Page 91 - Clinical Small Animal Internal Medicine

7 Pituitary-Dependent Hyperadrenocorticism in Dogs and Cats 59

time was 617 days for all cats (range 80–1278 days). Based on the above literature review, we offer the fol­
VetBooks.ir Complications included weight loss, urinary tract infec­ lowing recommendations for monitoring canine patients
receiving trilostane therapy.
tions, chronic kidney disease, seizures, and recurrent
pancreatitis. Hypocortisolemia was documented in one
case. Cause of death occurred as a result of nonadre­ Unwell Dogs, Stressed Dogs, and Dogs With Concurrent Illness
nal or nondiabetic illnesses (renal failure, seizures Perform an ACTH stimulation test.
[caused by hypoglycemia or unknown]), or lymphoma. ● Perform an electrolyte panel and evaluate for signs of
Trilostane ameliorates clinical signs of HAC in cats, is ● mineralocorticoid suppression.
tolerated well in the long term, and can lead to improved
regulation of diabetes. It should be considered as first‐ Clinically Well and Controlled Dogs (Per Client Questionnaire
line therapy for cats undergoing medical management and/or History)
of PDH.
Adrenocorticotropic hormone stimulation testing ● Pre‐trilostane cortisol <1.4 μg/dL: decrease dose by
should be performed 10, 30, and 90 days after start of 10% or perform an ACTH stimulation test.
treatment and 30 days after each dose adjustment. ● Pre‐trilostane cortisol 1.4–5 μg/dL: continue current
Trilostane is well tolerated in most dogs. Adverse effects dose.
that are usually mild and self‐limiting include diarrhea, ● Pre‐trilostane cortisol >5 μg/dL: reevaluate history and
vomiting, and lethargy in up to 63% of treated dogs. consider splitting dose to twice daily (if currently once
The ACTH stimulation test is the monitoring method daily), or a small dose increase, based on clinical signs.
for patients on trilostane therapy for which we have the
most clinical experience and have reliably used for clini­ Clinically Undercontrolled Dogs
cal decision making for a decade. However, the correla­ Pre‐trilostane cortisol <1.4 μg/dL: reevaluate history
tion of test results with the patient’s clinical well‐being ● and diagnosis; perform an ACTH stimulation test;
has been questioned by multiple researchers. As with consult with a specialist.
many endocrine tests, there is not one definitive meth­ Pre‐trilostane cortisol 1.4–5 μg/dL: this is currently a
odology that can be applied to all patients. ● gray zone. Depending on the patient, consider splitting
The ACTH stimulation test remains the test of choice
in any canine patient found to be clinically unwell by the dose to twice daily, if currently on once‐daily dos­
ing, or consider a dose increase if >3 μg/dL.
either the owner or the veterinarian. Oversuppression Pre‐trilostane cortisol >5 μg/dL: increase dose fre­
of cortisol production can occur with any medical ther­ ● quency (from once daily to twice daily) or dose.
apy for hyperadrenocorticism and can develop insidi­
ously or acutely. Occasionally, dogs have developed hypoadrenocorticism,
Recently in Europe, the cost of cosyntropin has incre­ which is generally glucocorticoid deficient only, although
ased significantly. This, along with the multiple publica­ dogs with evidence of mineralocorticoid deficiency have
tions showing a lack of correlation between the ACTH been reported. Hypoadrenocorticism induced by trilos­
stimulation test results and patients’ clinical well‐being, tane is generally reversible, although in rare cases this
led a group of researchers to investigate the value of may take several months, likely because of adrenocorti­
examining a single, unstimulated, cortisol result prior to cal necrosis. There have been anecdotal reports of acute
the administration of trilostane. death shortly after starting trilostane treatment.

Mitotane vs Trilostane
Procedure/Protocol
Studies have been performed comparing trilostane with
1) Owners are instructed to bring their dog to the veteri­ mitotane in dogs with PDH or adrenal tumors. In a ret­
nary hospital prior to receiving the morning dose of rospective study of dogs treated with either mitotane
trilostane. (n = 25) or trilostane (n = 123), long‐term survival was not
2) The owners are then asked questions regarding con­ statistically different between the groups. Median sur­
trol of clinical signs, with or without the use of a ques­ vival in the mitotane group was 708 days (range 33–1399),
tionnaire. If any signs of cortisol oversuppression are and in the trilostane group was 662 days (range 8–1971).
noted, such as vomiting, anorexia, hyporexia, or leth­ Of the dogs that died in this study, 11% died due to causes
argy, trilostane is not given, and a baseline cortisol that were attributed to the underlying PDH, and a fur­
and/or an ACTH stimulation test is performed to rule ther 17% died of causes that could have been related to
out hypoadrenocorticism. their underlying PDH. In 38% of cases, the cause of death
3) A serum sample is collected for the measurement of could not be directly attributed to PDH, and in 34% the
cortisol. cause of death was unknown.