(Boston)– A substantial minority of participants from the Framingham Heart Study, (nearly nine percent), had potentially clinically significant liver fibrosis (scarring). This the first study of this size and scale done in the United States.
“Before this study, we did not know how common asymptomatic liver fibrosis (scarring) was among adults living in the community,” said corresponding author Michelle T. Long, MD, Msc, assistant professor of medicine at Boston University School of Medicine (BUSM).
More than 3,000 middle-aged Framingham Heart Study participants (over a three-year period) underwent a test called a Fibroscan© or vibration-controlled transient elastography that quantifies how much fat is in the liver and also measures the stiffness of the liver. Liver stiffness correlates with the degree of liver scarring.
“We found that liver fibrosis was associated with more adverse cardiometabolic risk factors, even after accounting for liver fat which is a known risk factor for cardiometabolic disease. In particular, we observed that approximately one-quarter of the participants with diabetes had evidence of possibly clinically significant liver fibrosis,” explained Long, who also is a hepatologist at Boston Medical Center.
According to the researchers, these findings support the consideration of screening for liver fibrosis in high-risk groups, though additional studies are needed to determine the benefits/costs of screening. “Liver biopsy is the gold standard for diagnosing liver fibrosis; however, new non-invasive tests exist that can quickly and painlessly help doctors determine if you are at risk for having clinically significant liver fibrosis.”
If liver fibrosis is identified early, before cirrhosis is established, it is treatable. Long believes greater recognition of and awareness of liver fibrosis as a consequence of nonalcoholic fatty liver disease will hopefully allow more patients to receive treatment to prevent complications of advanced liver disease.
These findings appear online in the journal Hepatology.
The Framingham Heart Study is supported by 75N92019D00031. Dr. Long is supported in part by the National Institute of Diabetes and Digestive and Kidney Diseases K23 DK113252, Gilead Sciences, Echosens Corporation, the Doris Duke Clinical Scientist in Development Award, the Boston University School of Medicine Department of Medicine Career Investment Award and the Boston University Clinical Translational Science Institute UL1 TR001430. Dr. Benjamin is supported in part by NHLBI R01HL128914; 2R01 HL092577; American Heart Association, 18SFRN34110082. Dr. Chung is supported in part by the MGH Research Scholars Program. Dr. Loomba receives funding support from NIEHS (5P42ES010337), NCATS (5UL1TR001442), NIDDK (U01DK061734, R01DK106419, P30DK120515, R01DK121378, R01DK124318),NHLBI (P01HL147835), and DOD PRCRP (W81XWH-18-2-0026).
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