Using aspirin could lower fibrosis indices among patients at risk of liver fibrosis, according to results from a new peer-reviewed study published in Alimentary Pharmacology & Therapeutics. The study used records taken from the National Health and Nutrition Examination Survey III (NHANES III). The sample included a total of 1,907 subjects with suspected chronic liver disease while a group of 13,654 with no risk of liver disease were identified for comparison.

The use of aspirin (n=520) among the group at risk of liver disease was tied to a decrease of 0.23 standard deviation (SD) in the composite fibrosis index (95% CI: -0.41 to -0.06; P=0.009). On the other hand, Ibuprofen (n=332) use showed no significant changes in the composite fibrosis index in parallel analyses.

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Using a lower alanine aminotransferase test (ALT) cut off (20 U/L or above), the researchers tested whether the association between aspirin and lower fibrosis index could be sensitive to the chronic liver disease selection criteria. Results found that out of the 2,108 individuals identified through this method, the use of aspirin remained significantly associated with a decrease in composite fibrosis index of 0.22 SD (95% CI: -0.38 to -0.06; P=0.008).

In addition to lowering indices, aspirin was also associated with significantly reduced odds of stage 3–4 fibrosis among those with suspected alcoholic liver disease by APRI. To authenticate this finding, researchers also examined a larger subgroup with alcohol abuse — as individuals with advanced liver disease may display normal function — finding aspirin was associated with OR of 0.37 and 0.16 as predicted by FIB4 and APRI respectively.

Aspirin promotes antiplatelet activity, which has been used for the prevention and treatment of coronary artery disease. In animal tests, platelet activation has been shown to trigger liver fibrosis. Aspirin’s antiplatelet component can possibly halt this process, and the progress of liver fibrosis. The authors contend that their research further supports the emerging evidence for a critical pathological link between platelet activation and liver fibrosis. They suggest further trials to determine anti-platelet’s ability to delay liver fibrosis in patients who are at risk.

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