Hypervitaminosis A results from excessive intake of preformed vitamin A. A genetic variance in tolerance to vitamin A intake may occur.[22] Children are particularly sensitive to vitamin A, with daily intakes of 1500 IU/kg body weight reportedly leading to toxicity.[20]
Types of vitamin A[edit] => Provitamin carotenoids - such as beta carotene - are “largely impossible” to cause toxicity, as their conversion to retinol is highly regulated.[20] No vitamin A toxicity has ever been reported from ingestion of excessive amounts.[23] 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.[20] When ingested, 70-90% of preformed vitamin A is absorbed and used.[20
Sources of toxicity[edit] => Diet - liver is high in vitamin A. The liver of certain animals — including the polar bear, bearded seal,[24][25] walrus,[26] moose,[27] — 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.[28
Types of toxicity[edit] => 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[edit] => Tests may include:[1]
bone X-rays&blood calcium test&cholesterol test&liver function test&blood test for vitamin
Retinol concentrations are nonsensitive indicators[edit] => 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.[20] 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[20]
Retinol esters have been used as markers[edit] => 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.[20]
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.[20] 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.[20]
Symptoms may include:[1]
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[2]&Heart valve calcification[3]&Hypercalcemia&Increased intracranial pressure manifesting as cerebral edema, papilledema, and headache[4] (may be referred to as Idiopathic intracranial hypertension)&Irritability&Liver damage[5][6][7][8][9][10][11][12][13]&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[14][15][16][17][18]&Skin peeling, itching&Spontaneous fracture[19][20]&Yellow discoloration of the skin (aurantiasis cutis)&Uremic pruritus[21]&Vision changes&Vomitin