Pituitary vs. adrenal Cushing’s in dogs is a distinction most owners are never asked to think about – and it changes the treatment. A dog with pituitary-dependent hyperadrenocorticism and a dog with adrenal-dependent hyperadrenocorticism can walk into the same exam room looking exactly alike. Both drink too much. Both are hungry all the time. Both may have a thinning coat, a pot-bellied silhouette, and panting that never quite settles. From the outside, the two are almost indistinguishable.
Underneath, they are different diseases with different origins, different prognoses, and — importantly — different treatment paths. Getting the distinction right is one of the more consequential steps in managing canine Cushing’s, and it is worth understanding what your veterinarian is doing when they order that next round of tests.
The Two Forms, in Plain Terms
Pituitary-dependent hyperadrenocorticism (PDH) accounts for the large majority of canine Cushing’s cases — roughly 80 to 85 percent. The problem starts in the pituitary gland at the base of the brain, usually with a small benign adenoma. That tumor oversecretes ACTH (adrenocorticotropic hormone), and ACTH is the signal that tells the adrenal glands to make cortisol. The adrenals themselves are healthy; they are simply being shouted at continuously. Both adrenal glands respond by enlarging and overproducing.
Adrenal-dependent hyperadrenocorticism (ADH) is the minority form, making up the remaining 15 to 20 percent. Here the pituitary is behaving normally. One adrenal gland has developed a tumor — an adenoma or an adenocarcinoma — that produces cortisol autonomously, ignoring the body’s signalling entirely. Because circulating cortisol is high, the pituitary correctly suppresses its own ACTH output, and the *opposite*, non-tumored adrenal gland shrinks from disuse.
That last detail is the key to the whole diagnostic puzzle. In PDH, both adrenals are enlarged. In ADH, one is enlarged and the other is atrophied. The body’s own feedback loop leaves a signature.
The Tests That Separate Them
Screening tests confirm that a dog *has* Cushing’s. Differentiating tests establish *which kind*. They are not the same step, and the second one often gets skipped when owners are anxious to begin treatment.
Abdominal ultrasound is usually the most informative and least invasive place to start. A skilled sonographer measuring both adrenal glands can often answer the question outright: two symmetrically enlarged glands point to PDH, while one mass with a small or non-visualized partner strongly suggests ADH. Ultrasound also allows assessment of whether an adrenal mass is invading nearby vasculature, particularly the caudal vena cava — a finding that carries real surgical and prognostic weight.
Low-dose dexamethasone suppression testing (LDDS) frequently serves double duty. It is a screening test, but the pattern of the results can also be informative. A dog whose cortisol suppresses at the four-hour mark and then escapes by eight hours is displaying a pattern consistent with PDH. Adrenal tumors, functioning independently of feedback, typically show no meaningful suppression at any point.
High-dose dexamethasone suppression testing (HDDS) applies a stronger signal on the theory that most pituitary adenomas retain at least partial responsiveness to negative feedback, while autonomous adrenal tumors do not. Suppression supports PDH. Failure to suppress is less decisive than it sounds, because a meaningful minority of PDH cases also fail to suppress — so a non-suppressing result narrows the field without closing it.
Endogenous ACTH measurement is the most direct answer available. High or high-normal ACTH indicates the pituitary is driving the process (PDH). Low or undetectable ACTH indicates the pituitary has been appropriately suppressed by an autonomous source (ADH). The caveat is practical rather than scientific: the sample is fragile, requires careful handling and prompt processing, and not every practice is set up to run it reliably.
Why the Distinction Actually Matters
This is not academic tidiness. The two forms diverge on treatment.
PDH is generally managed medically, and often managed well. Trilostane is the mainstay, reducing cortisol production by inhibiting an enzyme in the steroid synthesis pathway. It does not treat the pituitary tumor itself; it manages the downstream consequence. Many dogs live comfortably for years on a stable protocol with periodic monitoring.
ADH introduces a surgical question. If the tumor is confined and has not invaded surrounding vasculature, adrenalectomy can be genuinely curative — a meaningfully different proposition from lifelong medical management. That decision hinges on tumor characteristics, the dog’s overall condition, and access to an experienced surgical team. Where surgery is not an option, medical management remains available, though expectations differ.
There is also a prognostic difference worth being prepared for. Adrenal tumors carry a risk of malignancy, and staging — chest radiographs, careful abdominal imaging — becomes part of the conversation in a way it does not for uncomplicated PDH.
The Question Worth Asking
If your dog has been diagnosed with Cushing’s and treatment has already started, it is entirely reasonable to ask which form was identified and what evidence supported that conclusion. In practice, screening and differentiation sometimes get compressed — a dog is confirmed positive, trilostane is started, and the ultrasound that would have distinguished PDH from ADH never happens.
For most dogs, that shortcut turns out fine, because the odds favor PDH. But the 15 to 20 percent with an adrenal tumor include the subset for whom a surgical cure was genuinely on the table.
For owners weighing adjunct natural support alongside conventional treatment — lignans and melatonin among them — the same principle applies. Know which disease you are managing first. You can read more about the evidence behind those options at lignans.com.
The Bottom Line
Pituitary and adrenal Cushing’s present almost identically and are treated differently. Abdominal ultrasound, dexamethasone suppression patterns, and endogenous ACTH measurement are the tools that separate them. If you do not know which form your dog has, that is a fair and useful question to bring to your veterinarian at the next visit.
Sources
- Merck Veterinary Manual — Cushing Disease (Pituitary-Dependent Hyperadrenocorticism) in Animals. https://www.merckvetmanual.com/endocrine-system/the-pituitary-gland/cushing-disease-pituitary-dependent-hyperadrenocorticism-in-animals
