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Hyperadrenocorticism, Suspect/Conflicting Results 487

○ Twice-daily administration is recom- ○ Glucocorticoid deficiency common; if • Large carcinomas and AT with widespread
mended. occurs by itself, adrenal glands recover metastasis: poor to fair
VetBooks.ir • Mitotane (o,p′-DDD, Lysodren) ○ Glucocorticoid and mineralocorticoid PEARLS & CONSIDERATIONS Diseases and Disorders
○ See treatment algorithm on p. 1427.
function, usually within a few weeks but
can take months
○ Causes selective destruction of adrenocorti-
cal glucocorticoid-secreting cells; zone that
and treatment for hypoadrenocorticism
secretes aldosterone is relatively spared. deficiency uncommon; often permanent Comments
• The LDDST requires very small volumes of
○ Goal is control of cortisol secretion by needed (p. 512) dexamethasone; it may need to be diluted
PDH and ATH. ○ Mineralocorticoid insufficiency alone for accurate dosing.
○ For ATH, alternative goal is tumor possible but less well understood • Adrenal necrosis can occur with trilostane.
destruction. ○ Hepatopathy with mitotane • If the patient cannot be adequately monitored
ATH treatment requires higher doses (e.g., owner unwilling or unable to provide
■
than PDH because AT is relatively Recommended Monitoring necessary follow-up for ACTH stimulation
resistant to mitotane. • Frequent ACTH stimulation tests needed testing), mitotane and trilostane should not
○ Used in two treatment phases: 1) induc- to assess efficacy of therapy and adjust dose; be used.
tion (or loading), which consists of frequency depends on many factors (see
daily administration, ideally q 12h; 2) treatment algorithms [pp. 1426, and 1427]) Technician Tips
maintenance, in which drug is dosed on • Post-pill timing important with trilostane For endocrine tests, it is best to consult with
a weekly basis, divided into 2-3 doses over but controversial the laboratory concerning testing protocol and
the course of a week. ○ Starting an ACTH stimulation test 2-6 sample handling.
○ Should be given with food to increase hours after pill recommended
drug absorption ○ Post-pill interval should always be the Client Education
○ See treatment algorithm on p. 1426. same for a patient Therapy is lifelong, and close monitoring is
needed; the frequency of testing decreases
Drug Interactions PROGNOSIS & OUTCOME with stabilization. Owners must be able to
• Mitotane: increases barbiturate and warfarin recognize hypoadrenocorticism and know how
metabolism; decreases insulin requirements • Untreated HAC: poor for quality of life; to intervene.
in diabetics. progression rate variable
• Trilostane: do not use in combination with • Treated PDH: good; median survival time SUGGESTED READING
other treatments for HAC. approximately 2 years; dogs tend to die of Behrend EN: Canine hyperadrenocorticism. In
causes unrelated to HAC Feldman EC, et al, editors: Canine and feline
Possible Complications • Macroadenomas and neurologic signs: poor endocrinology, St. Louis, 2015, Elsevier, pp
• For adrenalectomy (p. 35) to grave; macroadenomas with no or mild 377-451.
• For mitotane and trilostane neurologic signs: fair to good with radiation AUTHOR & EDITOR: Ellen N. Behrend, VMD, PhD,
○ Gastrointestinal complications common therapy and medical therapy DACVIM
○ With mitotane, neurologic signs (e.g. • Adrenal adenomas: good to excellent; small
ataxia) uncommon carcinomas (not metastasized): fair to good

Hyperadrenocorticism, Suspect/Conflicting Results Client Education
Sheet

BASIC INFORMATION on biopsy) suggests HAC, but other results are • Clinical signs may be due to presence of a
normal or contradictory. large pituitary tumor: inappetence, anorexia,
Definition stupor, pacing, behavior changes
A scenario in which clinical features and results HISTORY, CHIEF COMPLAINT • Clinical signs may be due to an adrenal
of general biochemical and/or endocrine testing • History sometimes includes clinical signs tumor: ascites, hindlimb edema if it has
conflict with regard to hyperadrenocorticism typical of HAC (p. 485): polyuria/polydipsia, invaded the vena cava
(HAC; Cushing’s disease) polyphagia, panting, pot belly, and skin
changes. PHYSICAL EXAM FINDINGS
Epidemiology • The absence of polyuria/polydipsia makes a • Physical exam abnormalities present would
SPECIES, AGE, SEX diagnosis of HAC unlikely. be typical of HAC (p. 485): alopecia, thin
Middle-aged to older dogs (i.e., those in which • Ensure that the complaint is a new develop- skin, comedones, and others.
HAC occurs commonly) ment (e.g., some dogs are always good eaters). • Rarely, findings suggest abdominal mass or
If polyphagia is due to HAC, it should have pituitary tumor.
Clinical Presentation developed recently.
DISEASE FORMS/SUBTYPES • Finding suggesting HAC is sometimes dis- Etiology and Pathophysiology
One clinical sign (e.g., polyuria/polydipsia, covered incidentally (e.g., increased alkaline • HAC is a slowly progressive disease that can
endocrine alopecia, systemic hypertension), phosphatase [ALP] value on predental blood manifest in multiple ways.
one biochemical abnormality (e.g., increased tests). • Clinical signs, for the most part, are the
alkaline phosphatase activity, proteinuria), or • Inquire about the use of any type of gluco- same whether the HAC is adrenal-dependent,
one other finding (e.g., vacuolar hepatopathy corticoid, including topical preparations. pituitary-dependent, or iatrogenic.

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