Most theories behind the mechanism of clubbing include an association with right to left circulatory shunting, possibly leading to increased vascular growth factors in systemic capillaries. For example, the most popular current theory is that megakaryocytes, normally filtered in the pulmonary capillaries form the venous circulation are released in the the arterial circulation due to right to left shunts in cyanotic heart disease or certain inflammatory lung diseases, like pulmonary fibrosis and bronchiectasis. This pertains to cirrhosis because it is thought that cirrhosis leads to increased humoral factors that cause inappropriate vasodilatation or shunts, such as those seen in spider angiomas. This is thought to occur in the lung due to cirrhosis, leading to right to left shunt and clubbing.
Stoller, J K, et al. “Reduction of intrapulmonary shunt and resolution of digital clubbing associated with primary biliary cirrhosis after liver transplantation.” Hepatology 11.1 (1990):54-58.
The observation that both intrapulmonary abnormalities and digital clubbing can be improved by liver transplantation is consistent with earlier hypotheses that a humoral factor may be responsible for these vascular changes. Because the intrapulmonary shunt and digital clubbing were reduced when hepatic function improved after transplant, attractive possibilities are that the diseased liver either produces a humoral factor responsible for promoting arteriovenous channels or that the diseased liver fails to clear a preexisting circulating factor.