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I remain skeptical that the association between acetaminophen use and incident hypertension observed by Curhan et al¹ was a causal one. It is established that traditional nonsteroidal anti-inflammatory drugs (NSAIDs) can exacerbate hypertension, but the authors' suggestion that acetaminophen—even when taken infrequently—can cause hypertension has limited plausibility. As the authors point out, short-term studies on acetaminophen use have not identified an adverse effect of this drug on blood pressure. Given its short half-life and duration of action, coupled with the absence of documented hemodynamic effects, it seems more likely that acetaminophen was a marker for chronic or frequent intermittent pain, rather than a direct culprit.

The authors note that scant information is available on the impact of chronic pain on blood pressure. This may be true, but the chronically increased catecholamines and glucocorticoids that may be associated with sustained physiological or psychological stress could certainly lead to hypertension.^2-3 The authors . . . [Full Text of this Article]