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Response

We thank Drs Lin and Tsai for their interest in and comments on our article.¹ We concur with their suspicion that clinicians may have tended to use pantoprazole in sicker patients, but as we point out in the article, acuity has not specifically been identified as a risk factor for upper gastrointestinal bleeding in critically ill patients. Also, despite the higher acuity scores among the patients receiving pantoprazole, with the exception of the incidence of upper gastrointestinal bleeding, the outcome parameters did not differ, calling into question the clinical significance of the difference in the Acute Physiology and Chronic Health Evaluation II scores between the 2 groups.^1–3

With regard to the dosing of pantoprazole, the prophylaxis regimens used at our institution are similar to those used elsewhere, and do not target gastric pH. Also, the dosing of pantoprazole was consistent with the dosing of PPIs in other studies.^4–6 The mechanism of bleeding in critically ill patients is quite different from that of typical peptic ulcer disease, being primarily due to mucosal ischemia and impaired mucosal barrier integrity, often associated in fact with decreased gastric acid production.⁷ Extrapolating from the literature on treating active bleeding and/or rebleeding of peptic ulcers may not be relevant to this population of patients.

Given the retrospective nature of our data, the small number of bleeding events, and the clearly established superiority of PPIs over histamine-2 receptor antagonists in terms of acid suppression and duration of action, it would seem premature to conclude that pantoprazole at a dose of 40 mg once daily is insufficient to prevent upper gastrointestinal bleeding in the population studied, although we would agree that on the basis of our data this class of drug seems to offer no routine advantage over histamine-2 receptor antagonists.

FINANCIAL DISCLOSURES
None reported.

REFERENCES

1. Ojiako K, Shingala H, Schorr C, et al. Famotidine versus pantoprazole for preventing bleeding in the upper gastrointestinal tract of critically ill patients receiving mechanical ventilation. Am J Crit Care. 2008;17(2):142–147.[Abstract/Free Full Text]
2. Cook DJ, Fuller HD, Guyatt GH, et al. Risk factors for gastrointestinal bleeding in critically ill patients. Canadian Critical Care Trials Group. N Engl J Med. 1994;330(6):377–381.[Abstract/Free Full Text]
3. Faisy C, Guerot E, Diehl J, Iftimovici E, Fagon J. Clinically significant gastrointestinal bleeding in critically ill patients with and without stress-ulcer prophylaxis. Intensive Care Med. 2003;29(8):1306–1313.[Medline]
4. Levy MJ, Seelig CB, Robinson NJ, Ranney JE. Comparison of omeprazole and ranitidine for stress ulcer prophylaxis. Dig Dis Sci. 1997;42(6):1255–1259.[Medline]
5. Lasky MR, Metzler MH, Phillips JO. A prospective study of omeprazole suspension to prevent clinically significant gastrointestinal bleeding from stress ulcers in mechanically ventilated trauma patients. JTrauma. 1998;44(3):527–533.
6. Kantorova H, Svoboda P, Scheer P, et al. Stress ulcer prophylaxis in critically ill patients: a randomized controlled trial. Hepatogastroenterology. 2004;51(57):757–761.[Medline]
7. Spirt MJ. Acid suppression in critically ill patients: what does the evidence support? Pharmacotherapy. 2003;23(10 Pt 2): 87S–93S.[Medline]

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