Hemorrhagic Cystitis Syndrome 2

Stress Boosts Feline Urinary Tract Signs

Authors: Baldwin NR, Buffington CAT (the Ohio State University, College of Veterinary Medicine, Columbus, OH) Summarized by Anthony Carr, DVM, Dip). ACVIM (Internal Medicine)

Journal of Veterinary Internal Medicine, Vol. 17, page 446, 2003.

Purpose of study: A variety of other abnormalities have been documented in cats with feline interstitial cystitis (FIC), or feline lower urinary track disease, suggesting that there may a systemic component to this disorder. This also holds true for humans with interstitial cystitis.
Design of the study: A structured interview technique was used to gather information on clinical disorders noted by owners. The study included 68 owners with cats that have FIC and 260 owners of healthy animals. The same interviewer asked questions about runny eyes, lower GI (diarrhea, constipation) and upper GI (vomiting, hairballs) problems and behavioral and lower urinary tract signs.
Results of the study: All cats had a similar rate of occurrence of ophthalmic problems. Sex and age were similar in both groups, as well. The cats with FIC were, however, much more likely to have signs of lower GI, upper GI and urinary problems.
Behavioral problems—aggression, fear and nervousness—were also more common in the FIC-afflicted animals.
Commentary: FIC can be very frustrating to treat. The rate of recurrence is variable and can be quite high. Few, if any, effective prophylactic or, for that matter, effective acute treatments are available.
Van de Merwe, et al, established a link to other systemic disorders in humans (International Journal of Urology, 2003).
People with interstitial cystitis more frequently have Crohn's disease, allergies, irritable bowel syndrome, fibromyalgia, systemic lupus erythematosus, Sjogren's syndrome as well as other immune-mediated diseases.
The link to allergies is especially intriguing because mast cell degranulation is involved both with allergic signs and symptoms of interstitial cystitis.
There are indications that FIC episodes may be precipitated by stressors, just as with people. This suggests that the sympathetic nervous system may be involved.
In previous studies, Buffington found increased plasma norepinephrine concentrations have been found in these cats (Journal of Urology, 2001).
This would be expected if the sympathetic nervous system were activated. The hypothalamic-pitu-itary-adrenal (HPA) axis was also tested in these cats by administering a corticotrophin-releasing hormone (CRH) and was found to be normal.
Further investigation of the HPA axis, however, Buffington and others showed that responses were different in cats with FIG (Journal of Veterinary Internal Medicine, 2002).
The effects of stress on plasma catecholamine concentrations and urine cortisol excretion in 12 normal cats and 12 cats with FIG was investigated.
All plasma catecholamine concentrations (dopamine, norepinepi-nephrine, epinephrine and various metabolites thereof) were elevated in FIC cats when compared to normal cats going along with an increased response to stress.
Surprisingly, however, the urine cortisol to urine creatinine ratio was not the same in these two groups. Under normal circumstances, increased cortisol excretion should occur with stress. This suggests that the HPA axis is uncoupled in these cats from sympathetic nervous system activation.
There is evidence that supports that adrenal glands and adrenal gland function in cats with FIC are different than in normal cats. In yet another study, Buffington found the adrenal glands of 13 necropsied cats with FIC were smaller than those adrenal glands of normal cats. The medulla was of normal size, but the cortex was smaller. This publication also included data on adrenocorticotrophic hormone (ACTII) stimulation, testing 20 cats with FIC, five of which
were later necropsied for the adrenal gland comparison.
The response to ACTH was significantly lower in cats with FIC than normal cats, though this adrenal insufficiency was very mild. The response to ACTH and adrenal gland size did not correlate.
Many other studies have reviewed stress and response to stress in patients with interstitial cystitis, both human and feline. There is evidence to support that the stress response is dysregulated.
This dysregulation may partially be responsible for some of the clinical signs seen. Of course, it cannot be discounted that chronic clinical disease can lead to dysregulation of the stress response as well, leading to the classic chicken and egg conundrum. By understanding these processes better, more effective therapies might be designed to help with this and similar debilitating diseases. There certainly is a need for this, since our current therapeutic armamentarium is woefully inadequate to deal with this problem.