Hyperadrenalcorticism
or Cushing’s syndrome is one of the most common endocrinopathies of
the dog. Characteristically
represented by excessive circulating levels of cortisol,
hyperadrenalcorticism has two primary origins:
pituitary-dependent (PDH) and adrenal dependent (ADH).
PDH is the most common form of Cushing’s accounting for
approximately 80-85% of all cases with 90% of those being pituitary
adenomas. In the presence of a
pituitary adenoma, pituitary hyperplasia, or adenocarcinoma, the
secretion of ACTH is not inhibited by the physiologic levels of cortisol.
The excessive secretion of ACTH leads to adrenal cortical
hyperplasia with resultant hypercortisolemia.
In
approximately 60% of dogs with PDH, both adrenal glands will be enlarged
(width and length) and often “plump” in appearance.
The adrenal glands will be well defined and show no evidence of
regional invasiveness. The
adrenal glands may push on, but will not invade into regional blood
vessels such as the caudal vena cava or aorta.
In the other 40% of dogs with PDH, the adrenal glands will be
normal in size, shape and location.
In either case, it is rare to define the inner architecture of
the adrenal glands.
In dogs that
have ADH, typically one adrenal gland is significantly enlarged and the
opposite adrenal gland is small (suppressed).
The enlarged adrenal gland may be well defined, oval to round in
shape (adenoma) or it may be very irregular in shape and may show
evidence of regional invasiveness into adjacent tissues or blood vessels
(adenocarcinoma or pheochromocytoma).
Other
sonographic findings that support a diagnosis of hyperadrenalcorticism
include a diffuse increase in echogenicity of the liver and possibly
decrease definition of the intrahepatic blood vessels (steroid
hepatopathy).
