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Ojiako and colleagues¹ report a retrospective study comparing the effectiveness of famotidine and pantoprazole to prevent stress ulcers in critically ill patients receiving mechanical ventilation. This study showed that patients in the pantoprazole group were sicker and had a significantly higher incidence of upper gastrointestinal bleeding than did patients in the famotidine group (0.38% vs 3.2%, P = .03).

The evidence for histamine-2 receptor antagonists (H₂RAs) is much stronger than that for proton pump inhibitors (PPIs) in this clinical setting. In current practice, H₂RAs (eg, famotidine) are the first-line agents for stress ulcer prophylaxis in critically ill patients, and PPIs (eg, pantoprazole) are generally used in patients who were perceived to be at higher risk (eg, those with previous history of peptic ulcer disease). If the risk profiles were similar, one would not use PPIs due to the lack of data on their efficacy and safety.

In this study, the number of patients in the pantoprazole group (95) was significantly lower than that in the famotidine group (522). The reasons for selecting pantoprazole (rather than famotidine) were not mentioned in the study. Given that patients in the pantoprazole group were sicker (ie, they had higher scores on the Acute Physiology and Chronic Health Evaluation [APACHE]), it seems likely that they were perceived by attending physicians to be at higher risk for stress ulcer bleeding. If the 2 groups were different in terms of risk profile and severity of illness (famotidine being used in lower risk and less sick patients and pantoprazole being used in sicker and higher risk patients), these 2 groups of patients could not be compared and this would invalidate the study.

Second, the authors quoted the landmark study by Cook et al² showing that mechanical ventilation for more than 48 hours and coagulopathy were the 2 independent risk factors for clinically significant bleeding from stress ulcers. Unfortunately, patients with coagulopathy (prothrombin time or activated partial thromboplastin time = 1.5 times the upper limit of normal without the use of anticoagulants) were excluded in this study. A significant number of critically ill patients might have been excluded, as this degree of coagulopathy is common in intensive care patients. Therefore, one would be justified in assuming a degree of caution when applying the results of this study to routine clinical practice.

Third, the definition of clinically significant bleeding in this study is different from definitions used in previous studies. In this study, clinically significant bleeding was defined as blood loss from the upper part of the gastrointestinal tract that required transfusion of 1 unit or more of blood products; however, in a previous study³ it was defined as clinically overt bleeding associated with a decrease in hemoglobin level of more than 2 g/dL or hemodynamic instability within 24 hours after bleeding or failure to increase hemoglobin concentration after transfusion by at least the number of units transfused minus 2. The significance of this discrepancy for comparing the results with those of previous studies is also questionable.

Therefore, the role of PPIs as the first-line agent in stress ulcer prevention is still unclear and should be assessed by means of a high-quality randomized controlled trial.

Aung A. Lwin, MBBS, MRCP
Sheffield, United Kingdom

REFERENCES

1. Ojiako K, Shingala H, Schorr C, Gerber DR. 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. Cook D, Guyatt G, Marshall J, et al. A comparison of sucralfate and ranitidine for the prevention of upper gastrointestinal bleeding in patients requiring mechanical ventilation. N Engl J Med. 1998;388:791–797.

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