| Hypervitaminosis A |
|
| Classification and external resources |
| Specialty |
endocrinology |
| ICD-10 |
E67.0 |
| ICD-9-CM |
278.2 |
| DiseasesDB |
13888 |
| MedlinePlus |
000350 |
| eMedicine |
med/2382 |
|
[edit on Wikidata]
|
Cod liver oil - a potentially toxic source of Vitamin A: Hypervitaminosis A can result from ingestion of too much vitamin A from diet, supplements, or prescription medications.
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.
Contents
- 1 Signs and symptoms
- 2 Causes
- 2.1 Types of vitamin A
- 2.2 Sources of toxicity
- 2.3 Types of toxicity
- 3 Mechanism
- 3.1 Delivery to tissues
- 3.1.1 Absorption
- 3.1.2 Storage
- 3.1.3 Transport
- 3.2 Effects
- 3.2.1 Increased bone turnover
- 3.2.2 Altered fat-soluble vitamin metabolism
- 3.2.2.1 Mitochondrial toxicity
- 4 Diagnosis
- 4.1 Tests
- 4.2 Relevance of blood tests
- 4.2.1 Retinol concentrations are nonsensitive indicators
- 4.2.2 Retinol esters have been used as markers
- 5 Prevention
- 5.1 Daily Tolerable Upper Level
- 6 Treatment
- 7 History
- 8 Other animals
- 9 See also
- 10 References
- 11 External links
Signs and symptoms
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
- Vomiting
Causes
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
- 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
- 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
- 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.
Mechanism
Absorption and storage in the liver of preformed vitamin A occur very efficiently until a pathologic condition develops.[20]
Delivery to tissues
Absorption
When ingested, 70-90% of preformed vitamin A is absorbed and used.[20]
Storage
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.[20]
Transport
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.[29]
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.[20]
Effects
Effects include increased bone turnover and altered metabolism of fat-soluble vitamins. More research is needed to fully elucidate the effects.
Increased bone turnover
Retinoic acid suppresses osteoblast activity and stimulates osteoclast formation in vitro,[23] resulting in increased bone resorption and decreased bone formation. It is likely to exert this effect by binding to specific nuclear receptors (members of the retinoic acid receptor or retinoid X receptor nuclear transcription family) which are found in every cell (including osteoblasts and osteoclasts).
This change in bone turnover is likely to be the reason for numerous effects seen in hypervitaminosis A, such as hypercalcemia and numerous bone changes such as bone loss that potentially leads to osteoporosis, spontaneous bone fractures, altered skeletal development in children, skeletal pain, radiographic changes,[20][23] and bone lesions.[30]
Altered fat-soluble vitamin metabolism
Vitamin A is fat-soluble and high levels have been reported affect metabolism of the other fat-soluble vitamins D,[23] E, and K.
The toxic effects of vitamin A might be related to altered vitamin D metabolism, concurrent ingestion of substantial amounts of vitamin D, or binding of vitamin A to receptor heterodimers. Antagonistic and synergistic interactions between these two vitamins have been reported, as they relate to skeletal health.
Stimulation of bone resorption by vitamin A has been reported to be independent of its effects on vitamin D.[23]
Mitochondrial toxicity
Vitamin A exerts several toxic effects regarding redox environment and mitochondrial function [31]
Diagnosis
Tests
Tests may include:[1]
- bone X-rays
- blood calcium test
- cholesterol test
- liver function test
- blood test for vitamin A
Relevance of blood tests
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.[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
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]
Prevention
Hypervitaminosis A can be prevented by not ingesting more than the US Institute of Medicine Daily Tolerable Upper Level of intake for Vitamin A. This level is for synthetic and natural retinol ester forms of vitamin A. Carotene forms from dietary sources are not toxic. 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.
Daily Tolerable Upper Level
| Life stage group category |
Upper Level (μg/day) |
| Infants
0–6 months
7–12 months
|
600
600 |
| Children
1–3 years
4–8 years
|
600
900 |
| Males
9–13 years
14–18 years
19 – >70 years
|
1700
2800
3000 |
| Females
9–13 years
14–18 years
19 – >70 years
|
1700
2800
3000 |
| Pregnancy
<19 years
19 – >50 years
|
2800
3000 |
| Lactation
<19 years
19 – >50 years
|
2800
3000 |
See the USDA Nutrient Database for the amount of Vitamin A http://ndb.nal.usda.gov/
Treatment
- Stopping high Vitamin A intake is the standard treatment. Most people fully recover.[1]
- Phosphatidylcholine (in the form of PPC or DLPC), the substrate for Lecithin retinol acyltransferase, which converts retinol into Retinyl esters (the storage forms of vitamin A).
- Vitamin E may alleviate hypervitaminosis A.[32]
- Liver transplantation may be a valid option if no improvement occurs.[33]
If liver damage has progressed into fibrosis, synthesizing capacity is compromised and supplementation can replenish PC. However, recovery is dependent on removing the causative agent; stopping high Vitamin A intake.[34][35][36][37]
History
Vitamin A toxicity is known to be an ancient phenomenon; fossilized skeletal remains of early humans suggest bone abnormalities may have been caused by hypervitaminosis A.[20]
Vitamin A toxicity has long been known to the Inuit and has been known by Europeans since at least 1597 when Gerrit de Veer wrote in his diary that, while taking refuge in the winter in Nova Zemlya, he and his men became severely ill after eating polar bear liver.[38]
In 1913, Antarctic explorers Douglas Mawson and Xavier Mertz were both poisoned (and Mertz died) from eating the livers of their sled dogs during the Far Eastern Party.[39] Another study suggests, however, that exhaustion and diet change are more likely to have caused the tragedy.[40]
Other animals
Some Arctic animals demonstrate no signs of hypervitaminosis A despite having 10-20 times the level of vitamin A in their livers as other Arctic animals. These animals are top predators and include the polar bear, Arctic fox, bearded seal, and glaucous gull. This ability to efficiently store higher amounts of vitamin A may have contributed to their survival in the extreme environment of the Arctic.[41]
Hypervitaminosis A causes hypothyroidism in mouse.[42]
Treatment
These treatments have been used to help treat or manage toxicity in animals. Although not considered part of standard treatment, they might be of some benefit to humans.
- Vitamin E appears to be an effective treatment in rabbits,[43] prevents side effects in chicks[44]
- Taurine significantly reduces toxic effects in rats.[45] Retinoids can be conjugated by taurine and other substances. Significant amounts of retinotaurine are excreted in the bile,[46] and this retinol conjugate is thought to be an excretory form, as it has little biological activity.[47]
- Cholestin - significantly reduces toxic effects in rats.[48]
- Vitamin K prevents hypoprothrombinemia in rats and can sometimes control the increase in plasma/cell ratios of vitamin A.[49]
See also
- Vitamin poisoning
- Far Eastern Party
- Retinoic acid syndrome
- Piblokto
References
- ^ a b c http://www.ncbi.nlm.nih.gov/pubmedhealth/PMH0001390/[full citation needed]
- ^ Gorospe M, Fadare O (May 2007). "Gastric mucosal calcinosis: clinicopathologic considerations". Advances in Anatomic Pathology. 14 (3): 224–8. PMID 17452819. doi:10.1097/PAP.0b013e31805048ea.
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- ^ Wall M (March 2008). "Idiopathic intracranial hypertension (pseudotumor cerebri)". Current Neurology and Neuroscience Reports. 8 (2): 87–93. PMID 18460275. doi:10.1007/s11910-008-0015-0.
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- ^ Tholen W, Paquet KJ, Rohner HG, Albrecht M (August 1980). "[Cirrhosis of the liver and esophageal bleeding after chronic vitamin A intoxication (author's transl)]". Leber, Magen, Darm. 10 (4): 193–7. PMID 6969836.
- ^ Jorens PG, Michielsen PP, Pelckmans PA, Fevery J, Desmet VJ, Geubel AP, Rahier J, Van Maercke YM (December 1992). "Vitamin A abuse: development of cirrhosis despite cessation of vitamin A. A six-year clinical and histopathologic follow-up". Liver. 12 (6): 381–6. PMID 1470008. doi:10.1111/j.1600-0676.1992.tb00592.x.
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- ^ Cho DY, Frey RA, Guffy MM, Leipold HW (November 1975). "Hypervitaminosis A in the dog". American Journal of Veterinary Research. 36 (11): 1597–1603. PMID 1190603.
- ^ Kodaka T, Takaki H, Soeta S, Mori R, Naito Y (July 1998). "Local disappearance of epiphyseal growth plates in rats with hypervitaminosis A". The Journal of Veterinary Medical Science. 60 (7): 815–21. PMID 9713809. doi:10.1292/jvms.60.815.
- ^ Soeta S, Mori R, Kodaka T, Naito Y, Taniguchi K (March 1999). "Immunohistochemical observations on the initial disorders of the epiphyseal growth plate in rats induced by high dose of vitamin A". The Journal of Veterinary Medical Science. 61 (3): 233–8. PMID 10331194. doi:10.1292/jvms.61.233.
- ^ Soeta S, Mori R, Kodaka T, Naito Y, Taniguchi K (March 2000). "Histological disorders related to the focal disappearance of the epiphyseal growth plate in rats induced by high dose of vitamin A". The Journal of Veterinary Medical Science. 62 (3): 293–9. PMID 10770602. doi:10.1292/jvms.62.293.
- ^ Rothenberg AB, Berdon WE, Woodard JC, Cowles RA (December 2007). "Hypervitaminosis A-induced premature closure of epiphyses (physeal obliteration) in humans and calves (hyena disease): a historical review of the human and veterinary literature". Pediatric Radiology. 37 (12): 1264–7. PMID 17909784. doi:10.1007/s00247-007-0604-0.
- ^ Wick JY (February 2009). "Spontaneous fracture: multiple causes". The Consultant Pharmacist. 24 (2): 100–2, 105–8, 110–2. PMID 19275452. doi:10.4140/TCP.n.2009.100.
- ^ a b c d e f g h i j k l m n o p Penniston KL, Tanumihardjo SA (February 2006). "The acute and chronic toxic effects of vitamin A". The American Journal of Clinical Nutrition. 83 (2): 191–201. PMID 16469975.
- ^ Corić-Martinović V, Basić-Jukić N (2008). "[Uremic pruritus]". Acta Medica Croatica. 62 Suppl 1: 32–6. PMID 18578330.
- ^ Carpenter TO, Pettifor JM, Russell RM, Pitha J, Mobarhan S, Ossip MS, Wainer S, Anast CS (October 1987). "Severe hypervitaminosis A in siblings: evidence of variable tolerance to retinol intake". The Journal of Pediatrics. 111 (4): 507–12. PMID 3655980. doi:10.1016/s0022-3476(87)80109-9.
- ^ a b c d e Barker ME, Blumsohn A (November 2003). "Is vitamin A consumption a risk factor for osteoporotic fracture?". The Proceedings of the Nutrition Society. 62 (4): 845–50. PMID 15018484. doi:10.1079/PNS2003306.
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- ^ The Phoca barbata listed on pages 167–168 of the previous reference is now known as Erignathus barbatus
- ^ "Walrus, liver, raw (Alaska Native)". Mealographer. Retrieved 2010-03-25.
- ^ "Moose, liver, braised (Alaska Native)". Mealographer. Retrieved 2012-10-15.
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- ^ Hough S, Avioli LV, Muir H, Gelderblom D, Jenkins G, Kurasi H, Slatopolsky E, Bergfeld MA, Teitelbaum SL (June 1988). "Effects of hypervitaminosis A on the bone and mineral metabolism of the rat". Endocrinology. 122 (6): 2933–9. PMID 3371268. doi:10.1210/endo-122-6-2933.
- ^ de Oliveira MR (2015). "Vitamin A and Retinoids as Mitochondrial Toxicants". Oxidative Medicine and Cellular Longevity. 2015: 140267. PMC 4452429 . PMID 26078802. doi:10.1155/2015/140267.
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- ^ Okiyama W, Tanaka N, Nakajima T, Tanaka E, Kiyosawa K, Gonzalez FJ, Aoyama T (June 2009). "Polyenephosphatidylcholine prevents alcoholic liver disease in PPARalpha-null mice through attenuation of increases in oxidative stress". Journal of Hepatology. 50 (6): 1236–46. PMC 2809859 . PMID 19398233. doi:10.1016/j.jhep.2009.01.025.
- ^ Wu J, Zern MA (2000). "Hepatic stellate cells: a target for the treatment of liver fibrosis". Journal of Gastroenterology. 35 (9): 665–72. PMID 11023037. doi:10.1007/s005350070045.
- ^ Navder KP, Lieber CS (March 2002). "Dilinoleoylphosphatidylcholine is responsible for the beneficial effects of polyenylphosphatidylcholine on ethanol-induced mitochondrial injury in rats". Biochemical and Biophysical Research Communications. 291 (4): 1109–12. PMID 11866479. doi:10.1006/bbrc.2002.6557.
- ^ Lips P (January 2003). "Hypervitaminosis A and fractures". The New England Journal of Medicine. 348 (4): 347–9. PMID 12540650. doi:10.1056/NEJMe020167.
- ^ Nataraja, Anjali (2002). "Man's best friend?". Student BMJ. 10: 131–70.
- ^ Carrington-Smith D (2005). "Mawson and Mertz: a re-evaluation of their ill-fated mapping journey during the 1911-1914 Australasian Antarctic Expedition". The Medical Journal of Australia. 183 (11–12): 638–41. PMID 16336159.
- ^ Senoo H, Imai K, Mezaki Y, Miura M, Morii M, Fujiwara M, Blomhoff R (October 2012). "Accumulation of vitamin A in the hepatic stellate cell of arctic top predators". Anatomical Record. 295 (10): 1660–8. PMID 22907891. doi:10.1002/ar.22555.
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- ^ St Claire MB, Kennett MJ, Besch-Williford CL (July 2004). "Vitamin A toxicity and vitamin E deficiency in a rabbit colony". Contemporary Topics in Laboratory Animal Science. 43 (4): 26–30. PMID 15264766.
- ^ Weiser H, Probst HP, Bachmann H (September 1992). "Vitamin E prevents side effects of high doses of vitamin A in chicks". Annals of the New York Academy of Sciences. 669: 396–8. Bibcode:1992NYASA.669..396W. PMID 1444058. doi:10.1111/j.1749-6632.1992.tb17134.x.
- ^ Yeh Y, Lee Y, Hsieh H, Hwang D (2008). "Effect of taurine on toxicity of vitamin a in rats". Food Chemistry. 106: 260–8. doi:10.1016/j.foodchem.2007.05.084.
- ^ Skare KL, DeLuca HF (July 1983). "Biliary metabolites of all-trans-retinoic acid in the rat". Archives of Biochemistry and Biophysics. 224 (1): 13–8. PMID 6870249. doi:10.1016/0003-9861(83)90185-6.
- ^ Skare KL, Sietsema WK, DeLuca HF (August 1982). "The biological activity of retinotaurine". The Journal of Nutrition. 112 (8): 1626–30. PMID 7097369.
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External links
- Facts about Vitamin A and Carotenoids, from the National Institutes of Health's Office of Dietary Supplements.
|
Malnutrition or nutrition disorders (E40–E68, 260–269)
|
| Malnutrition |
Protein-energy
malnutrition |
- Kwashiorkor
- Marasmus
- Catabolysis
|
| Vitamin deficiency |
| B vitamins |
- B1: Beriberi / Wernicke–Korsakoff syndrome (Wernicke's encephalopathy
- Korsakoff's syndrome)
- B2: Riboflavin deficiency
- B3: Pellagra (Niacin deficiency)
- B6: Pyridoxine deficiency
- B7: Biotin deficiency
- B9: Folate deficiency
- B12: Vitamin B12 deficiency
|
Other
vitamins |
- A: Vitamin A deficiency/Bitot's spots
- C: Scurvy
- D: Vitamin D deficiency/Rickets/Osteomalacia
- E: Vitamin E deficiency
- K: Vitamin K deficiency
|
|
Mineral
deficiency |
- Sodium
- Potassium
- Magnesium
- Calcium
- Iron
- Zinc
- Manganese
- Copper
- Iodine
- Chromium
- Molybdenum
- Selenium (Keshan disease)
|
|
| Overnutrition |
|
|
- Childhood obesity
- Obesity hypoventilation syndrome
- Abdominal obesity
|
| Vitamin poisoning |
- Hypervitaminosis A
- Hypervitaminosis D
- Hypervitaminosis E
|
| Mineral overload |
- see inborn errors of metal metabolism, toxicity
|
|