Hypervitaminosis A
| Hypervitaminosis A | |
|---|---|
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| Classification and external resources | |
| Specialty | endocrinology |
| ICD-10 | E67.0 |
| ICD-9-CM | 278.2 |
| DiseasesDB | 13888 |
| MedlinePlus | 000350 |
| eMedicine | med/2382 |
Hypervitaminosis A refers to the toxic effects of ingesting too much preformed vitamin A. Symptoms arise as a result of altered bone metabolism and altered metabolism of other fat-soluble vitamins. Hypervitaminosis A is believed to have occurred in early humans, and the problem has persisted throughout human history.
Toxicity results from ingesting too much preformed vitamin A from foods (such as fish or animal liver), supplements, or prescription medications and can be prevented by ingesting no more than the recommended daily amount.
Diagnosis can be difficult, as serum retinol is not sensitive to toxic levels of vitamin A, but there are effective tests available. Hypervitaminosis A is usually treated by stopping intake of the offending food(s), supplement(s), or medication. Most people make a full recovery.
High intake of provitamin carotenoids (such as beta carotene) from vegetables and fruits does not cause hypervitaminosis A, as conversion from carotenoids to the active form of vitamin A is regulated by the body to maintain an optimum level of the vitamin. Carotenoids themselves cannot produce toxicity.
Symptoms may include:
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.
Absorption and storage in the liver of preformed vitamin A occur very efficiently until a pathologic condition develops.
When ingested, 70-90% of preformed vitamin A is absorbed and used.
80-90% of the total body reserves of vitamin A are in the liver (with 80-90% of this amount being stored in hepatic stellate cells and the remaining 10-20% being stored in hepatocytes). Fat is another significant storage site, while the lung and kidneys may also be capable of storage.
Until recently, it was thought that the sole important retinoid delivery pathway to tissues involved retinol bound to retinol-binding protein (RBP4). More recent findings, however, indicate that retinoids can be delivered to tissues through multiple overlapping delivery pathways, involving chylomicrons, very low density lipoprotein (VLDL) and low density lipoprotein (LDL), retinoic acid bound to albumin, water soluble β-glucuronides of retinol and retinoic acid, and provitamin A carotenoids.
The range of serum retinol concentrations under normal conditions is 1–3 μmol/l. 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. Candidate mechanisms for this increase include decreased hepatic uptake of vitamin A and the leaking of esters into the bloodstream from saturated hepatic stellate cells.
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