Elevated 24,25-Dihydroxyvitamin D Serum Concentrations in Two Dogs with Cholecalciferol Toxicosis

Vitamin D toxicosis poses a health threat to dogs, with cases often stemming from cholecalciferol rodenticide ingestion. This case report investigates two clinical cases of canine cholecalciferol toxicosis, shedding light on the persistent elevation of 25-hydroxyvitamin D (25(OH)D) and the adaptive response of 24,25-dihydroxyvitamin D (24,25(OH)2D). Serum samples from affected dogs were analyzed over several months, revealing sustained increases in 25(OH)D concentrations. Notably, concurrent measurements of 24,25(OH)2D unveiled a marked elevation, suggesting a compensatory mechanism to mitigate calcitriol excess and hypercalcemia. These findings highlight the potential role of upregulating 24-hydroxylase activity as a therapeutic target for managing cholecalciferol toxicosis. These cases underscore the importance of understanding vitamin D metabolism in canine toxicology and prompt further exploration into novel treatment strategies and other research areas.