Comparison of efficacy of oral and parenteral cobalamin supplementation in normalising low cobalamin concentrations in dogs: A randomised controlled study

Abstract

The aim of this study was to compare the efficacies of parenteral and oral cobalamin supplementation protocols in dogs with chronic enteropathies and low cobalamin concentrations. It was hypothesised that both treatments would increase serum cobalamin concentrations significantly. Fifty-three dogs with chronic enteropathies and serum cobalamin concentrations<285ng/L (reference interval 244-959ng/L) were enrolled. Dogs were randomised to treatment with either daily oral cobalamin tablets (0.25-1.0mg cyanocobalamin daily according to body weight) or parenteral cobalamin (0.4-1.2mg hydroxycobalamin according to body weight). Serum cobalamin concentrations were analysed 28±5days and 90±15days after initiation of supplementation. After 28 days, all dogs had serum cobalamin concentrations within the reference interval or above. In the parenteral group (n=26), median (range) cobalamin concentrations were 228 (150-285) ng/L at inclusion, 2107 (725-10,009) ng/L after 28days and 877 (188-1267) ng/L after 90 days. In the oral group (n=27), median (range) serum cobalamin concentrations were 245 (150-285) ng/L at inclusion, 975 (564-2385) ng/L after 28days and 1244 (738-4999) ng/L after 90 days. In both groups, there were significant differences in serum cobalamin concentrations between baseline and 28 days, and between 28days and 90days (P<0.001). In conclusion, both parenteral and oral cobalamin supplementation effectively increase serum cobalamin concentrations in dogs with chronic enteropathies and low cobalamin concentrations.

Clinical utility of currently available biomarkers in inflammatory enteropathies of dogs

“…However, hypocobalaminemia is not specific for CIE and also can be observed in dogs with exocrine pancreatic insufficiency 31. Also, a normal serum cobalamin concentration does not rule out a diagnosis of CIE. Subnormal or low normal serum cobalamin concentrations (<400 ng/L) indicate a need for parenteral (50 μg/kg SQ once weekly for 6 weeks, then every 2‐4 weeks) or PO supplementation (50 μg/kg PO q24h for at least 12 weeks) with cyanocobalamin 51, 52…”

“…Hypocobalaminemia is a negative prognostic factor in dogs with CIE and is associated with hypoalbuminemia. 5,9 However, hypocobalaminemia is not specific for CIE and also can be 51,52 Methylmalonic acid (MMA) is a metabolite that accumulates when the activity of methylmalonyl-CoA mutase is decreased because of a lack of intracellular cobalamin. 53 Thus, increased MMA production is a useful marker for cobalamin deficiency at the cellular level as a result of cobalamin malabsorption, decreased cobalamin transport, or both.…”

In dogs with chronic enteropathy that have hypocobalaminaemia, can oral tablets be used instead of injectable protocols?

“…This requires frequent visits to veterinary clinics, can be distressing for both owners and dogs, and costly. Toresson et al, (2018) found that one dog was hypocobalaminaemic (38 ng/L) at day 90 after following this parenteral protocol. This suggests that the parenteral protocol was not adequate at supplementing cobalamin in this case.…”

“…Toresson et al (2016) produced a retrospective study based on a review of medical records of dogs that had been treated with oral cobalamin; the study concluded that dogs treated with oral cobalamin had normal cobalamin blood serum levels (>270 ng/L). A randomised clinical trial was later performed by Toresson et al (2018). This experimental trial concluded that both oral and parenteral cobalamin supplementation in dogs provided a significant increase in serum cobalamin concentrations >285 ng/L.…”

“…Normocobalaminaemia has been described as serum levels between 252-908 ng/L, (Vaden et al, 2009). However, in the studies described cobalamin is supplemented once levels are below 285 ng/L as this level represents the lowest 5% of the reference range (Toresson et al, 2018). Cobalamin is necessary for the methylmalonyl CoA mutase (MCM) system (Solomon, 2007) and deficiencies can result in the production of methylmalonic acid (Stabler et al, 1986).…”