Vitamin and Mineral Deficiencies in Gastrointestinal Disease

Vitamin and mineral deficiencies are commonly recognized in human patients with inflammatory bowel disease.¹ The mechanisms whereby micronutrient deficiencies may come about include reduced voluntary intake because of inappetence, increased losses as a result of diarrheal disease, compromised uptake as a consequence of loss of absorptive surface area, loss of specific mucosal receptors, or compromised fat absorption in diseases characterized by steatorrhea. In the veterinary literature, the greatest attention has been paid to (a) vitamin deficiencies resulting from fat malassimilation and (b) deficiencies in cobalamin (vitamin B₁₂) and folic acid or folate (vitamin B₉) as a result of loss of specific receptors. Hypovitaminosis D, with concurrent disorders of calcium homeostasis, has been reported in dogs in association with protein-losing enteropathies,^2,3 while in the cat severe organic acidemias have been recognized in patients with gastrointestinal disease and subnormal serum cobalamin concentrations.^4,5 Hypocobalaminemia has been identified as a negative prognostic factor in dogs with chronic enteropathies.⁶

Recent studies have focused on the prevalence of cobalamin deficiency in the cat and dog with gastrointestinal disease.^7,8 In both species, cobalamin deficiency was common in patients with gastrointestinal disease. In an open-label, uncontrolled study, cobalamin supplementation in cats with gastrointestinal disease and severe hypocobalaminemia was associated with positive clinical benefit and normalization of biochemical parameters.⁹

Cobalamin malabsorption because of intestinal disease cannot be successfully treated with dietary supplementation. Parenteral therapy is essential in deficient patients.⁹ A dose range previously described for use in cats with cobalamin deficiency as a consequence of intestinal disease is 250 µg/cat injected subcutaneously, once a week for 6 weeks, once every 2 weeks for 6 weeks, and once a month thereafter.⁹ The concentration of cobalamin in standard injectable multivitamin preparations (5 µg/mL) is insufficient to supply this amount of cobalamin in a reasonable injection volume. Therefore a pure preparation of cobalamin is recommended, in addition to multivitamin products, in dogs and cats with documented cobalamin deficiency.

Reduced serum concentrations of folic acid/folate most commonly occur in companion animals because of loss of specific duodenal mucosal receptors. Although subnormal serum folate concentrations have been recognized cats with gastrointestinal disease,¹⁰ the clinical significance of this finding, or of similar findings in dogs, is currently unclear. At the time of writing there is no well-defined threshold for folic acid supplementation in either species, and no peer-reviewed literature that specifically addresses the benefit, if any, of folate supplementation in adult patients with gastrointestinal disease. Empirically, treatment with oral or injectable folic acid (1 to 5 mg/dog or 1 mg/cat PO daily) results in dramatic increases in serum folate concentrations in most animals (unpublished data).

Vitamin and Mineral Deficiencies in Liver Disease

Liver disease patients often present with vitamin and/or mineral deficiencies. Several factors, including reduced voluntary intake, fat malabsorption, reduced gastrointestinal mucosal function, and loss of hepatic reserves, all contribute to the development of vitamin and mineral deficiencies.

Water-soluble vitamins such as folic acid, thiamine, cobalamin, niacin, and riboflavin are cofactors for many enzymatic reactions carried out in hepatic cells. Deficiencies in these vitamins are detected frequently in cats with hepatic lipidosis.¹¹ Most water-soluble vitamins do not have substantial body stores and daily replacement from dietary sources is necessary. Administration of multivitamin supplements is cost-effective and simple, and should be included in any nutritional support plan for patients with liver disease. In the cat, cobalamin malabsorption because of small intestinal disease is commonly documented in association with liver disease.⁵

In animals with long-standing liver disease, fat malabsorption and subsequent deficiencies of fat-soluble vitamins can occur. Vitamin E deficiency may reduce cellular defenses against oxidant-mediated damage, potentially playing a role in copper-associated hepatoxicity.^12,13 Empirically, regular supplementation of vitamins E, A, and D by intramuscular injection at 3- to 4-month intervals is recommended in companion animals with long-standing liver disease, particularly if this is complicated by steatorrhea. Cats with hepatic lipidosis should be screened for vitamin K deficiency, particularly if there is any evidence of bleeding tendencies. If detected (ideally via protein-induced vitamin K absence [PIVKA] assay), subcutaneous vitamin K administration at 1 to 5 mg/kg/day for 2 to 3 days is indicated.