Hypoadrenocorticism, commonly called Addison’s disease, is a condition in which the adrenal glands fail to produce enough of two critical hormones: cortisol and aldosterone. It affects both humans and dogs, though it is especially well-known in veterinary medicine, where it has earned the nickname “the great pretender” for its ability to mimic other common illnesses. The condition is manageable with lifelong hormone replacement, but without treatment it can become life-threatening.
What the Adrenal Glands Normally Do
You have two adrenal glands, one sitting on top of each kidney, and dogs have the same setup. These small glands produce two main hormones that keep the body running smoothly.
Cortisol, often called the stress hormone, does far more than help you handle stressful moments. It regulates blood pressure, controls blood sugar, reduces inflammation, and manages how the body uses energy from food. Aldosterone handles a different job entirely: it maintains the balance of sodium and potassium in the blood. That balance controls how much salt and water your body retains, which in turn keeps blood pressure stable, nerves firing correctly, and the heart beating in a regular rhythm.
When the adrenal glands are damaged or stop receiving the right signals, production of one or both hormones drops. That shortfall is what defines hypoadrenocorticism.
Primary vs. Secondary Forms
In primary hypoadrenocorticism, the adrenal glands themselves are damaged. The most common cause in both humans and dogs is an autoimmune process, where the body’s own immune system attacks and destroys the outer layer of the adrenal gland. Less frequently, infections, tumors, or certain medications can cause the same destruction. Because the gland itself is the problem, both cortisol and aldosterone production typically drop.
Secondary hypoadrenocorticism originates in the brain. The pituitary gland normally sends a signaling hormone to the adrenals telling them to produce cortisol. When the pituitary fails to send that signal, cortisol production falls, but aldosterone usually remains near normal because it is regulated by a separate system. One common trigger for secondary disease is the abrupt withdrawal of steroid medications after long-term use. The body becomes dependent on the external steroids and the pituitary stops sending its signal; when the medication is suddenly removed, cortisol levels plummet.
How It Presents in Dogs
Hypoadrenocorticism is uncommon in the general dog population, with an estimated prevalence between 0.06% and 0.28%. Certain breeds face dramatically higher risk. Great Pyrenees dogs have a prevalence near 9.7%, and bearded collies and standard poodles have been reported at roughly 9.4% and 8.6%, respectively. West Highland white terriers, Great Danes, Portuguese water dogs, Saint Bernards, and soft-coated wheaten terriers also appear predisposed.
The symptoms can look like almost any other illness, which is exactly why diagnosis is so often delayed. The most common signs owners report are loss of appetite (88% to 95% of cases), lethargy or depression (85% to 95%), and vomiting (68% to 75%). Beyond those, roughly half of affected dogs show weakness and weight loss, and about a third have diarrhea. Less common signs include increased thirst and urination, shaking or tremors, and collapse.
What makes the disease particularly tricky is its pattern. In 25% to 43% of cases, symptoms wax and wane. A dog may seem sick for a few days, then bounce back, only to relapse weeks later. This episodic quality often leads owners and veterinarians to attribute the signs to dietary indiscretion or a mild infection before the real cause is identified.
Symptoms in Humans
People with Addison’s disease experience many of the same core problems: fatigue, weakness, unexplained weight loss, nausea, vomiting, diarrhea, and abdominal pain. Darkening of the skin, particularly in skin creases, scars, and the gums, is a hallmark of the primary form in humans. Dizziness, low blood pressure, and salt cravings are also common because of the aldosterone deficit. Like the canine version, symptoms often develop gradually and can be mistaken for depression, chronic fatigue, or gastrointestinal disorders.
How It Is Diagnosed
The gold-standard test is the ACTH stimulation test. A synthetic version of the pituitary’s signaling hormone is injected, and cortisol levels are measured 30 to 60 minutes later. Healthy adrenal glands respond by producing a surge of cortisol. Damaged glands do not.
Historically, a stimulated cortisol level at or above 18 micrograms per deciliter was considered normal. More recent research using modern, more specific lab assays suggests the true cutoff is closer to 14 to 15 micrograms per deciliter, depending on the testing method. The older threshold was generating a significant number of false positive diagnoses. A baseline cortisol below 2 micrograms per deciliter, before the stimulation injection is even given, is strongly predictive of adrenal insufficiency.
Blood chemistry panels often provide early clues. In the primary form, low sodium and high potassium are classic findings because aldosterone is not doing its job of maintaining that mineral balance. In veterinary practice, a low sodium-to-potassium ratio on routine bloodwork is one of the red flags that prompts the ACTH stimulation test.
Adrenal Crisis: The Emergency
An adrenal crisis, sometimes called an Addisonian crisis, occurs when cortisol levels drop so low that the body can no longer maintain basic functions. Triggers include physical stress such as surgery, illness, or injury in someone (or an animal) whose adrenal glands are already compromised. Symptoms escalate quickly: severe weakness, dehydration, confusion, fainting, fever, abdominal pain, and sometimes seizures or loss of consciousness. Without immediate treatment, an adrenal crisis is fatal. Emergency care centers on rapid intravenous fluid resuscitation and injectable cortisol replacement.
In dogs, the presentation can range from mild dehydration in an alert animal to full cardiovascular collapse with weak pulses and dangerously slow heart rate. About 24% to 29% of dogs with hypoadrenocorticism are in shock or collapse at the time of diagnosis.
Long-Term Treatment
Hypoadrenocorticism requires lifelong hormone replacement. The goal is straightforward: give the body back the hormones the adrenal glands can no longer make.
In dogs, treatment involves two components. A glucocorticoid, typically prednisone, replaces cortisol and controls the gastrointestinal symptoms like vomiting and poor appetite. A mineralocorticoid replaces aldosterone and corrects the sodium-potassium imbalance. The mineralocorticoid can be given as a monthly injection or as a daily oral tablet. The injectable form has no cortisol-like activity, so dogs on that regimen always need a separate glucocorticoid. The oral form does carry some cortisol-like effect, so about half of dogs on it can eventually taper off the separate glucocorticoid.
After diagnosis, dogs typically start on a higher dose of prednisone that is gradually reduced over several weeks to find the lowest effective amount. Larger breeds often do well on very small doses. Regular blood work to monitor sodium, potassium, and overall electrolyte balance guides dose adjustments over time.
Human treatment follows the same logic: daily oral cortisol replacement plus, for primary disease, a mineralocorticoid to manage sodium and potassium. People with Addison’s disease also carry emergency injectable cortisol for situations where oral medication cannot be absorbed, such as during severe vomiting or trauma.
Living With the Condition
With consistent medication, both dogs and people with hypoadrenocorticism can live full, normal-length lives. The key adjustment is recognizing that the body can no longer mount its own stress response. During illness, injury, surgery, or any significant physical stress, hormone doses need to be temporarily increased to mimic the cortisol surge a healthy body would produce on its own. Missing this step is the most common trigger for an adrenal crisis in an otherwise well-managed patient.
For dog owners, this means keeping your veterinarian informed before any procedures, staying alert during times of stress like boarding or travel, and knowing the early warning signs of a relapse: sudden loss of appetite, vomiting, weakness, or unusual lethargy. Because symptoms tend to wax and wane even before diagnosis, some owners initially dismiss early relapses as “just an off day,” which can delay critical care.