Sindrome De Cushing Em Cães

Cushing's isn't always obvious on paper, but it shows up everywhere in the clinic

You see a middle-aged golden retriever come in with polyuria, polydipsia, and a potbelly. Owner says the dog drinks from every puddle in the yard now. Your first instinct is diabetes mellitus. Second is chronic kidney disease. Third — and this one sneaks up — is hyperadrenocorticism, commonly called Cushing's disease. The thing is, these three conditions can look nearly identical in the earliest stages. You need the right tests to separate them, and you need to know which test actually matters when you're staring at a wall of results at 7pm on a Friday.

O que é sindrome de cushing em cães: diagnóstico e tratamento na prática

Cushing's in dogs happens when there's too much cortisol circulating. Cortisol is a steroid hormone produced by the adrenal glands. It's supposed to be part of the stress response. The problem starts when it's always on. There are three main forms. Pituitary-dependent hyperadrenocorticism (PDH) accounts for about 80 to 85 percent of cases. The pituitary gland produces too much ACTH, which drives the adrenals to overproduce cortisol. Adrenal-dependent Cushing's — a tumor on one of the adrenal glands — makes up most of the rest. Iatrogenic Cushing's comes from prolonged glucocorticoid administration, usually steroids given for allergies or autoimmune disease. That one is reversible once you taper off the drug, though it takes months for the HPA axis to recover. The classic signalment is a dog between 6 and 12 years old, female intact, medium to large breed. But I've seen it in a 5-year-old Miniature Schnauzer and a 14-year-old Chihuahua. Age and breed are hints, not criteria.

Diagnosis starts with a chemistry panel and urinalysis. You'll see hypercholesterolemia, elevated ALP, mild ALT elevation, and a low urine specific gravity — usually below 1.030. That USG is your first red flag. A dog drinking that much water should concentrate urine. When it doesn't, something is interfering with the renal concentrating mechanism. Cortisol does exactly that. But here's the trap: USG can also be low in diabetes insipidus, pyometra, and some kidney diseases. So you can't stop there. The screening tests are the ACTH stimulation test and the low-dose dexamethasone suppression test (LDDST). Neither is perfect. The ACTH stim has a sensitivity around 78 percent and specificity near 90 percent. That means roughly one in five Cushing's cases will have a normal response on that test. The LDDST is more sensitive — about 92 percent — but slightly less specific. In my experience, running both together catches the vast majority of cases. If the ACTH stim is borderline and the LDDST is equivocal, I run a second LDDST a few weeks later. Dogs with exogenous steroid exposure or severe non-endocrine illness can throw off both tests.

Once you've confirmed hypercortisolism, you need to localize the problem. The high-dose dexamethasone suppression test (HDDST) helps distinguish pituitary from adrenal disease. Pituitary tumors often still suppress slightly at high doses, while adrenal tumors never suppress. But here's where people get tripped up: about 15 percent of PDH cases won't suppress on HDDST either. And a small adrenal carcinoma can sometimes show partial suppression. MRI or abdominal ultrasound is the definitive localization tool at this point. I recommend ultrasound first — it's cheaper, faster, and can reveal adrenal asymmetry or a pituitary macroadenoma in most cases. Skip straight to MRI only when ultrasound is inconclusive and surgery is being considered. Treatment depends on the form. For PDH, the drug of choice is trilostane. It inhibits 3-beta-hydroxysteroid dehydrogenase, blocking cortisol synthesis. The starting dose is typically 2 to 5 mg per kilogram once daily, given with food. You recheck an ACTH stimulation test 4 to 6 hours after dosing on day 14. The goal is a post-ACTH cortisol between 1.4 and 5.6 mg/dL. Some dogs do well at 2.0, others need the upper end. You adjust the dose based on those numbers and clinical response. If the pre-ACTH cortisol is below 0.5, you've overdosed and risk Addisonian crisis. That's an emergency. Reduce the dose by 25 to 50 percent and recheck in a week.

Mitotane is the older alternative. It's cheaper but more unpredictable. It destroys the adrenal cortex in a staged way, which means monitoring is more involved and side effects like gastrointestinal upset and liver enzyme changes are more common. I reserve mitotane for cases where trilostane isn't tolerated or isn't available. Adrenal tumors are a different story. Surgical removal is curative if the tumor is confined, but about 10 to 15 percent are malignant and have already metastasized. Pre-op CT scanning is worth it if your facility has one. It maps the tumor's relationship to the caudal vena cava and portal vein — structures that bleed dangerously during removal. If surgery isn't an option, trilostane can manage the clinical signs, though the required doses tend to be higher than for PDH.

Iatrogenic Cushing's requires no drug treatment. Slow taper of the offending glucocorticoid over 4 to 8 weeks allows the adrenal glands to recover. Some dogs need temporary supportive care during the withdrawal phase, especially if they've been on high doses for longer than three months. The hypothalamic-pituitary-adrenal axis suppression can persist for months after the drug is stopped. Don't rush the taper just because the skin lesions are improving. Monitoring is where most owners and some clinicians cut corners. Every three months on trilostane, you need a clinical recheck and an ACTH stim. Blood work every six months catches the early signs of kidney or liver changes. Owners should track water intake at home. A sudden spike in consumption often means the dose is too low. Sudden vomiting, lethargy, and anorexia — that's too high. I give every owner a printed log sheet. They write down the daily water consumption in milliliters. It's the single most useful data point between vet visits.

One edge case I want to mention: concurrent disease. I had a case last year — a 9-year-old Labrador with what looked like straightforward Cushing's. The ACTH stim was diagnostic, trilostane was started, and the polydipsia improved. But the dog kept losing weight. The Cushing's was controlled, so why the weight loss? Turns out there was a subtle exocrine pancreatic insufficiency hiding underneath. Cushing's can mask EPI because the two conditions affect appetite and stool quality in opposite directions. Once we added pancreatin supplementation, the weight came back. Always think about comorbidities. Cushing's doesn't exist in a vacuum. Prognosis is generally good for PDH managed with trilostane. Median survival times exceed three years in most studies, and many dogs live out their natural lifespan. Quality of life is usually excellent once the dose is stabilized. Adrenal tumor cases depend entirely on whether the tumor is benign or malignant. Benign tumors removed surgically have a median survival of over two years. Malignant ones vary widely — some respond to trilostane for a year or more, others progress quickly.

The hardest part isn't the diagnosis or the medication. It's the owner compliance. This is a lifelong condition. Miss a dose for two days and the symptoms return. Skip the recheck ACTH stim for six months and you might miss developing hypoadrenocorticism. It requires patience and a willingness to deal with blood draws and dosing adjustments indefinitely. Dogs that get consistent care do well. Dogs that fall out of the monitoring program are the ones that end up in crisis.