In patients with community-acquired pneumonia, PPI use was associated with a twofold increased risk for infection with oropharyngeal bacteria but not other pathogenic agents.
The decrease in gastric acidity that results from treatment with proton-pump inhibitors (PPIs) has been linked with bacterial colonization of the stomach and outcomes such as nosocomial pneumonia in the inpatient setting (Ann Intern Med 1994; 120:653) and community-acquired pneumonia (CAP; JAMA 2004; 292:1955).
To further investigate the possible link between PPI use and CAP, investigators prospectively assessed PPI use and microbiological etiology of pneumonia in patients treated for CAP in the emergency room of a large general hospital in the Netherlands. A diagnosis of CAP was based on symptoms and radiographic findings. Microbiological etiology of the pneumonia infection was assessed using sputum and blood cultures, urine antigen tests, and serum antibody tests. Relevant demographic and clinical covariates (e.g., medication use, comorbidities, severity of illness) and treatment outcomes (e.g., length of hospital stay, in-hospital mortality) were assessed.
Of 463 patients with CAP, 29% were using PPIs. The cause of pneumonia in PPI users was more likely to be oral flora than in nonusers (adjusted odds ratio, 2.0; 95% confidence interval, 1.22–3.72). PPI users were more likely than nonusers to be infected with Streptococcus pneumoniae (28% vs. 14%; adjusted OR, 2.23; 95% CI, 1.28–3.75) and had a lower rate of infection with Coxiella burnetii than nonusers (8% vs. 19%), which was not significant after adjustment for covariates. PPI use was not associated with any other pathogens. CAP severity, length of hospital stay, and in-hospital mortality did not differ between PPI users and nonusers.
The authors conclude that PPI use doubles the risk for CAP, possibly from infection with oropharyngeal flora, including S. pneumoniae.
Comment: This study confirms the previously observed increased risk for developing pneumonia from oropharyngeal bacteria in patients with reduced gastric acid. However, in the absence of a controlled study design, a possible mechanism for causality cannot be determined. We can only conclude that in this cohort of patients with CAP, oropharyngeal bacteria — specifically S. pneumoniae — were more common pathogens in PPI users than in nonusers. PPI users in this study had more comorbidities and poorer baseline lung function than the comparison group, suggesting that despite the attempt to control for comorbidities, other factors might have also contributed to the observed difference in risk for CAP.
Source: Journal Watch Gastroenterology