Page 120 - Clinical Small Animal Internal Medicine

88 Section 2 Endocrine Disease

Patients with both atypical HOAC and secondary HOAC, the administered glucocorticoid or progestogen
VetBooks.ir HOAC have similar clinical signs of isolated cortisol causes decreased ACTH production from the pituitary
gland. Decreased ACTH production results in atrophy
deficiency. Endogenous ACTH concentrations should be
measured to differentiate between secondary and pri-
to decreased cortisol production. Since ACTH is not
mary hypoadrenocorticism. High concentrations indi- of the zonae fasciculata and reticularis, leading
cate that the patient has primary HOAC (due to lack of required for the synthesis of aldosterone from the zona
cortisol’s negative feedback on the pituitary), whereas glomerulosa, electrolyte abnormalities do not occur.
low to unmeasurable concentrations are consistent with
secondary HOAC. If secondary HOAC is diagnosed, Epidemiology
imaging of the brain is recommended, to rule out a pitui-
tary/hypothalamic lesion; however, a distinct anatomic Hypoadrenocorticism is rare in cats, with fewer than 50
lesion may not be identified. cases reported in the literature.

Therapy Signalment
Therapy for atypical HOAC consists of glucocorticoid
replacement, usually with prednisone, given at 0.1– Unlike in dogs, there are no sex, age, or breed predisposi-
0.25 mg/kg/day. Some patients do well on even lower tions. Affected cats range in age from 1.5 to 14 years. The
dosages, particularly big dogs. The author has used majority of reported cases have been domestic short‐ or
dosages as low as 0.03 mg/kg/day. The goal is to admin- long‐haired cats, but two British shorthair cats have also
ister enough prednisone to control the clinical signs of been reported.
HOAC, while not causing steroid side‐effects.
Additional prednisone (2–4 times the normal dose) is History and Clinical Signs
recommended during times of stress.
Approximately 10% of dogs with atypical hypoadreno- Clinical signs and historical findings are similar to
corticism develop signs of mineralocorticoid deficiency those described in dogs. The signs may be chronic
(electrolyte abnormalities) weeks to months after the ini- (months) or acute (several days), and may wax and
tial diagnosis (usually within one year). It is impossible to wane. Owners may note improvement following
predict which dogs will develop electrolyte abnormali- treatment with fluids and/or glucocorticoids. The
ties, so reevaluation of the electrolytes is recommended most commonly reported signs include lethargy,
at one and three months following initial diagnosis, and inappetence, and weight loss. Vomiting, PU/PD, and
then every six months thereafter. constipation can also occur. In contrast to dogs, diar-
rhea has not been reported.
Prognosis Physical examination usually reveals depression, weak-
Prognosis for atypical hypoadrenocorticism is excellent, ness, dehydration, and hypothermia. About half of the
provided that the owners continue to administer medi- cats present in hypovolemic shock, characterized by pro-
cation as recommended. Almost all patients die of dis- longed capillary refill time and weak femoral pulse.
ease unrelated to hypoadrenocorticism. Collapse, ataxia, bradycardia, and abdominal pain are
less common.

Hypoadrenocorticism in Cats Diagnosis
Clinicopathologic findings in cats with HOAC are sim-
Etiology/Pathophysiology
ilar to those in dogs with HOAC. Hyponatremia and
Hypoadrenocorticism is rare in cats. Most cases are idi- hyperkalemia are almost always present, although one
opathic, but suspected to be due to immune‐mediated may occur without the other. Most cats are also
destruction of the adrenal cortex. Neoplastic infiltration hypochloremic, azotemic, and hyperphosphatemic.
and abdominal trauma have also been reported to cause Although the azotemia is usually prerenal, most
HOAC in cats. Concurrent glucocorticoid (cortisol) Addisonian cats have a urine specific gravity <1.030.
and mineralocorticoid (aldosterone) deficiency occurs in Hypercalcemia, hypoglycemia, and acidemia are less
most cats, and isolated glucocorticoid deficiency (“atypi- common than in Addi sonian dogs, but can be severe.
cal” hypoadrenocorticism) is rare. Secondary iatrogenic Alanine aminotransferase, alkaline phosphatase, and
hypoadrenocorticism can result from glucocorticoid bilirubin may be mildly increased. Complete blood
or progestogen (megesterol acetate) administration, but count may reveal mild anemia and lymphocytosis;
this is uncommon. In cases of secondary iatrogenic alternatively, lack of a stress leukogram (neutrophilia