Hypervitaminosis A

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief:

Hypervitaminosis A
File:Retinol structure.svg
ICD-10 E67.0
ICD-9 278.2
DiseasesDB 13888
eMedicine med/2382 

Overview

Hypervitaminosis A refers to the effects of excessive vitamin A (specifically retinoid) intake.

Presentation

Effects include:

Signs

Signs of acute toxicity include nausea and vomiting, headache, dizziness, blurred vision, and loss of muscular coordination.

Pathophysiology

Hypervitaminosis A occurs when the maximum limit for liver stores of retinoids is exceeded. The excess vitamin A enters the circulation causing systemic toxicity. Vitamin A in the form of betacarotene is only selectively converted into retinoids, and hence does not cause toxicity.

Although hypervitaminosis A can occur when large amounts of liver are regularly consumed, most cases of vitamin A toxicity result from an excess intake of vitamin A in the form of vitamin supplements. Toxic symptoms can also arise after consuming very large amounts of preformed vitamin A over a short period of time.

Recommended supplement limits

The Institute of Medicine has established Daily Tolerable Upper Levels (UL) of intake for vitamin A from supplements that apply to healthy populations, in order to help prevent the risk of vitamin A toxicity. These levels for preformed vitamin A in micrograms (µg) and International Units (IU) are:

  • 0-3 years: 600 µg or 2000 IU
  • 4-8 years: 900 µg or 3000 IU
  • 9-13 years: 1700 µg or 5665 IU
  • 14-18 years: 2800 µg or 9335 IU
  • 19+ years: 3000 µg or 10,000 IU

The dose over and above the RDA is among the narrowest of the vitamins and minerals. Possible pregnancy, liver disease, high alcohol consumption, and smoking are indications for close monitoring and limitation of vitamin A administration. However, vitamin A has also been repeatedly tested and used therapeutically over several decades in larger amounts, 100,000 - 400,000 IU total dosage, for treatment of severe pediatric measles in areas where vitamin A deficiency may be present, in order to reduce childhood mortality.[1][2]

Toxicity from eating liver

The liver of certain animals — including the polar bear, seal, and husky — is unsafe to eat because it is extraordinarily high in vitamin A. This danger has long been known to the Inuit and has been recognized by Europeans since at least 1597 when Gerrit de Veer wrote in his diary that, while taking refuge in the winter in Nova Zembla, he and his men became gravely ill after eating polar-bear liver.[3] In 1913, Antarctic explorers Douglas Mawson and Xavier Mertz were both poisoned, the latter fatally, from eating the liver of their sled dogs.[4]

Vitamin A itself was not discovered until 1917.

The livers of many other animals have lower levels of vitamin A and are commonly eaten.

See also

External links

References

  1. Hussey GD, Klein M (1990). "A randomized controlled trial of vitamin A in children with severe measles". NEJM. 323: 160–164. 
  2. Ellison JB (1932). "Intensive vitamin therapy in measles". Br Medical J. ii: 708–711. 
  3. The New England Journal of Medicine : Hypervitaminosis A and Fractures
  4. Student BMJ Man's best friend?



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