Cobalamin deficiency in dogs and cats

Abstract

Cobalamin is a member of the B-group of vitamins and a cofactor for metabolic processes like nucleic acid synthesis, amino acid synthesis, and the citric acid cycle. Mammals are unable to synthesize cobalamin and therefore rely on adequate food intake. Cobalamin absorption is a complex process in the stomach, duodenum, and ileum, requiring a functional exocrine pancreas. Thus, a great number of gastrointestinal diseases like chronic enteropathies, intestinal lymphoma, or exocrine pancreatic insufficiency can lead to hypocobalaminemia. Furthermore, some dog breeds (Giant Schnauzer, Border Collie, Australian Sheperd Dog, and Beagle) can have a primary, hereditary cobalamin deficiency (Imerslund-Gräsbeck syndrome). Clinical signs of cobalamin deficiency comprise anorexia, vomiting, diarrhoea, failure to thrive, and neuropathies. Laboratory findings like non-regenerative anemia, leukopenia, hypoglycemia, and hyperammonaemia have also been described. When hypocobalaminemia is suspected usually in dogs and cats, the cobalamin concentration is usually measured by immunoassay. Because the concentrations of cobalamin in blood and cells can differ the sole measurement of the vitamin concentration is of limited informative value. Treatment depends on the underlying disease aiming at eliminating the cause of hypocobalaminemia. However, successful therapy of gastrointestinal diseases often requires an additional oral or parenteral cobalamin supplementation. In patients with Imerslund-Gräsbeck syndrome, a regular and lifelong cobalamin supplementation is essential.