The results of a low dose dexamethasone suppression test may suggest ADH vs PDH, but do not confirm it.
In ADH, the adrenal tumour(s) secrete excess cortisol which inhibits the release of endogenous ACTH. In PDH, the pituitary lesion produces excess ACTH which stimulates the adrenal glands to produce excess cortisol. The measurement of endogenous ACTH has been found to be useful in discriminating between the two conditions. An elevated ACTH is evidence of pituitary-dependent hyperadrenocorticism, but it is important to note that a normal ACTH does not rule out pituitary hyperadrenocorticism as some dogs with pituitary disease do not have elevated endogenous ACTH (this is assumed to be due to the pulsatile nature of ACTH secretion, even by pituitary tumours).
ACTH Levels (Scott-Moncrieff et al)
(Note: lower limit of detection is 10 pg/mL)
| Normal dogs |
<15.3 pg/mL |
| ADH |
<10 pg/mL |
| PDH |
>15.6 pg/mL** |
**Scott-Moncrieff reported that approximately 55% of cases (6/11) confirmed as having PDH had elevated endogenous ACTH (this is similar to the proportion reported for other methods). In a preliminary study at VETPATH, 75% of dogs (9/12) with LDDST results consistent with hyperadrenocorticism (PDH or ADH) had elevated ACTH levels indicative of PDH.