By Courtney North
For the next few postings I plan to address typical hyperadrenocorticism (Cushing’s syndrome) – this is one of the most common sources of questions addressed to me (I’ll try to pull together some interesting information on atypical Cushing’s at a later date). And I agree – it can be a pretty confusing process. It looks simple in the textbook but is more complicated in the real world. I decided to address this because right now I’m dealing with a weird case – does the dog have Cushing’s or not? And is that adrenal nodule the start of a functional tumor or just a red herring? The owner and I are working our way through it now.
As a quick review, there are a few forms of hyperadrenocorticism (Cushing’s syndrome – hyperadrenocorticism was first described by Dr. Harvey Cushing in 1932). Cushing’s syndrome occurs in both dogs and cats though, of course, it is MUCH more common in dogs than in cats.
The first, which is the only form we call Cushing’s disease, refers to hypersecretion of ACTH from the pituitary gland (pituitary dependent hyperadrenocorticism). This is by far the most common form of Cushing’s syndrome (accounting for 80-85% of diagnosed cases), usually occurs in older small breed dogs and is usually due to a pituitary microadenoma.
The second form refers to excess secretion of cortisol by an adrenal tumor. These are more likely to occur in older, large breed dogs. The tumor in question is usually either an adenoma or a carcinoma.
Last, in humans, though not in domestic animals, there have been cases of nonendocrine tumors secreting ectopic ACTH, resulting in Cushing’s syndrome.
The treatment of pituitary dependent hyperadrenocorticism and adrenal tumors is very different so it really is important that we determine what form our patient has.
Clinical signs in hyperadrenocorticism are usually straightforward but definitely not pathognomonic! The most common complaint by owners of affected pets is increased thirst and urination. But, of course, there are lots of diseases that have these same signs. Other common signs include excessive panting, a poor haircoat (particularly bilateral truncal alopecia), recurrent infections (particularly skin or urinary tract infections), increased appetite, a pot belly, thin skin, muscle wasting… It’s a long and not very specific list! Animals with Cushing’s may also have insulin resistance and/or high blood pressure. And of course, there are sometimes those patients who have bloodwork changes consistent with Cushing’s but no clinical signs. Or vice versa.
A common question is whether there is a link between Cushing’s disease and SARDs (sudden acute retinal degeneration syndrome). This arises because loss of vision due to SARDS is often preceded by clinical signs similar to those noted in dogs with hyperadrenocorticism, particularly excessive thirst and urination and panting. When tested during this time period, about 17% of dogs will have cortisol excess. However, this is likely a stress response as most of these dogs, when reevaluated a few weeks later, will have normal cortisol levels. A true relationship between Cushing’s and SARDS has not been established. So, contrary to internet postings, there is no proof that Cushing’s causes SARDS!
On another note, there may be a link between hyperadrenocorticism and development of gall bladder mucoceles but this is still being investigated. One study (Pike et al.) found that 9 out of 30 dogs with cortisol excess went on to develop a gall bladder mucocele. But a definitive link remains to be proven. A 2009 retrospective study (Mesich et al.) did not find a significant increase in gall bladder mucoceles in dogs with other common endocrinopathies (diabetes mellitus and hypothyroidism) but found that dogs with hyperadrenocorticism were 29 times more likely to develop mucoceles than those normal adrenal function. So, while waiting for additional studies to be published, I do test all dogs with gall bladder mucoceles for hyperadrenocorticism (I usually wait 4-6 weeks after surgery in order to reduce the risk of a false positive).
Next…testing options….
Welcome to my first IM blog! Please check out the Capital Area Veterinary Specialists homepage for a link – in the interest of saving trees I’m going to post online rather than faxing in the future. In general I hope to use the blog to address some of the topics that I receive lots of phone calls about or that are just of interest. Obviously I’m not claiming that these should replace your own judgement or research but I hope to clarify some issues and maybe encourage some additional discussion.
Please don’t hesitate to contact me with any comments or if there are particular topics you’d like to discuss (cnorth@cavstvo.com).
I just returned from the ACVIM conference in Denver, CO and had a great time! I’ve actually never been to Colorado before (!) and Denver is a neat city – it has an interesting history and fun people. At night it really comes alive with terrific food and music and some pretty fun street entertainment (yes, I watched a mime). It’s been a few years since I last attended an ACVIM conference so it was really great catching up with friends from vet school and beyond. And I saw a few faces from Austin too! I hope we can make a good showing at next year’s conference – it’s scheduled for New Orleans, one of my favorite cities!
The conference provided a good review of several topics as well as some fresh insights. Below is just a quick summary of some of the things I found interesting, either for clinical purposes or just as “gee whiz” information. Enjoy!
-the World Small Animal Veterinary Association Renal Standardization Study Group (which includes Texas A&M’s own Dr. George Lees) presented a really nice review of what we do and do not understand regarding proteinuric dogs, in particular those with true glomerular nephropathy. Of particular interest – it is always controversial whether steroids should be implemented or not. We all know that steroids used in the wrong context can be detrimental and we emphasize the importance of obtaining renal biopsies to determine whether steroid therapy would benefit that patient. But steroid therapy is widely used in treating proteinuric human patients. In our desire to “first do no harm”, are we actually harming our patients by withholding steroids? Currently one of their studies is evaluating the outcome of proteinuric dogs started on steroids either with or without advanced diagnostics such as renal histopathology. It will be interesting to see the outcomes of the two groups. They have a couple of different studies and would love to include your patients whenever possible – check out their website at World Small Animal Veterinary Association
-I enjoyed the presentation by Dr. Dan Fletcher on advances in continuous glucose monitors. I had the opportunity to use these as a resident and they are really nice, particularly in a critical care setting. However, there are still some kinks to be ironed out, which is why I haven’t invested in one yet. Some of the monitors in development are really intriguing so I can’t wait to see how that progresses. Maybe I’ll be looking into such a system in the future…
-I was surprised by the wide range of aspirin doses cited for anticoagulant properties – anywhere from 0.5 mg/kg/day all the way up to 5 mg/kg/day. I generally stick with doses of 0.5-1 mg/kg/day and it’s not clear whether a higher dose is really beneficial or just more aspirin (and potentially more side effects)
-A really fascinating discussion of aspirin resistance was presented. One of the big debates is whether “aspirin resistance” represents treatment failure (i.e. insufficient dosing) or true resistance. Approximately 28% of people are aspirin resistant and have increased morbidity from hypercoagulable events and cardiac complications in the face of aspirin therapy. Interestingly these same individuals also appear to be resistant to most other anticoagulant therapies as well, so simply switching them from aspirin to another anticoagulant such as Plavix may not accomplish much in most cases. Researchers are still trying to evaluate whether different dosing schemes might be of help. The incidence of aspirin resistance in companion animals is, of course, unknown. Human studies indicate increased expression of COX2 may be predictive of increased aspirin resistance so we’ll have to see what the significance of this is for our patients.
-Dr. Jody Lulich from the University of Minnesota’s urolith lab discussed ciprofloxacin urolithiasis. The bad news is that it does occur in dogs but the good news is that there is a good chance of being able to dissolve them and thus potentially avoid cystotomy. They dissolve best in acidic or alkaline urine rather than in neutral urine so acidifying the patient’s urine may be a reasonable option.
-I am a big fan of polyunsaturated fatty acids (particularly fish oils) as supplements in neoplasia and many renal disease cases so it was gratifying to see studies validating their use. Unfortunately, it still remains unknown what dosing is optimal for various conditions and what ratio of omega 3s to 6s we should be aiming for. I generally just recommend something along the lines of 100 mg/kg of a high quality oil and hope the rest falls in line.
-women are four times more likely than men to live to be 100 years old. When you talk about living to be 110 years old, the ratio becomes 20:1!!! Lots of room for good jokes here…
-An ongoing Purdue University study of very aged Rottweilers (>13yrs old) demonstrates that prolonged exposure to ovaries (specific hormones were not identified) correlates with prolonged life span. This held true even when potential increased incidence of cancer (for example, increased risk of mammary neoplasia in intact females) was taken into account. Human studies seem to mirror this (retrospective studies of women who have undergone hysterectomy versus ovariohysterectomy). This certainly adds to the confusion surrounding OHEs and castration in veterinary medicine. I’d love to see a study evaluating the impact of hormone supplementation following OHE and how it does or does not impact quality of life and longevity.
-Hill’s Science Diet revealed some information about their upcoming diet for hyperthyroid cats. Is it a panacea? Probably not, but it does hold promise for many cats. In essence it is a diet that is extremely low in iodine and most of the hyperthyroid cats who were fed the diet exclusively became euthyroid, negating the need for methimazole, surgery , or I131. So far the diet has only been tested on a limited number of cats and I think the data so far only follows the cats for about a year. It is not recommended for euthyroid cats and is probably not suitable for cats with other specific dietary needs (such as IBD or renal disease) but it definitely holds promise and may fill a need for a specific population of cats. I’m interested to see what follow up studies reveal.
-Last, we are thinking of implementing some additional noninvasive procedures. I was scoping out equipment. We are looking at fluoroscopy units (which would allow Dr. Meier to perform additional cardiac studies, too) and stenting equipment. For now I am focusing on tracheal and urethral stenting. I may be working with a group to get some additional training in the near future and we may have a relevant CE evening to discuss it. CAVS would love to get your feedback on whether you would be interested in being able to offer these services to your clients and their pets.
Of course there was lots of interesting information presented but these issues really caught my eye. I’d love to hear from others who went to the conference!
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