Vitamin D toxicity of dietary origin in cats fed a natural complementary kitten food

Abstract

Case series summaryThis case series describes two young sibling cats and an additional unrelated cat, from two separate households, that developed hypercalcaemia associated with hypervitaminosis D. Excessive vitamin D concentrations were identified in a natural complementary tinned kitten food that was fed to all three cats as part of their diet. In one of the cases, there was clinical evidence of soft tissue mineralisation. The hypercalcaemia and soft tissue mineralisation resolved following withdrawal of the affected food and medical management of the hypercalcaemia.Relevance and novel informationThis case series demonstrates the importance of obtaining a thorough dietary history in patients presenting with hypercalcaemia and the measurement of vitamin D metabolites when investigating such cases. Complementary foods may have the potential to induce nutritional toxicity even when fed with complete, nutritionally balanced diets.

The Role of Vitamin D in Small Animal Bone Metabolism

“…Asymptomatic patients with mild hypercalcemia and with normal Ca × P product may not require immediate treatment, while individuals with severe acute increase in Ca levels may require more aggressive treatment. Accidental nutritional vitamin D toxicosis was reported in cats [22][23][24] and in those cases, respiratory discomfort was an important clinical sign among them due to soft tissue calcinosis. All of them were treated according to their symptoms, but only in a study by Crossley et al [24], was bisphosphonate used and had a good clinical outcome.…”

“…Accidental nutritional vitamin D toxicosis was reported in cats [22][23][24] and in those cases, respiratory discomfort was an important clinical sign among them due to soft tissue calcinosis. All of them were treated according to their symptoms, but only in a study by Crossley et al [24], was bisphosphonate used and had a good clinical outcome. It is worth mentioning that in the study by Crossley et al [24], of the three cats intoxicated with vitamin D and with hypercalcemia, pamidronate was administered in only one of them, since conventional therapy for hypercalcemia (fluid therapy, furosemide, prednisone) had no effect on circulating calcium concentrations, unlike in the others two cats, who had a good response to conventional therapy.…”

“…All of them were treated according to their symptoms, but only in a study by Crossley et al [24], was bisphosphonate used and had a good clinical outcome. It is worth mentioning that in the study by Crossley et al [24], of the three cats intoxicated with vitamin D and with hypercalcemia, pamidronate was administered in only one of them, since conventional therapy for hypercalcemia (fluid therapy, furosemide, prednisone) had no effect on circulating calcium concentrations, unlike in the others two cats, who had a good response to conventional therapy. An important observation of the before mentioned study is the fact that the cats were not made ill by a single food with inadequate amounts of vitamin D, but they received, as part of their diet, complimentary food in addition to dry extruded food, such as canned food and cat milk daily, and these were responsible for the reported vitamin D toxicosis.…”

“…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.…”

“…It promotes hydroxylation on carbon 23 of calcitriol, producing 1α,23,25-trihydroxyvitamin D 3 (1α,23,25(OH) 3 D 3 ) which, in turn, undergoes an oxidation process giving rise to 1α,25-dihydroxyvitamin D 3 -26,23-lactone.Through a second metabolic pathway, 24-hydroxylase promotes hydroxylation on carbon 24 of calcidiol and calcitriol, resulting in the formation of 24,25-dihydroxyvitamin D 3(24,25(OH) …”