Vitamin d toxicity disease
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Understanding Vitamin D Toxicity Disease
Introduction to Vitamin D Toxicity
Vitamin D toxicity, also known as hypervitaminosis D, is a rare but potentially serious condition resulting from excessive intake of vitamin D. This condition can lead to severe hypercalcemia, which can cause various health issues if not promptly identified and treated1 2 5.
Causes of Vitamin D Toxicity
Overdose and Manufacturing Errors
Vitamin D toxicity often arises from the inadvertent or improper intake of high doses of vitamin D supplements. This can be due to errors in prescription, self-administration of doses higher than recommended, or manufacturing errors in vitamin D-containing products1 2 6. For instance, cases have been reported where patients consumed supplements with vitamin D content far exceeding the labeled amount, leading to severe toxicity6.
Endogenous Factors
Endogenous vitamin D toxicity can occur due to excessive production of active vitamin D metabolites in certain diseases, such as granulomatous disorders and some lymphomas, or due to genetic conditions like Williams-Beuren syndrome2. These conditions can lead to elevated levels of 1,25-dihydroxyvitamin D, contributing to hypercalcemia2.
Symptoms of Vitamin D Toxicity
The clinical manifestations of vitamin D toxicity are primarily related to hypercalcemia. Common symptoms include confusion, apathy, recurrent vomiting, abdominal pain, polyuria, polydipsia, and dehydration2 4 8. In severe cases, hypercalcemia can lead to life-threatening conditions such as acute kidney injury and cardiovascular complications6 7.
Diagnosis and Biochemical Indicators
Serum Vitamin D and Calcium Levels
Diagnosis of vitamin D toxicity is typically based on elevated serum levels of 25-hydroxyvitamin D (25(OH)D) and calcium. Serum 25(OH)D concentrations higher than 150 ng/mL are indicative of vitamin D toxicity due to overdosing2. Hypercalcemia, with serum calcium levels significantly above the normal range, is a hallmark of this condition1 5.
Free 1,25-Dihydroxyvitamin D Levels
Recent studies suggest that elevated free levels of 1,25-dihydroxyvitamin D, despite normal total levels, might contribute to the pathogenesis of hypercalcemia in vitamin D toxicity. This is due to the displacement of 1,25-dihydroxyvitamin D from its binding protein by high levels of 25(OH)D and other metabolites7.
Risk Factors and Public Awareness
Increased Supplement Use
The growing public awareness of the health benefits of vitamin D has led to an increase in its consumption, raising the risk of vitamin D toxicity. Self-administration of vitamin D in doses higher than recommended can lead to hypercalcemia and other toxic effects2 8.
Pediatric Considerations
In children, vitamin D toxicity is rare but can occur due to high total intake from supplements or errors in manufacturing and prescription. Cases of severe hypercalcemia and nephrocalcinosis have been reported in pediatric patients3.
Conclusion
Vitamin D toxicity, though rare, is a serious condition that can result from excessive intake of vitamin D supplements or endogenous overproduction of active vitamin D metabolites. The primary clinical manifestation is severe hypercalcemia, which can lead to significant health complications. Increased public awareness and careful monitoring of vitamin D intake are essential to prevent toxicity. Medical practitioners should be vigilant in identifying and managing this condition to mitigate its potentially life-threatening effects.
Sources and full results
Most relevant research papers on this topic
Development of Vitamin D Toxicity from Overcorrection of Vitamin D Deficiency: A Review of Case Reports
Vitamin D intoxication is rare but can occur due to manufacturing errors, overdosing by patients or prescribers, and combinations of these factors.
Systematic Review
Very Rigorous Journal
Highly CitedVitamin D Toxicity–A Clinical Perspective
Vitamin D toxicity (VDT) can result from excessive long-term intake of vitamin D, malfunctions in the vitamin D metabolic pathway, or coincidental diseases, and can cause severe health effects if not identified and treated promptly.
Highly CitedVitamin D supplementation and risk of toxicity in pediatrics: a review of current literature.
Vitamin D toxicity in children is rare but life-threatening, and monitoring levels is recommended for infants receiving long-term supplementation at or above the recommended upper intake.
Systematic Review
Rigorous JournalHighly CitedVitamin D Toxicity: A Clinical Perspective
Vitamin D toxicity (VDT) is caused by excessive long-term intake of vitamin D, malfunctions in the vitamin D metabolic pathway, or coincidental disease, and can result in severe hypercalcemia if not promptly identified.
Highly CitedVitamin D toxicity – causes, symptoms and diagnosis
Overdosing vitamin D can lead to vitamin D toxicity, which can range from asymptomatic to life-threatening, and medical practitioners should be alert to identify it quickly.
Systematic ReviewVitamin D Toxicity from an Unusual and Unexpected Source: A Report of 2 Cases
Two cases of hypervitaminosis D were caused by a manufacturing error in a creatine supplement, despite not claiming to contain vitamin D.
Case ReportSerum Levels of Free 1,25-Dihydroxyvitamin D in Vitamin D Toxicity
High levels of 25-hydroxyvitamin D may cause increased free 1,25-dihydroxyvitamin D levels, which may contribute to the hypercalcemia and hypercalciuria in vitamin D toxicity patients.
Highly CitedVitamin D toxicity syndrome: a toxicologist's view
Overuse of vitamin D, particularly through pharmaceuticals and dietary supplements, can lead to vitamin D toxicity, requiring regular monitoring and awareness-raising among family physicians.
Literature ReviewVitamin D toxicity related to its physiological and unphysiological supply
Large oral intake of vitamin D can cause hypercalcaemic toxicity, while moderate oral intake over time may lead to atherosclerosis.
Pharmacokinetics of vitamin D toxicity.
Vitamin D toxicity occurs when 25(OH)D(3) concentrations exceed 750 nmol/L, with potential mechanisms including over-stimulation of gene transcription, or displacement of 1alpha,25(OH)(2)D(3) from binding.
Very Rigorous JournalHighly Cited