it may mean malabsorption, tenesmus or true diarrhoea. Serious disorders not to be missed include neoplasia, AIDS, various serious infections such as amoebiasis, and inflammatory bowel disease.
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PMID:Diarrhoea. 152 Jan 38

The clinical significance of the fastidious organism DF-3 isolated from stool cultures is unclear. We sought to improve our understanding of this organism and to further define its association with human disease. Stool cultures for DF-3 were obtained from three sources: an ongoing study of enteric pathogens in patients infected with the human immunodeficiency virus, a screening procedure in which all stool samples submitted for Clostridium difficile toxin assay were cultured for DF-3, and stool samples submitted specifically for DF-3 culture. Retrospective clinical data were obtained from chart reviews of patients with positive cultures. Antimicrobial susceptibility testing and cell wall fatty acid analysis were performed for each DF-3 isolated. Eight isolates of DF-3 were obtained over a period of 8 months. All patients either had severe underlying disease or were immunocompromised, including three patients coinfected with human immunodeficiency virus and two patients with inflammatory bowel disease. The spectrum of clinical disease ranged from chronic diarrhea with a well-defined response to therapy for DF-3 to an asymptomatic carrier state. Cell wall fatty acid analysis of these isolates demonstrated a consistent pattern with a large peak of 12-methyltetradecanoate. DF-3, a fastidious gram-negative coccobacillus, can be recovered from stool cultures of immunocompromised patients by using selective media. The presence of 12-methyltetradecanoate in cell wall fatty acid analysis assists in identification. The increased use of a selective medium-(cefoperazone-vancomycin-amphotericin B) in the evaluation of diarrhea in immunocompromised hosts, including persons with inflammatory bowel disease, may better define the association of DF-3 with human gastrointestinal disease.
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PMID:Clinical illnesses associated with isolation of dysgonic fermenter 3 from stool samples. 153 8

Arachidonic acid metabolites formed by both the cyclooxygenase and lipoxygenase pathways may contribute to the clinical diarrhea and colitis of inflammatory bowel disease. Patients with active ulcerative colitis have increased levels of leukotriene B4 in their rectal mucosa, and these levels tend to correlate with severity of the disease. In this study, we evaluated the efficacy of ingestion of fish oil n-3-omega-fatty acids, inhibitors of leukotriene synthesis, in the treatment of ulcerative colitis. Eleven patients with ulcerative colitis of mild to moderate severity were studied in a 8-month, double-blind, placebo-controlled, crossover trial of dietary supplementation with fish oil, which provided about 4.2 g of omega-3- fatty acids per day. A disease activity index based on patient symptoms and sigmoidoscopic appearance was used to assess efficacy. Mucosal leukotriene B4 production was measured by radioimmunoassay. Mean disease activity index declined 56% for patients receiving fish oil and 4% for patients on placebo (p less than 0.05). There were no statistically significant differences in histopathologic scores or colonic mucosal leukotriene B4 levels. All patients tolerated fish oil ingestion and showed no alteration in routine blood studies. No patient worsened; anti-inflammatory drugs could be reduced or eliminated in eight patients (72%) while receiving fish oil. We conclude that fish oil dietary supplementation results in clinical improvement of active mild to moderate ulcerative colitis but is not associated with significant reduction in mucosal leukotriene B4 production, compared with placebo therapy. Further studies are needed to elucidate the mechanism of action and optimal dose and duration of fish oil supplementation in ulcerative colitis.
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PMID:Fish oil fatty acid supplementation in active ulcerative colitis: a double-blind, placebo-controlled, crossover study. 155 30

A patient who presented with chronic inflammation of the colon, and initially also the terminal ileum, accompanied by marked diarrhea, is described. Repeated high-dose steroid therapy was only temporarily successful, and symptoms recurred upon dose reduction. During the further course of the disease, a marked elevation of alkaline phosphatase and transaminases, as well as soft tissues swelling occurred. Clinically, the diagnosis of inflammatory bowel disease with primary sclerosing cholangitis was made. Irregularities in the walls of the common bile duct and the intrahepatic ducts seen at endoscopic retrograde cholangiopancreatography were consistent with the latter diagnosis. However, extreme eosinophilia of peripheral blood, bone marrow and bowel mucosa was present, and liver histology showed eosinophilic cholangiohepatitis. Under the diagnosis of hypereosinophilic syndrome with involvement of bowel, liver and biliary system, therapy with hydroxyurea was initiated. The patient's condition improved promptly. Eosinophil count and liver enzymes have remained normal under long-term medication with 1.0 g per day of this drug.
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PMID:Hypereosinophilic syndrome resembling chronic inflammatory bowel disease with primary sclerosing cholangitis. 155 10

The age-specific sero-prevalence of amoebiasis and giardiasis was estimated in 91 pediatric diarrhoea and in 70 non-diarrhoeal cases from Southern India. Anti-amoeba/giardia IgG assays on 20 children with inflammatory bowel disease from the UK yielded base-line levels in a non-endemic symptomatic population. IgG, IgM, and IgA levels were estimated to E. histolytica and G. lamblia using an ELISA. Concomittant faecal examinations were done for the Indian children. There was a significant correlation between acquisition of sero-positivity and age. A rise in the IgG response to both organisms was evident between 38 and 47 and 13-24 months, respectively, in diarrhoeal and non-diarrhoeal cases. An appreciable IgM response occurred predominantly in diarrhoea cases and at a younger age (less than 24 months). IgA responses were low. Anti-protozoal IgG levels in the UK children were negligible. There was no relationship between faecal excretion and sero-positivity. The study shows an age-related antibody response to E. histolytica and G. lamblia.
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PMID:Age-specific sero-prevalence of amoebiasis and giardiasis in southern Indian infants and children. 156 36

The history, pharmacology, pharmacokinetics, clinical uses and efficacy, adverse effects, drug interactions, and dosage and administration of rectal mesalamine and oral olsalazine in the treatment of inflammatory bowel disease (IBD) are reviewed. The high incidence of toxicity associated with sulfasalazine led to the development of the nonsulfonamide 5-aminosalicylic acid products mesalamine and olsalazine. The exact mechanism of action of these agents in the treatment of IBD is unknown. In clinical trials, mesalamine was shown to be as effective as or more effective than sulfasalazine or corticosteroids in treating active ulcerative colitis, proctitis, and proctosigmoiditis. Mesalamine is effective in the maintenance of remission in patients with ulcerative colitis. Several studies have demonstrated the effectiveness of olsalazine in the treatment of active mild to moderate ulcerative colitis. Olsalazine is also effective in the maintenance of remission of ulcerative colitis. The most common adverse effect associated with mesalamine enemas is perianal irritation or trauma secondary to insertion. The most common adverse effects associated with olsalazine are dose-dependent watery diarrhea and gastrointestinal upset. The recommended dosage of the mesalamine enema for the treatment of active mild to moderate ulcerative colitis is one 4-g (60-mL) retention enema daily for three to six weeks. The dosage of mesalamine suppositories for the treatment of active ulcerative proctitis is one 500-mg suppository inserted rectally twice daily for three to six weeks. The dosage of olsalazine is 1 g daily in divided doses for the maintenance of remission of ulcerative colitis. Both rectal mesalamine and oral olsalazine provide clinicians with an effective therapeutic option for the treatment of ulcerative colitis, proctosigmoiditis, and proctitis in patients unresponsive to or intolerant of the effects of sulfasalazine or corticosteroids.
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PMID:Mesalamine and olsalazine: 5-aminosalicylic acid agents for the treatment of inflammatory bowel disease. 160 Jun 85


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