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Therapeutic Success with the Suppression of Helicobacter pylori of Intractable Gastric Ulcers
Author(s) -
ARAKAWA Tetsuo,
KIMURA Shuji,
UCHIDA Toshiyuki,
HIGUCHI Kazuhide,
FUKUDA Takashi,
NAKAMURA Hajime,
KOBAYASHI Kenzo
Publication year - 1994
Publication title -
digestive endoscopy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.5
H-Index - 56
eISSN - 1443-1661
pISSN - 0915-5635
DOI - 10.1111/j.1443-1661.1994.tb00379.x
Subject(s) - lansoprazole , medicine , helicobacter pylori , proton pump inhibitor , rabeprazole , gastroenterology , refractory (planetary science) , antagonist , antacid , amoxicillin , gastric mucosa , pharmacology , stomach , receptor , antibiotics , physics , astrobiology , microbiology and biotechnology , biology
Three patients with a long history of gastric ulcers refractory to treatment first with an H 2 ‐receptor antagonist, then with a prostaglandin E t analogue plus an antagonist, and next with a proton‐pump inhibitor, lansoprazole, were given amoxicillin together with an H 2 ‐receptor antagonist, and the ulcers finally healed. The patients were men aged about 60, and two were smokers. Reduction of gastric acidity by lansoprazole may have been satisfactory in these patients because one dose of the drug raised the gastric pH to more than 3.0 for about 97% of the next 24h in all three of the patients, as by the continuous measurement of intraluminal pH. The gastric mucosa of these patients was found to be infected with Helicobacter pylori when tested at the end of treatment with this inhibitor. Their medication was changed from the proton‐pump inhibitor to amoxicillin plus an H 2 ‐receptor antagonist, and all of the ulcers healed within 6 weeks. H. pylori was not detected at the end of this treatment. These results indicate that reduction of gastric acidity alone was insufficient to cure the ulcers in these patients. H. pylori may be related to some ulcers being refractory to many antiulcer agents, even proton‐pump inhibitors.