Helicobacter pylori in duodenal and gastric ulcer disease.
The decision to treat a patient should in general always be based on potential risk and advantage. Widespread and uncontrolled use of all kinds of anti-H. pylori regimens may promote development of antimicrobial resistant strains. In particular, antimicrobial monotherapy is associated with failure to eradicate H. pylori and induction of resistant strains. Polychemotherapy is much more effective and has a lower risk for development of antimicrobial resistant H. pylori strains but carries the risk of significant drug-related side effects. If the prescribed anti-H. pylori regimen is not effective in at least 80%, or if the patient is not compliant, this type of therapy should not be considered. Also if reinfection is to be expected, the risk may outweigh potential benefits (Graham, 1993). Guidelines published in 1990 by an international working party during the World Congress of Gastroenterology recommended H. pylori eradication only in patients where duodenal ulcer was a serious management problem requiring lifelong maintenance therapy, and in whom complications (bleeding, perforation) had occurred or surgery was considered (Tytgat et al, 1990). Recently less stringent guidelines were recommended. A National Institutes of Health (NIH) Consensus Development Conference has recommended that all patients with gastric or duodenal ulcer who are H. pylori infected should be treated with antimicrobials including patients presenting with an ulcer for the first time. In addition, patients on maintenance antisecretory medication should also be contacted and treated for H. pylori infection (Anonymous, 1994). The ulcer relapse rate during prolonged follow-up after H. pylori eradication is very low. Despite this, it is advised that antisecretory medication is continued after successful H. pylori eradication in patients with previous ulcer complications. In all other patients maintenance antisecretory medication can be stopped after successful eradication. It is not known whether H. pylori eradication lowers the risk of NSAID-induced ulceration or whether the risk of ulcer complications is reduced.
Rauws
E J
EJ
Department of Gastroenterology and Hepatology, Academic Medical Centre, Amsterdam, The Netherlands.
Tytgat
G N
GN
D000894:Anti-Inflammatory Agents, Non-Steroidal / Q000627:therapeutic use; D003906:Developing Countries; D004381:Duodenal Ulcer / Q000188:drug therapy / Q000453:epidemiology / Q000382:microbiology*; D016481:Helicobacter Infections / Q000188:drug therapy / Q000453:epidemiology; D016480:Helicobacter pylori; D006801:Humans; D012008:Recurrence; D013276:Stomach Ulcer / Q000188:drug therapy / Q000453:epidemiology / Q000382:microbiology*
D000894:Anti-Inflammatory Agents, Non-Steroidal