In Reply: Dr Corica and colleagues question
the appropriateness of our speculation about potential therapeutic interventions
targeting elevated leptin in obese patients. Our results and those of others1- 3 indicate that
leptin may promote platelet aggregation by interacting with the leptin receptor
on platelets. Furthermore, a recent clinical study identified plasma leptin
as an independent risk factor for cardiovascular events,4
although mechanisms other than increased platelet aggregation may relate to
this increased risk. Currently, the best treatment for reducing the potential
adverse effects of leptin is probably weight reduction, which is admittedly
difficult. Because of the well-known consequences of leptin deficiency on
weight gain and metabolism,5 we agree that
drug-induced leptin reduction or antagonism might cause more harm than good.
Therefore, targeting the platelet seems to be a more reasonable approach.
However, we certainly agree that there is much to be learned about the mechanism
of leptin-induced platelet aggregation and whether chronically elevated leptin
levels have an effect on thrombosis.
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