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  • Title: Are duodenal ulcer seasonal fluctuations paralleled by seasonal changes in 24-hour gastric acidity and Helicobacter pylori infection?
    Author: Savarino V, Mela GS, Zentilin P, Lapertosa G, Cutela P, Mele MR, Mansi C, Dallorto E, Vassallo A, Celle G.
    Journal: J Clin Gastroenterol; 1996 Apr; 22(3):178-81. PubMed ID: 8724253.
    Abstract:
    The occurrence of duodenal ulcer is characterized by seasonal variation, for poorly understood reasons. No previous study has assessed whether 24-h intragastric acidity and Helicobacter pylori infection have similar seasonal fluctuations in patients with this disorder. For this reason, we evaluated retrospectively the circadian gastric pH in 319 new patients (226 men and 93 women, mean age 45.2 years) with endoscopically proven duodenal ulcer, who agreed to undergo this examination during the years 1987-1992 in our center. The month-by-month occurrence of the disease over the global 6-year period was assessed, and the mean pH values were calculated for each patient during three time intervals of interest: 24 h, daytime (08:00-19:59 h), and nighttime (20:00-07:59 h). The mean pH values of these three time periods were then calculated month by month throughout the annual cycle. H. pylori infection was sought by histology in 171 patients examined in the period from 1990 to 1992. The percentage of H. pylori-positive duodenal ulcer patients was then calculated for each season. The calendar fluctuation of duodenal ulcer occurrence showed an evident increase (p < 0.001) in fall (October-December) and in winter (January-March) compared with spring (April-June) and summer (July-September). Both 24-h and nighttime gastric acidity showed no significant variation by month, whereas daytime gastric pH varied significantly (p < 0.05) with two evident decreases, meaning higher acidity, in April and August. H. pylori infection was detected in 152 of 171 patients (89%), and the percentage of H. pylori-positive duodenal ulcers did not differ from season to season. We conclude that there was no parallel circannual fluctuation of duodenal ulcer, gastric acidity, and H. pylori infection in the restricted sample of patients we studied. This reduces the apparent relevance of acid in inducing ulcer seasonal fluctuation. Also, the responsibility of H. pylori in this phenomenon can be excluded until a reliable diagnostic method capable of distinguishing recent from old infection is found.
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