A new hypothesis on the mechanism of digital clubbing secondary to pulmonary pathologies.

Our hypothesis concerns the chronic activation of macrophages, and the continual production of pro-fibrotic tissue repair factors, as a cause of digital clubbing in an array of pulmonary pathologies. The level of macrophage activation will differ between individuals, corresponding to the variable immune response to these pulmonary pathologies. Due to this variability, there is a corresponding inconsistency in the presentation of clubbing. Although testing of this hypothesis would be difficult, there is evidence to support our theory; including a link to chronic diseases involving granulomas, where there would be a large collection of macrophages present and pathologies in organs with large resident macrophage populations. This theory, therefore, could also be developed to include non-pulmonary causes of clubbing.