Introduction Hyaluronan is a glucosaminoglycan synthesized by the mesenchymal cells and degraded by hepatic sinusoidal endothelial cells by a specific receptor-mediated process. Elevated levels are associated with the sinusoidal capillarization that is seen in cirrhosis. Methodology Serum hyaluronan was measured, using a radiometric assay (Pharmacia, Sweden) in 221 patients with biopsy-proven chronic liver disease of a variety of aetiologies (alcoholn= 70, autoimmune chronic active hepatitisn= 23, primary biliary cirrhosisn= 17, hepatitis Cn= 69, cryptogenicn= 15, variousn= 27). All patients were fasted, and their liver function tests, full blood count, prothrombin time and Child-Pugh score were assessed at the time of the liver biopsy. Results Hyaluronan levels (μg/l) were significantly higher in patients with liver cirrhosis (cirrhosisn= 127, mean 440, 95% CI 367-515) (P<0.0001) compared with hepatic fibrosis (n= 23, mean 144, 95% CI 69-190), chronic hepatitis (n= 60, mean 63, 95% CI 37-91) and fatty liver (n= 11, mean 107, 95% CI 37-177). Within the cirrhotic population, there was no significant difference in hyaluronan levels between different aetiologies, but hyaluronan level increased proportionally to the severity of cirrhosis. Overall, a hyaluronan level > 100 μg/l had a 78% specificity and 83% sensitivity for diagnosing cirrhosis, while the specificity was increased to 96% for all patients with hyaluronan levels > 300 μg/l. The highest specificity and sensitivity were seen at a cut-off value of 100 μg/l in patients with alcohol-associated liver disease (89%, 87%) and hepatitis C (93%, 72%) respectively. Within patient cohorts, there was a significant correlation (P< 0.01) between hyaluronan and albumin, platelet count and bilirubin, but not with alanine aminotransferase. Conclusion Measurement of fasted serum hyaluronan reliably differentiated cirrhotic from non-cirrhotic liver disease and can be regarded as a useful test in the diagnosis of liver cirrhosis, particularly when a liver biopsy is contraindicated.
The Royal Infirmary, Edinburgh EH3 9YW, UK A selection of interesting papers that were published in the month before our press date in major journals likely to report important results in gastroenterology and hepatology.
Aliment Pharmacol Ther 31 , 679–692 Summary Background Non‐alcoholic fatty liver disease affects 10–35% of the adult population worldwide; there is no consensus on its treatment. Omega‐3 fatty acids have proven benefits for hyperlipidaemia and cardiovascular disease, and have recently been suggested as a treatment for non‐alcoholic fatty liver disease. Aims To review the evidence base for omega‐3 fatty acids in non‐alcoholic fatty liver disease and critically appraise the literature relating to human trials. Methods A Medline and PubMed search was performed to identify relevant literature using search terms ‘omega‐3’, ‘N‐3 PUFA’, ‘eicosapentaenoic acid’, ‘docosahexaenoic acid’, ‘non‐alcoholic fatty liver disease’ and ‘NAFLD’. Results Omega‐3 fatty acids are important regulators of hepatic gene transcription. Animal studies demonstrate that they reduce hepatic steatosis, improve insulin sensitivity and reduce markers of inflammation. Clinical trials in human subjects generally confirm these findings, but have significant design inadequacies. Conclusions Omega‐3 fatty acids are a promising treatment for non‐alcoholic fatty liver disease which require to be tested in randomized placebo‐controlled trials.
The Royal Infirmary, Edinburgh EH3 9YW, UK A selection of interesting papers that were published in the month before our press date in major journals likely to report important results in gastroenterology and hepatology.
The Royal Infirmary, Edinburgh EH3 9YW, UK A selection of interesting papers that were published in the month before our press date in major journals likely to report important results in gastroenterology and hepatology.
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