Some limitations of our study merit discussion. First, this was an analysis of administrative data, so misclassification of some exposures, covariates, and outcomes is always possible. We used validated end points of HF readmission and death to minimize misclassification of outcomes. The diagnosis of gout using administrative databases may also be prone to misclassification. We chose an inclusive definition of gout that accounted for any primary or secondary diagnosis in an effort to include all patients with a possible remote history of gout. In addition, we performed a sensitivity analysis using variable definitions of gout to ensure that our results were robust to our definition of gout. Nonetheless, despite our efforts, some patients may have been misclassified according to gout status, which could have biased our effect estimates for remote gout and may have led to some residual confounding. Second, despite adjustments in our models for many important confounders such as renal failure, myocardial infarction, history of gout, daily diuretic dose, and comorbidities (using the Charlson index), some degree of confounding may still modify our estimates. We could not adjust for obesity, alcohol use, or socioeconomic status since these variables were not available. We also could not adjust our models for ejection fraction because this covariate was not available. However, on the basis of the pathophysiological mechanisms of allopurinol, which is known to improve endothelial function, allopurinol should have similar benefits in systolic and diastolic HF. Third, because we used prescriptions to assess drug use, we could not account for use of over-the-counter drugs (such as NSAIDs) and could not measure compliance with prescribed drugs. Fourth, because we compared allopurinol users with nonusers, our results may be biased by confounding by indication. Because we were studying the unintended effects of allopurinol use on HF outcomes, our estimates are less likely influenced by such confounding. However, it is possible that in certain patients with HF and gout, lack of allopurinol use (or stopping allopurinol use) may itself represent a risk factor for adverse HF outcomes. Fifth, our analysis of acute gout may be inflated owing to reverse causality. We attempted to limit this problem by adjusting for covariates that suggested a recent worsening in HF (eg, a recent visit to a physician or ED for HF or a recent increase in diuretic dose).