Peer-reviewed veterinary case report
Vitamin D treatment for dogs with protein-losing gut disease and low
By Jablonski, Sara A et al.Ā·Published in Journal of veterinary internal medicineĀ·2025Ā·Department of Small Animal Clinical Sciences, United StatesĀ·View original on PubMed ā
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Original publication title: Treatment of Hypovitaminosis D With Cholecalciferol in Dogs With Protein-Losing Enteropathies: A Randomized, Double-Blind, Placebo-Controlled, Clinical Trial.
- Species:
- dog
Plain-English summary
A group of 28 dogs with protein-losing enteropathy (a condition that causes them to lose protein through their intestines) were given either a vitamin D supplement (cholecalciferol) or a placebo for six weeks. While the dogs receiving the vitamin D had higher levels of this nutrient in their blood, there was no noticeable improvement in their overall health or symptoms compared to those who received the placebo. Some dogs did experience high vitamin D levels, but without any related health issues. Overall, the vitamin D treatment did not provide the expected clinical benefits for these dogs.
People also search for: dog protein-losing enteropathy treatment Ā· vitamin D for dogs with PLE Ā· symptoms of low vitamin D in dogs
Abstract
BACKGROUND: The effects of vitamin D supplementation are unknown in dogs with protein-losing enteropathy (PLE). OBJECTIVE: To evaluate the safety, efficacy, and clinical benefit of orally administered cholecalciferol in dogs with PLE and decreased serum concentrations of 25OHD. ANIMALS: Twenty-eight dogs with PLE, decreased 25OHD, and serum ionized calcium (iCa) > 1.0 mmol/L (n = 15 treated with cholecalciferol, n = 13 treated with placebo). METHODS: Prospective, double-blinded, randomized, controlled trial. Dogs randomized to receive 400 IU/kg cholecalciferol or placebo PO daily along with standard therapy for 6 weeks. Clinical and biochemical variables were measured at baseline (T0) and monitored at 2 (T1), 4 (T2), and 6 (T3) weeks postmedication initiation. Clinical and biochemical variables were also measured 6 weeks following discontinuation of study medication (T4). Variables were compared in dogs with PLE receiving cholecalciferol versus placebo at T0-T4 using Student's t test or Mann-Whitney U tests and a mixed-effects model. Correlations between 25OHD and clinical and biochemical variables were also performed. RESULTS: Dogs with PLE treated with cholecalciferol had higher 25OHD concentrations at T2 compared to dogs treated with placebo (225 nmol/L, range 72-434 vs. 80 nmol/L, range 31-254 nmol/L; p = 0.004). Clinical and biochemical variables did not otherwise differ between dogs with PLE treated with cholecalciferol versus placebo at T0-T4. Serum albumin correlated with 25OHD at T0-T3(p < 0.005 for all comparisons). Hypervitaminosis D without ionized hypercalcemia occurred in five dogs (18%). CONCLUSIONS: While PLE dogs treated with cholecalciferol had higher 25OHD concentrations at study timepoints, a clinical benefit of supplementation was not observed.
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Search related cases āOriginal publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/40485009/