Can We Treat Hepatic Fibrosis?

Small amounts of fibrous tissue are normally found in the healthy liver in the capsule, peri-vascular connective tissue and surrounding portal triads. Excessive fibrosis is a common, important, nonspecific, secondary response to hepatic injury. Several serum biomarkers of hepatic fibroplasia have been validated in human medicine, including hyaluronate, alpha- smooth muscle actin, AST:platelet ratio and the ‘FibroTest’ which combines serum haptoglobin, alpha 2 macroglobin, GGT, apolipoprotein A1, bilirubin, age and gender. Investigation of some of these variables has occurred in horses although none has achieved significant clinical use. In this author’s experience serum globulin concentrations >50 g/l or bile acids >30 mmol/l found in horses with liver disease are almost invariably associated with significant hepatic fibrosis. Although there is evidence that ultrasonography can detect hepatic fibroplasia in horses (Durhamet al. 2003a), veterinary surgeons are essentially reliant on biopsy or autopsy specimens to recognise fibrosis in horses’ livers.

In one study, excessive hepatic fibrosis was found in 33 of 73 biopsy specimens collected from horses with suspected liver disease but not in any of 12 biopsy specimens collected from horses with no prior suspicion of liver disease (Durham et al.2003b). There are essentially 3 patterns of fibrosis in a diseased liver, all of which are controlled by hepatic stellate cells: fibroplasia extending between portal tracts (porto-portal), between central veins (centro-central) and from portal tracts to central veins (centro-portal). Porto-portal fibroplasia is by far the most commonly encountered pattern in equine liver disease. [...]