Journal of veterinary internal medicine · 2025
Treatment of Hypovitaminosis D With Cholecalciferol in Dogs With Protein-Losing Enteropathies: A Randomized, Double-Blind, Placebo-Controlled, Clinical Trial.
СтатьяRandomized Controlled Trial, VeterinaryНазвание и аннотация: Перевод в очереди
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Jablonski Sara A, Shropshire Sarah B, Watson Victoria E, Manchester Alison C, Cridge Harry, Lennon Elizabeth M, Tolbert M Katherine
Аннотация
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.
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.