Idiopathic cystitis

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Lateral radiograph of a two year old cat with feline idiopathic/interstitial cystitis. Note the bladder wall appears thickened and non-distensible
Endoscopic appearance of the bladder mucosa in a cat with lower urinary tract disease. The endoscopy demonstrates glomerulations consistent with feline idiopathic/interstitial cystitis.
Schematic representation of the proposed pathophysiological alterations in cats with feline idiopathic/interstitial cystitis
Normal urinary system in the male cat
FIC in the male cat
Recurrence rates of feline idiopathic cystitis on moist versus dry diet

Feline idiopathic (interstitial) cystitis (FIC) has been characterised as a form of Feline lower urinary tract disease (FLUTD) of unknown cause and with no widely accepted treatment. Clinically it appears less sinister than acute and life-threatening pseudomembranous cystitis.

FIC is not thought to be a single disease entity, since it presents with a comorbidity of a variety of unexplained clinical conditions in some patients with FIC. Recent studies in cats with severe FIC reveal the presence of an underlying neuroendocrine abnormality. It is hypothesized that there is uncoupling of sympathetic nervous system activity from the hypothalamic-pituitary-adrenal axis, since cats with FIC often have smaller adrenal glands[1].

Human patients with idiopathic cystitis appear to suffer from a wide variety of comorbid conditions and the data suggests the same is true in cats. For example, lower urinary tract signs have been reported to be a comorbid condition in cats with separation anxiety syndrome, hypertrophic cardiomyopathy and obesity. These findings suggest that FIC may not be a disease process localised to the bladder.

Cause

In FIC in cats, there appears to be an enhanced activation of the stress response system, primarily the sympathetic nervous system limb. Once stimulated by higher brain structures responding to the perception of a threat, corticotrophin-releasing factor (CRF) is released from the hypothalamus, which acts as a hormone to stimulate the anterior pituitary gland to release ACTH. CRF also acts as a neurotransmitter to stimulate neurones in the brainstem, including the locus coeruleus, to activate the sympathetic nervous system. Under mild stress conditions, cats with FIC had significantly higher plasma levels of dihydroxyphenylalanine (DOPA), norepinephrine (NE), and other catecholamine metabolites compared with healthy cats. These results support previous work documenting elevated tyrosine hydroxylase, the rate limiting step in catecholamine synthesis in the brainstem of cats with FIC.

Activation of the SNS can increase epithelial permeability and permit environmental agents greater access to sensory afferent neurones, which could result in increased sensory afferent firing and local inflammation. Altered bladder permeability has been reported in cats with FIC and may be mediated via the SNS. Sympathoneural-epithelial interactions apparently play an important role in permeability. For example, it has been shown that application of NE to bladder strips induces release of nitric oxide from uroepithelium. Application of capsaicin results in release of nitrous oxide from epithelium in addition to nervous tissue in the urinary bladder. In light of reports that nitrous oxide may increase urothelium permeability, these results suggest that some of the sympathetically mediated alterations in permeability may be mediated by norepinephrine via this mechanism. The increased permeability related to increased SNS activation does not require direct interaction with epithelial cells, nor is it restricted to the urinary bladder.

However, the presence of inflammation and altered permeability is not well correlated with pain, as anyone who has had a superficial bruise will know. In the bladder, we have reported the presence of submucosal petechial haemorrhages in cats with no signs of referable to the lower urinary tract, and other investigators have identified urothelial disruption and increased presence of inducible nitric oxide synthase (and presumable increased permeability) in painless bladder conditions. Moreover, emotional and environmental factors such as stress or depression can modulate the experience of pain through descending pathways from the midbrain. Therefore, even the increased activity of afferent nerves noted in FIC cats could result in different perceived bladder sensations at any given time, depending on the emotional state of the animal.

Although cortisol responses are subnormal in these severe FIC cats, cortisol replacement with prednisolone has not been demonstrably useful in this clinical syndrome. The apparent lack of long-term benefit of glucocorticoid therapy in patients with FIC suggests that inadequate production of other steroids also may play a role in the pathophysiology of this disease. The adrenal cortex is responsible for many different hormones, and the only one sufficiently investigated is cortisol. Preliminary studies in humans with interstitial cystitis have suggested alterations in the relationships between adrenal hormones, particularly the cortisol / dehydroepiandrosterone sulfate (SHEAS) ratio. Adrenocortical function also has been evaluated in human patients with other chronic, waxing and waning pain conditions (e.g. chronic fatigue syndrome) by measuring the cortisol/DHEAS ratio. This ratio was twofold to threefold higher in chronic fatigue patients than in controls. It has been suggested that serum levels of DHEAS may be low in patients with inflammatory and noninflammatory diseases because of an activate SNS. Sympathetic hyperactivity may be a common denominator for low levels of DHEAS in both inflammatory and noninflammatory diseases. Currently we have not investigated this in cats with FIC. In the meantime, we cannot advocate the use of steroids as a sole treatment for FIC, and based on clinical experience, cats do not seem to improve with the current antiinflammatory doses of prednisolone commonly administered.

Clinical signs

The clinical signs of FIC include variable combinations of dysuria, pollakiuria, haematuria and periuria (inappropriate urination).

FIC may be the most common cause of lower urinary tract signs. It affects two thirds of the 1.5% of cats that present to primary veterinary care with lower urinary tract signs.

Treatment

Indoor housing has been associated with increased risk for development of FLUTD, calcium oxalate urolithiasis, odontoclastic resorptive lesions, obesity and hyperthyroidism.

Environmental enrichment to attempt to reduce the cat's perception of threat often is sufficient to eliminate recurrence of signs.

Another strategy for treating cats with FIC includes application of feline pheromones. Pheromones are fatty acids that seem to transmit highly specific information between animals of the same species. Although the exact mechanisms of action are unknown, pheromones reportedly induce changes in the limbic system and the hypothalamus, which alter the emotional state of the animal.

Feliway, a synthetic analogue of this naturally occuring feline facial pheromone, was developed in an effort to decrease anxiety-related behaviours of cats. Although not specifically tested in cats with FIC, treatment with this pheromone has been reported to reduce the amount of anxiety experienced by cats in unfamiliar circumstances, a response that may be helpful for FIC patients and their owners.The spray can be used to treat areas of the house where the cat is urinating by use of a single spray to the affected spot daily for 30 days[2].

References

  1. Westropp JL (2003) Small adrenal glands in cats with feline interstitial cystitis. J Urol 170(6Pt1):2494-2497
  2. August, JR (2006) Consultations in Feline Internal Medicine, Vol 5. Elsevier Saunders
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