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One theory is that clubbing is a response to arterial hypoxaemia, in which release of an unknown humoral substance causes dilation of the vessels of the fingers and the toes.
Another is that clubbing results from a neurovascular abnormality. In support of this is the fact that a vagal section may reverse clubbing.
Recent research studies have shown that platelet-derived growth factors and vascular endothelial growth factors (which are released when platelet precursors are trapped in the peripheral circulation) acts as promoters of vascularity and eventually finger clubbing (1).
However, no theory adequately explains the sheer variety of diseases in which this phenomenon occurs.
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