In the future, assay of enteric inflammatory markers such as fecal calprotectin may prove useful in confirming the presence of enteric disease, but the relationship of inflammation to this enteropathy is currently uncertain. Even histologic examination of intestinal biopsy specimens may not provide evidence of a conclusive diagnosis; lesions may be patchy and interpretation of biopsy findings is inherently subjective. It is also likely that in cats, as in dogs, functional problems in the intestine may not be associated with either inflammation or villous atrophy but rather with intraluminal microbial changes and biochemical derangements in the enterocytes lining the small intestine that are not revealed by classic histologic evaluation.
In some cats, despite a thorough investigation, it is not possible to confirm enteropathy. A presumptive diagnosis of idiopathic enteropathy is the best that can be achieved. The approach to management in these instances is essentially the same as for patients with histologically confirmed IBD — that is, a dietary change (low-carbohydrate alternative fiber source, novel antigen, or hydrolyzed diet), prebiotic or probiotic supplementation, correction of low serum cobalamin/folate concentrations, supplementation with vitamin E and perhaps other antioxidants, antibiotic treatment with metronidazole or tylosin, and perhaps glucocorticoid therapy or immunomodulation with chlorambucil or cyclosporine.11 However, in the absence of specific laboratory abnormalities or any overt clinical signs to monitor, other than perhaps very slowly progressive weight loss, it is probably premature to recommend particularly aggressive treatment for these patients. A cautious, conservative approach is warranted.
As many of the observations about digestive disturbances in elderly cats are relatively new, appropriate clinical studies evaluating treatment interventions have not been performed. Dietary changes and supplements would certainly be the safest and most easily administered interventions. When specific abnormalities such as hypocobalaminemia are identified, they should be rectified.
The effect of dietary changes has to be evaluated on an individual trial-and-error basis, which can be difficult if gradual weight loss is the only clinical sign to evaluate. Observing improvements in the newer GI disease markers, such as fecal α1-proteinase inhibitor and serum fPL, may provide objective evidence of a positive response, but the value of this approach remains to be evaluated.
Careful observation of stool characteristics may provide some evidence of improved digestibility, especially if grossly apparent abnormalities were present at the outset. If there is no apparent response to dietary change after two to four weeks, an alternative diet should be tried. I prefer to select diet changes based on reduced carbohydrate content (generally associated with increased protein content) or different amounts or types of fermentable fiber. Adjusting the fat content of the diet does not appear to be particularly useful in treating feline enteropathies. Unfortunately, definitive studies in geriatric cats with malabsorption have not been done. Treatment needs to be individualized and evaluated on a trial-and-error basis.
With regard to older cats in general, there is some evidence that diet can play a role in maintaining body weight and fat mass — and prolonging life. A control diet (nutritionally complete and balanced adult cat food) supplemented with antioxidants (vitamin E and ss-carotene), a blend of n-3 and n-6 fatty acids, and a prebiotic (dried chicory root) was associated with reduced decline in body weight and increased longevity (by more than 1 year) compared with feeding either the control diet alone or the control diet supplemented with antioxidants alone.6 These striking observations illustrate the potential benefit to be gained from dietary and other interventions to address the gastrointestinal changes that appear to be so common in aging cats.
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7. Steiner JM, Peterson MA, Ruaux CG, et al. Serum cobalamin and folate concentrations in cats with hyperthyroidism. J Vet Intern Med 2005;19:474-475.
8. Cook AK, Suchodolski JS, Steiner JM, et al. The prevalence of hypocobalaminaemia in cats with spontaneous hyperthyroidism. J Small Anim Pract 2011;52(2):101-106.
9. Burke KF, Broussard JD, Craig G, et al. Evaluation of fecal alpha1-proteinase inhibitor concentrations in cats with idiopathic inflammatory bowel disease and cats with gastrointestinal neoplasia. Vet J 2013;196(2)189-196.
10. Williams DA, Czarnecki-Maulden G. Protein-losing enteropathy commonly co-exists with high fecal fat output in geriatric cats with idiopathic malabsorption and persists following correction of subnormal serum cobalamin concentration. In Proc 23rd Congress Europ Coll Vet Inter Med - Comp Anim, Liverpool, England, Sept. 2013.
11. Webb CB. Feline inflammatory bowel disease. NAVC Clinician’s Brief 2012;10:11-14.