Cause
Hyperadrenocorticism results from overproduction of adrenal glucocorticoids.
Approximately 80% of cases are caused by an ACTH secreting pituitary tumour.
This excess of ACTH causes bilateral symmetrical adrenal enlargement and
hyper-secretion of cortisol. The remaining cases are due to a primary adrenal
tumour.
Signalment and Clinical Signs
Clinical signs can be extensive but include polyuria, polydipsia, polyphagia,
generalised alopecia, hepatomegaly, muscle weakness, pot belly, thin skin,
bruising and in some cases neurological signs consequent upon a pituitary
tumour.
Diagnostic Tests
It is crucial to understand that all of the diagnostic tests have limitations
and all can give both false negative and false positive results. It is therefore
particularly important to use the tests to support a clinical suspicion
of hyperadrenocorticism: The diagnosis should not rely upon the results
of blood tests alone.
Routine biochemistry and haematological abnormalities
Increases in ALKP present in 80-90 % of cases. Mild hypercholesterolaemia
also common. Typical stress leukogram (mature neutrophilia, lymphopenia
and eosinopenia) often seen.
ACTH stimulation test
Collect fasting whole blood sample, administer 250mg synthetic ACTH intramuscularly,
collect a second blood sample one hour later. Request cortisol assay on
pre and post samples.
Low dose dexamethasone suppression test
Collect fasting whole blood sample, administer 0.015 mg/kg dexamethasone
intravenously, collect additional blood samples three and eight hours later.
Measure cortisol in each sample.
The interpretation of the ACTH stimulation and low dose
dex suppression tests is influenced by the history, routine laboratory findings,
and recent drug therapy. Please provide Axioms clinical pathologists with
the relevant history to help get the most out of the tests performed.
Treatment
Surgical removal of an adrenal tumour can be considered in those patients
with no evidence of metastatic spread. This is an intensive procedure requiring
appropriate facilities but is potentially curative. Most dogs are medically
managed. Vetoryl (Trilostane) has recently been licensed (see
Axiom Endocrine Factsheet 2.1). Mitotane (Lysodren) therapy remains
commonly used drug for treating HAC. Starting dose is approximately 50mg/kg
daily for 7-10 days. Once initial control is achieved this dose can be decreased
to weekly in most dogs.
Therapeutic Monitoring
Monitoring of therapy should consist of clinical evaluation and results
of an ACTH stimulation test. In dogs receiving Trilostane treatment, the
ACTH stimulation test should be performed 4-6 hours after giving that day's
medication. Cortisol results from 50-100 nmol/L pre and post-ACTH are indicative
of good control if receiving mitotane therapy. |