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Once the body stores of cobalamin are depleted, cobalamin deficiency can occur.105 The half‐life of cobalamin in healthy dogs is approximately 6‐16 weeks.106 It is assumed that this half‐life is decreased in dogs with CIE as a result of a reduced cobalamin absorption in the face of normal biliary excretion and enterohepatic circulation.49 Reported prevalences of hypocobalaminemia in dogs with CIE ranged from 19% to 38%,49, 65, 107, 108, 109, 110 and similar findings have been reported in cats.111 Dogs with suboptimal serum cobalamin status might not respond to treatment of the primary disease process unless given supplemental cobalamin, because cobalamin is essential for many cell functions and mucosal regeneration, and a deficiency can contribute to mucosal inflammatory infiltration and villous atrophy.72, 105 Correlation of hypocobalaminemia with histopathologic findings Histological lesions in dogs with CIE are often multifocally distributed, and different degrees of disease severity might be found among the different segments of the intestinal tract and also among different regions within the same segment (Dossin O, Tesseydre JF, Concordet D
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This injectable formulation allows for much higher plasma concentrations of vitamin C, bypassing the limitations of gastrointestinal absorption and providing rapid systemic availability
