Saturday, May 9, 2015

Hypervitaminosis A

Acute hypervitaminosis A results from ingestion of very large amounts of the vitamin during a relatively short period of time.

Chronic hypervitaminosis A in humans is more common than acute hypervitaminosis A. Serum levels of vitamin A are generally more than 3.49 umol/liter and there are increased levels of the unbound retinol resulting in a change in the ration of free retinal to retinal bound to RBP as well as increase in retinyl esters.

A symptoms of acute hypervitaminosis A include nausea, vomiting, double or blurred vision, increased intracranial pressure, headache, dizziness, skin desquamation, and muscle in-coordination.

Chronic hypervitaminosis A can result from high intakes of vitamin A over long period of time and/or in connection with liver or kidney disease.

The effects of hypervitaminosis A on the liver, the primary storage site for vitamin A, are multiple. They include fat storing cell hyperplasia and hyper trophy, fibrogenesis, sclerosis of veins, portal hypertension and congestion in perisinusoid cells, which leads to hepatocellular damage and cirrhosis o a cirrhosislike hepatic disorder.

Vitamin A in very large doses is known to be teratogenic in many animals. Excessive intake of vitamin A has also been associated with human congenital abnormalities in some cases reports although a causal relationship has not been established.

High intakes should be avoided by pregnant women. Hypervitaminosis A in pregnant women can lead to fetal abnormality, but such cases are very rare. Levels of vitamin A intake associated with hypervitaminosis A varies according to the health and size of the person.

As little as 12,000 IU per day, given to small children for an extended period, has been reportedly led to toxicity symptoms.

Hypervitaminosis A may result from acute ingestion of about 500,000 IU of vitamin A by an adult, or from a chronic daily intake of about 100,000 IU. Cases of hypervitaminosis A caused by natural food sources are rare but they have a very long history.

It has been hypothesized that pathological changes found in a Homo erectus skeleton from 1.5 million years ago were caused by hypervitaminosis A attributable to the consumption of carnivore livers.
Hypervitaminosis A

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