Chronic Enteropathy and Vitamins in Dogs

Abstract

Chronic enteropathy (CE) or chronic inflammatory enteropathy is a group of diseases with multiple and different etiologies characterized by chronic gastrointestinal signs such as vomiting, diarrhea, anorexia, weight loss for more than 3 weeks, and inflammatory cell infiltration, such as lymphoplasmacytic cells in the intestinal mucosal lamina propria. The diagnosis was histologically confirmed after excluding other diseases such as parasitic infections, tumors, pancreatitis, exocrine pancreatic insufficiency, metabolic diseases, and endocrine diseases, such as hypoadrenocorticism. Nutritional management depends on several important functions, such as digestion and absorption processes, digestive enzymes and nutritional transporters, and barrier functions. Intestinal dysbiosis may have been found to be involved in various functions. Recently, cobalamin (vitamin B₁₂) and vitamin D have been considered negative prognostic factors in dogs with CE. Cobalamin supplementation ameliorates clinical disease severity in dogs with CE, and vitamin D supplementation ameliorates hypocalcemia in dogs with CE and hypoalbuminemia. Therefore, the aim of this review is to provide an overview of CE and present treatment and nutritional management strategies for CE and prognostic vitamins.

Keywords: canine; chronic enteropathy; cobalamin; treatment; vitamin D.

Figure 1

Absorption of cobalamin by carnivores. Normal absorption of cobalamin requires the function of the stomach (acid, proteases, and IF), pancreatic exocrine (IF and proteases), and ileal mucosa (receptors for cobalamin plus IF). IF, intrinsic factors. Adapted from Ruaux, 2013 [54].

Figure 2

The major intracellular metabolic pathway requires cobalamin. In the mitochondria, adenosylcobalamin is required as a cofactor for methylmalonyl-CoA mutase, which converts L-methylmalonyl-CoA to succinyl-CoA. In the cytoplasm, methylcobalamin is required as a cofactor for methionine synthase, which converts homocysteine to methionine and 5-methylhydrofolate to tetrahydrofolate. Adapted from Toresson et al., 2019 [59].

Figure 3

Vitamin D metabolism. (a) Natural vitamin D is transported to the liver by VDBP and is converted to 25-hydroxyvitamin D [25(OH)D] by 25-hydroxylase. The biological activity of 25(OH)D₃ derived from vitamin D₃ (cholecalciferol) was better than that of 25(OH)D₂ derived from vitamin D₂ (ergocalciferol) because of its higher affinity for VDBP. This reaction is not strictly regulated and is thought to proceed in a substrate-dependent manner. (b) 25(OH)D is converted to 1,25-dihydroxyvitamin D [1,25(OH)₂D], an active form of vitamin D, by 1α-hydroxylase in the proximal tubule of the kidney. This reaction is tightly regulated, stimulated by PTH and hypophosphatemia, and inhibited by FGF-23 and 1,25(OH)₂D, hypercalcemia, and hyperphosphatemia. (c) 25(OH)D and 1,25(OH)₂D are inactivated by 24-hydroxylase in the proximal tubules of the kidney. FGF, fibroblast growth factor; PTH, parathyroid hormone; VDBP, vitamin D-binding protein.