One of the diseases that struck fear into my heart when I was a newbie vet was hyperadrenocorticism. AKA Cushing’s disease. I barely understood it, could hardly explain it to clients and dreaded diagnosing and treating it.
I’m still not too thrilled about diagnosing and treating it, it’s complicated and messy and requires some diligence, vigilance and more than a little financial output on the part of the clients. However, I have a fairly decent handle on the understanding and explaining of the disease.
I got to thinking about Cushing’s because I had to euthanize a sweet little Chihuahua stricken with it yesterday. She had developed diabetes mellitus as a complication (on top of the Cushing’s). That just opens up a Pandora’s Box of additional requirements for diligence, vigilance, and financial output for this client which proved insurmountable. Euthanasia was the best outcome under these circumstances because her quality of life was poor.
So I haven’t done a particularly educational blog in awhile so I decided to tackle this topic since it’s a bit slow at work today, and who doesn’t like to write about complicated endocrine maladies when they have some free time!
And yes, “Old Broad” (frequent Cone of Uncertainty commenter and confessed crazy cat lady), cats do get Cushing’s disease, but I’ve never seen one so don’t have enough comfort level with the topic to talk about it at the moment
The major players in Cushing’s disease are the adrenal glands and the pituitary gland. The pituitary is this vaguely testicular looking little gland that sits up in your dog’s brain, nestled in there behind the eyeballs. It is kind of like the remote control gland for all the other glands in the body. It secretes hormones that tell the other glands to secrete their hormones.
In about 90% of the cases, a little benign tumor pops up inside the pituitary gland that shoots out a bunch of ACTH (adrenocorticotropic hormone, for those of you playing along at home). This hormone tells the adrenal glands down by the kidneys to secrete cortisol. And secrete cortisol it does, in huge amounts. Way more than the body needs. (Under normal conditions, you need cortisol to deal with the stresses of every day life. Too much cortisol though, and you have problems.) This is “pituitary dependent hyperadrenocorticism”; I’m throwing in the big words for those who need reassurance that I am, indeed, a medical professional.
Cortisol is a steroid hormone (cortico-steroid not anabolic-steroid. It’s not going to, in the words of Hans and Franz of 90’s SNL fame, “pump you up”). Pretty much the natural version of Prednisone and some of the other anti-inflammatory steroids we use in practice every day. You know, the ones that make your dog pant like crazy, drink tons of water, pee everywhere and want to eat everything in sight.
These steroid side effects, incidentally, are the reasons people bring their dogs to the vet when they develop Cushing’s syndrome. The eating, the panting, the drinking and the peeing.
Especially the peeing.
There are myriad other symptoms, skin issues, hair loss, hypertension, abdominal distention, muscle weakness, etc. But the one that brings them to the vet is usually the peeing.
I imagine I’m losing people here, are you bored?
If you are still with me, I’ll mention that 10% of Cushing’s cases actually don’t have the little pituitary brain tumor, they instead have tumors in the adrenal gland. Symptoms are the same, but if not diagnosed properly (generally via ultrasound) the tumors are malignant will grow and invade things in that region (Like the vena cava, which is this giant vein that carries lots and lots of blood. Things do not go well when this vein gets eaten up by cancer). This is “adrenal dependent hyperadrenocorticism”, best treated with surgery, if caught early enough. I don’t know if any DVM’s read this blog, with different experiences, but in our practice, the dogs that go to surgery for this (and we refer this out to boarded surgeons); have about a 50:50 chance of surviving. Somehow there seems to be a high risk of complications involved with getting these tumors out. Sorry to be all gloom and doom. My “Bible” of endocrinology (Feldman and Nelson’s Canine and Feline Endocrinology and Reproduction) says that “Dogs diagnosed as having ATH have an excellent prognosis…if they survive the first two weeks after surgery”. So there’s that.
I’m not going to go into how we diagnose Cushing’s because it’s boring and painful and confusing and I hate it. Suffice to say that it can be expensive and there are lots of grey areas involved in the testing. There is not usually a really definitive “yes or no” test. It’s more of a “probably” or “probably not” test. Sometimes one expensive test is negative, so then we have to do another expensive test which may test positive. Plus we have to view all these results in light of the patient and his clinical signs. The art of veterinary medicine comes to play quite a bit when dealing with this syndrome. So bear with us, we really are doing our best and we aren’t just after your money.
Not only is diagnosing Cushing’s disease difficult, treating it is also. First and foremost, there is no cure for Cushing’s disease. (Unless your dog has adrenal dependent, and he survives the surgery, and he doesn’t subsequently develop metastasis, or a pituitary mass.)
You just manage the symptoms. The goal is to get them to not act like they’re starving to death, not drinking gallons of water, and most importantly, not peeing all over your carpet. Ultimately they live an average of three years, give or take. They may succumb to complications like diabetes or pulmonary thromboembolism (blood clot in the lungs). Sometimes the little pituitary tumor gets really big and the pet starts to have seizures that we manage with anticonvulsants.
There are several treatment (or symptom management) options. The two more common ones are Lysodren and Trilostane.
Lysodren has been around forever, it’s actually a derivative of the insecticide DDT (which almost wiped out the pelican population in the 70’s, if I remember correctly from my “Ranger Rick” magazines from elementary school). Used VERY carefully, it basically destroys just enough of the adrenal gland to reduce its cortisol secretion. Used not very carefully and it can wipe out the whole gland and cause HYPO adrenal corticism which, if untreated could result in death. This isn’t better than peeing all over the carpet. Usually. Guess it depends on who’s cleaning up all that urine.
Then there’s Vetoryl (generic name: Trilostane). About, what, 5 or 10 years ago we used to have to buy this stuff on the “grey” market from England and have it shipped over. It all felt very illicit and dicey because the product wasn’t FDA approved in the US, but it was supposed to be fantastic and much safer for managing Cushing’s. It’s available in the US now and we use quite a bit of it. It’s not cheap though. Theoretically it’s safer, but every now and then it randomly can melt down the adrenals and cause death by hypoadrenocorticism (see above). It works by shutting off cortisol production at the molecular level as opposed to randomly killing off adrenal gland cells like Lysodren.
There are many more things I could still tell you about Cushing’s disease, but I’ve got to stop somewhere. If you happen to have a dog (heck, or cat) with the syndrome and want to share your experience, feel free. I’m always open to questions too.