Abstract
Firstly, the evidence of prostaglandin deficiency in gastric ulcer is by no means complete ; Chris Hawkey in our laboratory, for example, shows mainly a difference between having gastritis and not having gastritis, not related to ulcer. Secondly, I would like to attribute the findings in Jerusalem to intervention by Jehovah, as you do, but I think I must really attribute them to the failure of intervention by a statistician. What you need, is to quote confidence intervals; I think this is true for all the studies, and you can then get a better appreciation of different means between studies. The third point I would like to make is in relation to enprostil. We have looked at relapse rates after stopping treatment, and these do not look very different from the relapse curves for ranitidine. It looks as though they are fundamentally the same (Hawkey CJ (1986) Synthesis of prostaglandin E2, thromboxane B2 and prostaglandin catabolism in gastritis and gastric ulcer. Gut 27: 1484–1492).
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© 1988 Springer-Verlag Berlin Heidelberg
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Domschke, W., Dammann, H.G., Peskar, B.M., Holtermüller, K.H. (1988). Discussion Following the Reports of Prof. Rachmilewitz and Dr. Sontag. In: Domschke, W., Dammann, H.G., Peskar, B.M., Holtermüller, K.H. (eds) Prostaglandins and Leukotrienes in Gastrointestinal Diseases. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-73316-1_40
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DOI: https://doi.org/10.1007/978-3-642-73316-1_40
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