Lansoprazole worsens asthma control in poor metabolizers: is nitric oxide involved?
Abstract
To the Editor:
We enjoyed the article of Lang and colleagues (1). This well-designed longitudinal study demonstrates that the proton pump inhibitor lansoprazole worsens asthma control in a cohort of children characterized as poor metabolizers of proton pump inhibitors as a result of cytochrome P450 polymorphism. The authors speculated that prolonged proton pump inhibitor treatment in poor metabolizers could result in oversuppression of gastric acid that could favor development of upper respiratory infections, as suppressed acidity is associated with prolonged retention of upper respiratory infection pathogens in gastric epithelium. However, as pointed out by the authors, they did not observe differences between the lansoprazole and placebo groups in asthma control after recent upper respiratory infections.
There is an alternative explanation for the findings of Lang and colleagues: The negative effect of proton pump inhibition on asthma control might be mediated by asymmetrical dimethylarginine. As a result of the degradation of some methylated proteins, asymmetrical dimethylarginine is generated by lung vascular and parenchymal cells. This molecule is an endogenous inhibitor of nitric oxide synthase (NOS) and may also induce oxidative stress by causing NOS to generate reactive oxygen species (2). Asymmetrical dimethylarginine is thought to exacerbate airway inflammation, increase airway hyperactivity, and promote lung collagen formation and deposition (3). Increased…
How strong is the evidence?
Evidence Hub reads this as a cohort study, done in people. Its evidence level is 3 of 5 (Moderate · trial / cohort / secondary analysis). Trials without a large randomized design, cohorts and secondary analyses give moderate evidence.
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