[H2-receptor antagonist-refractory ulcer--its pathophysiology and role of proton-pump inhibitors].
Among H2-receptor antagonist (H2RA)-refractory ulcers, non-responders that did not heal after 5 months therapy had high intraluminal pH in the basal condition and high sensitivity to inhibition of acid secretion by H2RA but possessed gastric mucosa to generate less prostaglandins. Combination therapy of PGE1-analogue with H2RA healed these ulcers by 60%. Proton-pump inhibitor (PPI) exerted a complete inhibition of acid secretion in these patients and the rate of healing was 88%. Helicobacter pylori was present in the mucosa of all 4 ulcer patients refractory to treatment with PPI. The ulcers healed in 3 out of 4 patients after eradication of H. pylori. It is suggested that PG supplement or complete inhibition of acid secretion is effective for ulcers in H2RA-non-responders. PPI-refractory ulcers may relate to H. pylori infection.
Third Department of Internal Medicine, Osaka City University Medical School.
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Arakawa
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D000251:Adenosine Triphosphatases / Q000037:antagonists & inhibitors*; D000818:Animals; D003864:Depression, Chemical; D004351:Drug Resistance; D005744:Gastric Acid / Q000378:metabolism; D005753:Gastric Mucosa / Q000378:metabolism / Q000382:microbiology; D017506:H(+)-K(+)-Exchanging ATPase; D006635:Histamine H2 Antagonists / Q000494:pharmacology*; D006801:Humans; D064747:Lansoprazole; D009853:Omeprazole / Q000031:analogs & derivatives* / Q000494:pharmacology / Q000627:therapeutic use; D011453:Prostaglandins / Q000096:biosynthesis; D013276:Stomach Ulcer / Q000188:drug therapy* / Q000382:microbiology / Q000503:physiopathology
D053799:2-Pyridinylmethylsulfinylbenzimidazoles; D006635:Histamine H2 Antagonists; D011453:Prostaglandins; D064747:Lansoprazole; D000251:Adenosine Triphosphatases; D017506:H(+)-K(+)-Exchanging ATPase; D009853:Omeprazole