HYALURONIC ACID

Hyaluronic Acid is associated with liver function and liver fibrosis.

Since 1996 the incidence of liver related deaths in the UK has risen by almost 50% from 8.6 deaths per 100,000 to 12.7 deaths per 100,000 of the male population. In 2001 chronic liver disease was the cause of death for 7% of UK men and 6% women who died under 45 years of age. This represents more men than died of Parkinson’s disease and more women than died of cervical cancer. Liver disease is now the fifth most common cause of death in the UK after heart disease, stroke, chest disease and cancer (http://www.statistics.gov.uk/. However, unlike the other main causes of death, liver disease mortality rates are increasing rather than declining.

Non-invasive Serum Markers

Significant scientific and commercial investment has been made over the last ten years to develop serum markers capable of predicting fibrotic stages of chronic liver disease. These markers include indirect markers (including most of the standard LFT’s) and direct markers.

Of the direct markers Hyaluronic Acid (HA) appears interesting. Hyaluronic Acid is removed by the liver via sinusoidal cell adhesion molecules. Fibrosis impedes this removal process and causes a rise in the serum Hyaluronic Acid. Rises in the level in serum Hyaluronic Acid increase with the development for liver fibrosis. The notion of being able to use a marker for routine assessment that reflects the function of the sinusoidal endothelial cells, rather than the hepatocytes themselves, is an exciting concept. (Journal of Clinical Pathology 2008)

Hyaluronic Acid would appear to be a reliable surrogate marker in distinguishing three clinically relevant stages of fibrosis: absent/minimal, intermediate, and advanced. It also has breadth of application to reflect the severity of liver inflammation, fibrosis, and fibrogenesis in patients with alcoholic liver disease, and is useful as a marker of pre-cirrhotic and cirrhotic stages. Hyaluronic Acid is also a valid non-invasive predictor of hepatic fibrosis in unselected children with liver disease.

We can accept serum markers may not discriminate the stage of fibrosis as accurately as biopsy and we can also accept that both indirect and direct markers have intrinsic limitations. We also know that there is no biochemical marker yet available that can differentiate between Fatty Liver or NASH – but serum markers can identify preliminary liver fibrosis and there is an overall opinion that the combination of non-invasive direct markers with indirect markers is a likely to continue to set future trends in liver fibrosis diagnosis.