Persistent Increase in Serum 25-Hydroxyvitamin D Concentration in a Dog Following Cholecalciferol Intoxication

Abstract

Cholecalciferol is becoming an increasingly utilized rodenticide in the United States due to changes implemented by the Environmental Protection Agency (EPA) to reduce unintended exposure of wildlife to second-generation anticoagulant rodenticides. The lipophilic properties of cholecalciferol and prolonged tissue elimination are well-documented; however, long-term clinical ramifications are unknown. This report describes unique clinicopathologic and treatment features during the acute phase of cholecalciferol rodenticide toxicosis in a 4-year-old neutered Shih-Tzu mix that presented for intermittent vomiting, anorexia, polyuria, and polydipsia. In addition, this report also highlights the potential benefit of serial measurements of serum 25-hydroxyvitamin D concentrations and long-term treatment in the chronic phase of cholecalciferol rodenticide toxicosis in dogs.

Vitamin D metabolism and disorders in dogs and cats

“…Hypervitaminosis D secondary to rodenticide consumption is well recognised and unfortunately, is likely to be an increasing problem as some rodenticide manufacturers switch to vitamin D containing products (DeClementi & Sobczak 2018, Gerhard & Jaffey 2019). Consumption of vitamin D containing medication is also an increasingly well-recognised cause of hypervitaminosis D in companion animals.…”

“…The lipid-soluble properties of vitamin D can lead to sequestration of the vitamin into fat deposits in the body. Consequently, it can take several months for the serum 25(OH)D concentrations to return to within the reference interval following a hypervitaminosis D episode (Gerhard & Jaffey 2019). Long term sequelae such as soft tissue mineralisation are well-recognised complications of prolonged hypercalcaemia secondary to hypervitaminosis D (Crossley et al 2017).…”

Investigation of the effects of dietary supplementation with 25-hydroxyvitamin D3 and vitamin D3 on indicators of vitamin D status in healthy dogs

“…At the highest D vitamer dose in that trial, the combined serum 25(OH)D 2 and 25(OH)D 3 concentrations ranged from approximately 42 to 146 ng/mL. Under these conditions, signs of vitamin D excess (eg, high ionized calcium and low to undetectable PTH concentrations in serum, decreased food intake, weight loss, and inactivity) 9 were absent.…”

“…An impediment to carrying out such studies is the lack of an established safe upper limit for dietary vitamin D in adult dogs. Negative health consequences of hypervitaminosis D in dogs have been described but are mostly reported following consumption of extraordinary amounts of vitamin D (eg, owing to dietary formulation error 8 or rodenticide ingestion 9 ). Another obstacle is that substantial variation in individual responses to ingested vitamin D 3 has been found in studies of people 10 and dogs.…”

The Role of Vitamin D in Small Animal Bone Metabolism

“…Excessive vitamin D is also harmful and causes of hypervitaminosis D in small animals. This can be due to commercial food formulation miscalculation [21][22][23][24], accidental consumption of rodenticides [25][26][27][28][29], consumption of certain plants that may contain calcitriol glycosides (such as jessamine [30]) and the use of topical ointments for psoriasis treatment, which are based on vitamin D analogs such as calcipotriol and maxacalcitol [31][32][33][34]. Acute vitamin D intoxication results in hypercalcemia, which causes clinical signs such as polydipsia, polyuria, anorexia, vomiting, constipation, seizures, etc.…”