Abstract:
BACKGROUND:Two studies were carried out in order to investigate the issue of meal-provoked nocturnal gastrooesophageal reflux. METHODS:In Experiment 1, 20 symptomatic reflux patients underwent both pH and polysomnographic monitoring on two nights. On one night, patients ate a non-provocative meal prior to 19.00 hours, while on the other night patients consumed a late evening meal (21.00 hours). In Experiment 2.17 symptomatic reflux patients were studied using pH and polysomnographic monitoring on two nights subsequent to a late evening provocative meal. On one night, patients received 75 mg of the H2-antagonist ranitidine, while on another night they received a placebo. The data from 12 of the 17 patients studied were used in the analysis. RESULTS:For Experiment 1, no significant differences in the number or duration of reflux events, acid exposure (total %), or polysomnographic measures of per cent of sleep stages between the two nights were observed. The results of the second experiment demonstrated that when given ranitidine, patients experienced significant decrease in acid contact time (total %), and mean duration of reflux events. Subjective reports of discomfort and sleep disturbance were also significantly improved on the drug night. However, significant differences in polysomnographic measures were not observed. CONCLUSIONS:Based on these results, we conclude that in some symptomatic reflux patients a late-night non-provocative meal may not increase the incidence of gastro-oesophageal reflux, and that a low dose of an H2-antagonist is effective in decreasing oesophageal acid contact time following a late evening provocative meal.
journal_name
Aliment Pharmacol Therjournal_title
Alimentary pharmacology & therapeuticsauthors
Orr WC,Harnish MJdoi
10.1046/j.1365-2036.1998.00407.xsubject
Has Abstractpub_date
1998-10-01 00:00:00pages
1033-8issue
10eissn
0269-2813issn
1365-2036journal_volume
12pub_type
临床试验,杂志文章abstract:BACKGROUND:Non-alcoholic fatty liver disease generally has a benign course; however, patients with non-alcoholic steatohepatitis (NASH) may progress to cirrhosis and hepatocellular carcinoma. Currently, there is a lack of consensus about optimal NASH treatment. AIM:To assess the efficacy of insulin-sensitizing agents ...
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