Page 906 - Small Animal Internal Medicine, 6th Edition

878 PART VI Endocrine Disorders

The prognosis for dogs with PDH depends in part on the hyperadrenocorticism, but transverse diameter did not differ
age and overall health of the dog and on the client’s commit- between PDH and occult hyperadrenocorticism dogs. The
VetBooks.ir ment to therapy. The mean life span of affected dogs after authors speculated that occult hyperadrenocorticism not
caused by an adrenal tumor may be due to increased 24-hour
diagnosis of PDH is approximately 30 months. Younger dogs
may live considerably longer (i.e., 5 years or longer). Many
dogs ultimately die or are euthanized because of complica- cortisol secretion, an increase that may not be detected using
routine screening tests.
tions related to hyperadrenocorticism (e.g., pituitary macro- Currently, an ACTH stimulation test with measurement
tumor syndrome) or other geriatric disorders. of serum and plasma adrenocortical steroid precursor hor-
mones is used to identify occult hyperadrenocorticism in
dogs. The most common finding is an increase in pre- and
OCCULT (ATYPICAL) post ACTH stimulation serum 17-hydroxyprogesterone con-
HYPERADRENOCORTICISM IN DOGS centrations. Currently, the only laboratory with established
reference ranges for precursor and sex steroids is the Endo-
Occult hyperadrenocorticism is defined as a syndrome in crinology Laboratory at the University of Tennessee, College
which a dog appears to have hyperadrenocorticism based on of Veterinary Medicine, in Knoxville, Tennessee. Treatment
history, physical examination and clinicopathologic findings, recommendations have included low dosages of mitotane
but results of the ACTH stimulation test, LDDS test, and and trilostane, although Sieber-Ruckstuhl et al. (2006) failed
UCCR are within reference ranges. Possible explanations for to document a decrease in 17-hydroxyprogesterone concen-
occult hyperadrenocorticism include dogs early in the course tration in dogs with PDH treated with trilostane.
of hyperadrenocorticism, dogs that have a disease that We do not routinely measure serum adrenocortical pre-
mimics some of the clinical manifestations of hyperadreno- cursor hormones when evaluating dogs for hyperadrenocor-
corticism (e.g., Alopecia X), and dogs that have increased of ticism. If results of the LDDS test and UCCR are normal or
adrenocortical precursor hormones such as progesterone equivocal, we look for another cause for the clinical signs. If
and 17-hydroxyprogesterone (see Fig. 50.15). Adrenal another cause is not identified and clinical signs are mild, we
tumors that secrete progesterone may cause a clinical syn- recommend waiting and testing for hyperadrenocorticism if
drome that mimics hyperadrenocorticism in dogs and cats. progression is noted. Readers are referred to Behrend et al.
Clinical signs presumably result from intrinsic glucocorti- (2013) in the suggested reading section for more information
coid activity of progestins, progestin-induced displacement on occult hyperadrenocorticism.
of cortisol from cortisol-binding protein in the circulation,
or both. Cortisol concentrations are inappropriately low on
hyperadrenocorticism screening tests in dogs and cats with HYPERADRENOCORTICISM IN CATS
progesterone secreting tumors.
Abnormal secretion of adrenocortical precursor hor- Hyperadrenocorticism is uncommon in cats. Although
mones has been proposed as a cause of occult hyperadreno- many of the clinical characteristics of feline hyperadrenocor-
corticism but this proposal is controversial, in part, because ticism are similar to those seen in dogs, some important
adrenocortical precursor hormones have not been proven to differences should be emphasized. Most notable is the very
cause occult hyperadrenocorticism. Results of studies aimed strong association with diabetes mellitus; the progressive,
at documenting a relationship between adrenocortical pre- relentless weight loss leading to cachexia; and dermal and
cursor hormones and generation of the clinical abnormali- epidermal atrophy leading to extremely fragile, thin, and
ties affiliated with this syndrome are conflicting and easily torn and ulcerated skin (i.e., feline fragile skin syn-
improvement of clinical signs after mitotane and trilostane drome) in cats with hyperadrenocorticism. Establishing the
treatment unpredictable. diagnosis can be difficult, abnormalities on routine blood
Alterations in concentrations of adrenocortical precursor and urine tests that are suggestive of hyperadrenocorticism
hormones before and after ACTH stimulation has been used in dogs are usually absent in cats, and medical treatment for
to establish the diagnosis. Because these precursor hormones hyperadrenocorticism in cats is not consistently effective.
precede cortisol in the production pathway, dogs with hyper-
adrenocorticism also have increased concentrations of pre- Etiology
cursor hormones, as can dogs with nonadrenal illness, and Hyperadrenocorticism in cats may be classified as pituitary
healthy female dogs during estrus, diestrus, and pregnancy. dependent (PDH) or adrenocortical tumor dependent
A recent study by Frank et al. (2015) documented higher (ADH). Approximately 80% of cats with hyperadrenocorti-
serum cortisol concentrations during a 9-hour blood sam- cism have PDH and 20% have ADH, with 50% of adrenal
pling period in dogs with occult hyperadrenocorticism com- tumors being adenomas and 50% carcinomas. Cats with
pared with control dogs but lower cortisol concentrations PDH have a pituitary microadenoma, macroadenoma, or
compared with dogs with pituitary-dependent hyperadreno- carcinoma identified at necropsy. Iatrogenic hyperadreno-
corticism. In addition, average transverse adrenal gland corticism is uncommon in cats; typically prednisone or pred-
diameter determined by abdominal ultrasound was less in nisolone administration for months is required before
control dogs compared with dogs with PDH and occult clinical signs occur.