Capsaicin, the active ingredient in chili, has been implicated as both a cytoprotective and a detrimental agent to the gastric mucosa. The effect of capsaicin on Helicobacter pylori has not been investigated previously. Therefore, we performed in vitro time- and concentration-dependent studies to examine the growth of H. pylori in the presence of capsaicin. Capsaicin specifically inhibited growth of H. pylori dose-dependently at concentrations greater than 10 micrograms ml-1 (P < 0.05) but did not inhibit the growth of a human fecal commensal Escherichia coli strain. Bactericidal activity was observed within 4 h. Capsaicin continued to exhibit bactericidal activity when incubated at pH values as low as 5.4. Ingestion of chili, therefore, could have a protective effect against H. pylori-associated gastroduodenal disease. This effect deserves further study in animal models.

Helicobacter pylori infection causes chronic-active gastritis and is associated with peptic ulceration. However, the link between gastric H pylori colonization and duodenal ulcers is not well understood. Therefore, a retrospective, case-controlled study was conducted to determine whether H pylori infection is associated with gastric metaplasia and mucosal inflammation in the duodenum. Biopsy specimens from the duodenal bulb were obtained from 31 of 47 children with H pylori-induced gastritis. Two control groups, matched for age and sex, consisted of 33 children with normal antral histologic evaluation and 33 with H pylori-negative gastritis. Coded duodenal sections were stained with periodic acid-Schiff, hematoxylin-eosin, and silver to examine for gastric metaplasia, mucosal inflammation, and Helicobacter-like organisms, respectively. Thirteen of 31 (42%) H pylori-infected children had gastric metaplasia, in contrast to 1 of 33 with normal histologic characteristics (P < .0001) and 2 of 33 with H pylori-negative gastritis (P < .001). H pylori was detected overlying ectopic gastric mucosa in only 2 of 13 cases. Duodenal ulcers were identified endoscopically in 10 of 13 children with gastric metaplasia and 9 of 18 H pylori-infected subjects without metaplasia (P = NS). Twenty-four of 31 (77%) children with H pylori gastritis had duodenitis compared with 4 of 33 (12%) with H pylori-negative gastritis (P< .001) and 2 of 33 (6%) with a normal antrum (P < .001). Duodenitis was present in 14 of 19 children with H pylori infection and duodenal ulcers and 10 of 12 infected patients without mucosal ulceration (P not significant). These findings demonstrate a higher frequency of both gastric metaplasia and mucosal inflammation in the proximal small intestine of H pylori-infected children. However, there was a lack of correlation between the presence of duodenal ulceration and both gastric metaplasia and duodenitis.

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Measurement of salivary clearance and urinary metabolites of caffeine is an excellent noninvasive tool for assessing liver function, particularly the activity of cytochrome P4501A2 (CYP1A2), N-acetyltransferase (NAT), and xanthine oxidase (XO). This study was undertaken to measure the clearance of caffeine using saliva as a biological fluid and to assess the activities of the above-mentioned enzymes in healthy children and pediatric patients with liver diseases using urinary molar ratios of different caffeine metabolites. The well-established two-sample saliva approach was used to measure the clearance of caffeine in nine pediatric patients with liver diseases (LD) and in nine healthy children. The caffeine metabolites were also measured in the urine of these subjects by high-performance liquid chromatography, and urinary molar ratios of 5-acetylamino-6-formylamino-3-methyluracil (AFMU), 1-methylxanthine (1X), 1-methyluric acid (1U), and 1,7-dimethyluric acid (17U) were employed to estimate the activities of CYP1A2, NAT, and XO. The caffeine salivary clearance and the percentage of the dose excreted in the form of various metabolites were significantly (p < 0.035) smaller in the LD patients than those in healthy children. The urinary molar ratio of [AFMU + 1U + 1X]/17U, which reflects the activity of CYP1A2, was also significantly (p < 0.0005) reduced in these patients. However, there were no significant differences between the two groups in the ratios of AFMU/1X and 1U/1X, which estimate the activities of NAT and XO, respectively. In conclusion, the data obtained suggest that liver disease in pediatric subjects significantly reduces the salivary clearance of caffeine and the activity of cytochrome P4501A2, but it has no impact on the activities of NAT and XO.

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