January 13, 2016
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Aspirin lowers indices in liver fibrosis, may reduce CLD

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In a cross-sectional analysis, researchers found aspirin use was associated with decreased indices for liver fibrosis, suggesting aspirin can reduce further liver injury and chronic liver disease, according to published findings.

Researchers evaluated data of 1,856 patients with suspected chronic liver disease (CLD) from the National Health and Nutrition Examination Survey III. The researchers sought to determine any association between aspirin use and liver fibrosis among adults with CLD, due to the fact that previous mouse models studied showed that anti-platelet agents, such as aspirin, decrease liver fibrosis. Using four validated fibrosis indices and a composite index, the researchers were able to measure liver fibrosis among this cohort of patients.

“Because fibrosis is typically a consequence of liver injury, we focused primarily upon individuals with liver disease or strong risk factors, such as viral hepatitis, alcohol abuse and nonalcoholic steatohepatitis,” the researchers wrote.

Overall, the use of aspirin was associated with a lower composite liver fibrosis index calculated from Fibrosis-4 score, aspartate aminotransferase-to-platelet ratio index (APRI) score, Forns score and nonalcoholic fatty liver disease fibrosis score (95% CI, − 0.42 to − 0.06; P = .009).

The association of aspirin with lower fibrosis scores was higher among patients with suspected CLD compared to those without suspected CLD (− 0.23 vs. − 0.03 standard deviation units; P = .05). Multivariate logistic regression analysis showed aspirin use was associated with a reduced odds of developing stage 3 or 4 fibrosis among patients with suspected alcoholic liver disease (OR =  0.21; 95% CI, 0.06-0.67) by APRI score.

The negative association between aspirin use and lower fibrosis index was similar across all four fibrosis indices (P = .002-.08) in patients with chronic viral hepatitis, suspected alcoholic liver disease and NASH.

In parallel analyses, ibuprofen use was not associated with any liver fibrosis index in any type of CLD (P = .1-1).

The researchers concluded: “Our observations support the emerging experimental and clinical evidence for a critical pathological link between platelet activation and liver fibrosis. Clinical equipoise is emerging that may justify prospective randomized trials of aspirin, and potentially other antiplatelet drugs to determine their ability to delay or diminish the progression of liver fibrosis in patients with various forms of chronic liver diseases.” – by Melinda Stevens

Disclosure: The researchers report no relevant financial disclosures.