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Archived Comments for: Cardioprotective aspirin users and their excess risk of upper gastrointestinal complications

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  1. aspirin, GI irritation, and copper and zinc

    Patrick Frank, Stanford University, Chemistry and SLAC

    4 October 2006

    There is a significant literature showing that both copper(II) and zinc(II) protect the GI system from the ulcerative effects of aspirin and other NSAIDs. As I recall, the complex zinc(aspirinate)2 itself is anti-ulcerative.

    These reports, mostly dating from the 1980's and early 1990's, have been only modestly followed up in the medical literature. They should be given greater attention because they promise an inexpensive and apparently effective treatment or prevention of GI ulceration.

    Recent examples: A. Garciaplaza, et al. (1996) "A multicentric trial of zinc acexamate versus famotidine in the treatment of acute duodenal ulcer" Revista Espanola de Enfermedades Digestivas 88, 757-762

    and

    E. Jimenez (1992) "Metaanalysis of Efficacy of Zinc Acexamate in Peptic Ulcer" Digestion 51, 18-26

    and

    C.T. Dillon, et al. (2003) "Gastrointestinal toxicity, antiinflammatory activity, and superoxide dismutase activity of copper and zinc complexes of the antiinflammatory drug indomethacin" Chemical Research in Toxicology 16, 28-37

    Competing interests

    No competing interests

  2. H.Pylori plays a important role in increasing risk for gastrointestinal bleeding.

    Venkataswamy Narayana Mahesh, University Hospital of North Durham

    10 October 2006

    Editor- Diaz et al have done a commendable job with this study and highlights the importance of recognising associated factors which might increasre the risk of complications. The authors mention paucity of data regarding the role of H.Pylori in upper gastrointestinal bleeding. In one study of 19 published studies(1), H.Pylori presence contributed to increased recurrence rates as in cured versus noncured H. pylori infection was 6% compared to 67% for duodenal ulcers and 4% compared to 59% for gastric ulcers.

    Also we have enough evidence (2) to prove that H.Pylori and NSAID use (including low dose aspirin) are both independent and synergistic risk factors (17.5 times higher the risk). It is thought that the increased inflammatory response to the presence of H.Pylori in the gastric mucosa' renders it susceptible to damage by the gastric secretions, and this play an important role in ulcer formation and its antecedent complications.(3). Current evidence points towards the need of H.Pylori detection and eradication in atleast high risk individuals i.e advancing age, male, previous hisory of gastrointestinal bleeding etc, as mentioned in this study. Although NICE in UK recommends use of proton pump inhibitors along with aspirin in this group of patients, further randomised studies to this regard is warrented.

    REFERENCES:

    1. Hopkins, RJ, Girardi, LS, Turney, EA. Relationship between Helicobacter pylori eradication and reduced duodenal and gastric ulcer recurrence: A review. Gastroenterology 1996; 110:1244.

    2. Papatheodoridis, GV, Sougioultzis, S, Archimandritis, AJ. Effects of Helicobacter pylori and Nonsteroidal Anti-Inflammatory Drugs on Peptic Ulcer Disease: A Systematic Review. Clin Gastroenterol Hepatol 2006; 4:130.

    3. Crabtree, JE. Gastric mucosal inflammatory responses to Helicobacter pylori. Aliment Pharmacol Ther 1996; 10 Suppl 1:29.

    Competing interests

    None declared

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