Hypervitaminosis A results from excessive intake of preformed vitamin A. A genetic variance in tolerance to vitamin A intake may occur. Children are particularly sensitive to vitamin A, with daily intakes of 1500 IU/kg body weight reportedly leading to toxicity.
- Types of vitamin A => Provitamin carotenoids-such as beta carotene-are “largely impossible” to cause toxicity, as their conversion to retinol is highly regulated. No vitamin A toxicity has ever been reported from ingestion of excessive amounts. Overconsumption of beta carotene can only cause carotenosis, a harmless and reversible cosmetic condition in which the skin turns orange.
- Preformed vitamin A absorption and storage in the liver occur very efficiently until a pathologic condition develops. When ingested, 70 – 90% of preformed vitamin A is absorbed and used.
- Sources of toxicity => Diet-liver is high in vitamin A. The liver of certain animals — including the polar bear, bearded seal, walrus, moose, — are particularly toxic.
- Supplements-usually when taken above recommended dosages-can be toxic. Cod liver oil is particularly high in vitamin A.
- Medications-at high doses of vitamin A-are often used on long-term basis in numerous preventive and therapeutic medical applications, which may lead to hypervitaminosis A.
- Types of toxicity => Acute toxicity occurs over a period of hours or a few days, and is less of a problem than chronic toxicity.
- Chronic toxicity-ingestion of high amounts of preformed vitamin A for months or years-results from daily intakes greater than 25,000 IU for 6 years or longer and more than 100,000 IU for 6 months or longer-are considered toxic.
Tests => Tests may include:
- bone X-rays
- blood calcium test
- cholesterol test
- liver function test
- blood test for vitamin.
Retinol concentrations are nonsensitive indicators => Assessing vitamin A status in persons with subtoxicity or toxicity is complicated because serum retinol concentrations are not sensitive indicators in this range of liver vitamin A reserves. The range of serum retinol concentrations under normal conditions is 1–3 μmol/l and, because of homeostatic regulation, that range varies little with widely disparate vitamin A intakes.
Retinol esters have been used as markers => Retinyl esters can be distinguished from retinol in serum and other tissues and quantified with the use of methods such as high-performance liquid chromatography.
Elevated amounts of retinyl ester (i.e. , > 10% of total circulating vitamin A) in the fasting state have been used as markers for chronic hypervitaminosis A in humans and monkeys. This increased retinyl ester may be due to decreased hepatic uptake of vitamin A and the leaking of esters into the bloodstream from saturated hepatic stellate cells.
Symptoms may include:
- Abnormal softening of the skull bone (craniotabes—infants and children)
- Blurred vision
- Bone pain or swelling
- Bulging fontanelle (infants)
- Changes in consciousness
- Decreased appetite
- Dizziness
- Double vision (young children)
- Drowsiness
- Headache
- Gastric mucosal calcinosis
- Heart valve calcification
- Hypercalcemia
- Increased intracranial pressure manifesting as cerebral edema, papilledema, and headache (may be referred to as Idiopathic intracranial hypertension)
- Irritability
- Liver damage
- Nausea
- Poor weight gain (infants and children)
- Skin and hair changes
- Cracking at corners of the mouth
- Hair loss
- Higher sensitivity to sunlight
- Oily skin and hair (seborrhea)
- Premature epiphyseal closure
- Skin peeling, itching
- Spontaneous fracture
- Yellow discoloration of the skin (aurantiasis cutis)
- Uremic pruritus
- Vision changes
- Vomitin