Page 906 - Equine Clinical Medicine, Surgery and Reproduction, 2nd Edition

Liver disease 881

VetBooks.ir biopsy specimens, then the most likely explanation increased in horses with hepatic failure, even in the
absence of an inflammatory hepatic disorder. This is
will be other non-hepatic diseases (often GI) that are
provoking these biochemical responses. This sce-
macrophagic Kupffer cells that normally line the
nario might be especially common in young perfor- thought to arise primarily from the loss of hepatic
mance horses, which may demonstrate progressively sinusoids in large numbers to screen and remove
increasing serum concentrations of liver enzymes GI-derived antigenic material arriving in the liver via
such as GGT through training. There are several the hepatic portal veins. Loss of Kupffer cell mass is
possible explanations for this, including increased likely to result in generalised systemic immune stim-
prevalence of GI diseases such as gastric ulceration ulation. The effect of hepatic failure on other acute
and colon acidosis, frequent visceral hypoxaemia phase proteins such as serum amyloid A and fibrino-
during maximal exercise as blood is diverted to exer- gen is variable. This reflects a balance between acute
cising muscles and perhaps even physical trauma to phase protein generation stimulated by the general
the liver during fast work given the hepatic position inflammatory conditions resulting from hepatic fail-
interposed between the diaphragm and colon. ure, versus failure of hepatic synthesis of these acute
One particularly useful application of serum bio- phase proteins. It is generally expected that early/
chemistry is in the establishment of liver disease as mild hepatic failure is associated with increases in
an outbreak, rather than as an individual case. When acute phase proteins, with abnormally low concen-
faced with a horse with evidence of liver disease, it is trations being found in end-stage disease. Hepatic
highly recommended that additional horses on the insufficiency is also sometimes associated with
same premises are evaluated using serum biochem- hypoalbuminaemia in horses, but this appears to be
istry, even if they appear perfectly healthy. In most a less common and milder effect than seen in many
instances this testing will reveal that the concern is other species. Hypoalbuminaemia may result as an
far greater than just the index case, and this diverts effect of a chronic inflammatory status (negative
epidemiological considerations towards possible acute phase protein), typical of hepatic failure, and
infectious or nutritional/toxic causes, which should also as a result of failure of hepatic synthesis of albu-
then be investigated. min. Horses appear to maintain reasonable levels of
Several further serum biochemical analytes can albumin synthesis and the protein appears to have a
be used to indicate remaining hepatic function as longer half-life in horses than other species, which
their serum concentrations relate to the effective- mitigates against this effect. Nevertheless, mild to
ness, or failure, of certain hepatic functions, and moderate hypoalbuminaemia may be seen in some
may have greater prognostic importance for the cases of hepatic failure but alternative causes of this
assessment of a case of liver disease. However, as for finding (especially intestinal disease) should always
serum enzymes, certain confounding factors should be considered. Both serum urea and creatinine have
always be considered when interpreting the results been reported to be abnormally low in cases of hepatic
of these functional markers. For example, normally failure. In the case of low urea, this might arise from
functioning hepatocytes effectively remove bile failure of ureagenesis by the liver. Additionally, both
acids and unconjugated bilirubin from the serum analytes might be lowered by increased diuresis fol-
before they are excreted into bile. Thus, accumu- lowing failure of hepatic aldosterone degradation.
lation in serum is indicative of failure of hepato- Derangements in serum concentrations of amino
cyte function. However, as the uptake of bile acids acids is commonly associated with hepatic insuf-
and bilirubin into hepatocytes depends on cellular ficiency, comprising increased concentrations of
receptors known to have very short half-lives (‘rapid methionine and the aromatic amino acids (AAAs)
turnover proteins’), this process is highly sensitive tyrosine and phenylalanine, and decreased concen-
to a catabolic status and therefore both bile acids trations of the branched-chain amino acids (BCAAs)
and bilirubin will be seen to increase during fast- valine, leucine and isoleucine. Increased AAAs results
ing, anorexia or hypophagia in the absence of hepatic from reduced hepatic clearance, whereas decreased
disease. Total serum globulins are often found to be BCAAs results from increased muscular metabolism.