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Letter: would aspirin alleviate fibrosis in alcoholic liver disease? Authors’ reply

Year: 2016

Type: article

Abstract: We appreciate the comments by Dr Lu regarding the association between aspirin and liver fibrosis.1, 2 To address the concern, we tested the interaction of aspirin use with ALD among all subjects and those with chronic liver disease. In these post hoc analyses, we observed an interaction between ALD status and aspirin use of borderline significance in the general population, with P-values for multiplicative interaction of 0.04 for FIB4 and 0.07 for APRI, whereas the test did not reach significance among those with CLD, with P-values for multiplicative interaction of 0.3 for FIB4 and 0.2 for APRI. In other words, our data suggest that there is an increase in the extent of association in those with ALD compared to the general population with borderline significance, but do not distinguish a difference between ALD and other forms of CLD. The possibility of reverse causation, i.e. patients with advanced fibrosis may not take aspirin for fear of bleeding, is possible, although we also observed a protective association among those with mild to moderate fibrosis (stage 0–2), in whom this scenario is less likely. We agree that FIB4 and APRI are not perfect fibrosis indices, but emphasise that this type of non-differential misclassification is expected to bias our results towards the null rather than to an overestimation. The impact of aspirin on ethanol metabolism is interesting, although it has been shown that aspirin still increases bleeding time even among individuals with recent alcohol ingestion.3 Currently, there is no evidence to suggest that ethanol influences the antiplatelet effect and inhibition of PDGF release mediated by aspirin. The authors’ declarations of personal and financial interests are unchanged from those in the original article.2

Source: Alimentary Pharmacology & Therapeutics

DOI: 10.1111/apt.13669