Vitamin D intoxication

Vitamin D (VD) toxicity requires serum levels of 25-hydroxyvitamin D (25(OH)D) above 150 ng/mL and is mainly associated with exposure to extreme doses due to manufacturing or intake errors. Symptoms are related to secondary hypercalcemia caused by increased calcium intestinal absorption and release from bone stores. VD supplementation is common in the cystic fibrosis (CF) population due to the high prevalence of vitamin D deficiency secondary to exocrine pancreatic insufficiency, reduced fat stores and decreased sunlight exposure. As a result of exocrine pancreatic insufficiency and secondary fat malabsorption, this supplementation is frequently combined with pancreatic enzymes and other liposoluble vitamins (A, E, K), either under the form of commercial products or, in countries where these are not available, under the form of compounding or magistral prescriptions. The latter is dependent on human intervention and has been associated with intoxications due to dosage errors. Vitamin D toxicity is associated with accidental overdoses due to manufacturing or intake errors and its secondary hypercalcemia can result in severe morbidity. Although patients with cystic fibrosis are potentially at increased risk for this intoxication as prescription of vitamin D preparations is a common practice in this population, the frequency of such events is currently unknown.

Vitamin D3 (D3) is currently the recommended form of substitution for patients with CF and it can be obtained from the transformation of 7-dehydrocholesterol to D3 by UV-light in the skin or through dietary intake. Circulating D3 undergoes a first hydroxylation step in the liver by vitamin D 25-hydroxylase, yielding 25(OH)D before being hydroxylated in the kidney to 1,25(OH)2D, its effective form under normal conditions. This metabolite is then capable of binding the vitamin D receptor (VDR) with a strong affinity, influencing the behaviour of cells implicated in bone turn-over, calcium-phosphate metabolism or immunity. The first hydroxylation step is much less controlled than the second one, resulting in high 25(OH)D levels in case of D3 overdose while 1,25(OH)2D levels remain normal or are slightly elevated. This excessive 25(OH)D is subsequently able to exceed the binding capacity of its transporter protein, the vitamin D-binding protein (VDBP) and to interact with the VDR, for which it has some affinity. Inappropriate interaction with the VDR can then mediate pathologic intestinal calcium reabsorption and mobilization from bone, resulting in hypercalcemia and gastro-intestinal (nausea, vomiting, constipation, polydipsia), neurological (confusion, depression, hallucination, coma), cardiac (QT shortening, ST-segment elevation, bradyarrythmias), or renal (polyuria, nephrocalcinosis, acute kidney injury) symptoms.

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