Vitamin A, toxicity

JN Hathcock, DG Hattan, MY Jenkins, JT McDonald, PR Sundaresan, YL Wilkening. Evaluation of vitamin A toxicity. Amer J Clin Nutr 52 183-202, 1990. 

Ellis JK, Russell RM, Makrauer FL, Schaefer EJ. Increased risk for vitamin A toxicity in severe hypertriglyceridemia. Ann Intern Med 1986 105(6) 877-9. 

Figure 29-4. Stellate cell lipid droplets present in a biopsy obtained from the liver of a patient experiencing vitamin A toxicity. Image obtained from electron microscopy of a biopsied human liver showing the characteristic lipid droplets (LD) found in hepatic stellate cells (SC).These lipid droplets are highly enriched in vitamin A, and the size and number of lipid droplets is influenced by dietary vitamin A intake and nutritional status. In this image of a human stellate cell, the nucleus (N) is compressed by the surrounding lipid droplets, and very little cell cytoplasm within the stellate cell can be seen in this view.Adjoining the stellate cell are two hepatocytes (H).

RETINOIDS VITAMIN A Risk of vitamin A toxicity Additive effect tretinoin is a form of vitamin A Avoid co-administration... 

Hathcock J, Hattan D, Jenkins M, McDonald J, Sundaresan P, and Wilkening V (1990) Evaluation of vitamin A toxicity. American Journal of Clinical Nutrition 52,183-202. 

Vitamin A toxicity in an adnlt woman resnlted in hjrper-calcemia with renal insnfficiency (31). 

In chronic vitamin A ingestion, risk factors for vitamin A toxicity are age, body weight, and renal insufficiency. The hypercalcemia cansed by chronic vitamin A ingestion is explained by npregnlation of osteoclasts by retinol meta-bohtes. 

Vitamin A toxicity appears to occur only when the amount of vitamin A exceeds the binding capability of the retinol binding protein. Hypervitaminosis A can canse severe anemia and thrombocytopenia, resulting from retinol-dependent bone marrow cell growth inhibition (39). 

Young children seem to be particularly at risk of vitamin A toxicity. Symptoms of chronic intoxication are seen with intakes of 800-16 000 micrograms/kg RE (2500-50 000 lU/kg) (21). Children with restricted protein intake may have reduced tolerance to vitamin A. 

At special risk of vitamin A toxicity are those whose liver function is compromised by drugs, viral hepatitis, or protein-energy malnutrition (12). Elderly people may also be at increased risk for similar reasons but also from different causes. In addition to protein deficiency, alcohol intake and co-existing liver and renal disease may be present (86). 

Two children with vitamin A toxicity have been reported (90). 

The effect of alcohol abuse, one of the most common aggravating factors in vitamin A toxicity, has been elucidated. Vitamin A toxicity was potentiated in patients who took 10 000 lU/day for sexual dysfunction, and this effect was attributed to excess alcohol consumption (95). In animals, potentiation of vitamin A toxicity by ethanol resulted in striking hepatic inflammation and necrosis accompanied by a rise in serum glutamate dehydrogenase and aspartate transaminase (96). 

Hathcock IN, Hattan DG, Jenkins MY, McDonald JT, Sundaresan PR, Wilkening VL. Evaluation of vitamin A toxicity. Am J Clin Nutr 1990 52(2) 183-202. 

Miksad R, de Ledinghen V, McDougall C, Fiel I, Rosenberg H. Hepatic hydrothorax associated with vitamin a toxicity. J Clin Gastroenterol 2002 34(3) 275-9. 

Coghlan D, Cranswick NE. Complementary medicine and vitamin A toxicity in children. Med J Aust 2001 175(4) 223. ... 

Ingestion of large amounts of zinc oxide may cause nausea, cramps, vomiting, and diarrhea. Zinc oxide is often used in ointments along with vitamins A and D, and toxicity usually develops to these added constituents rather than the zinc oxide. It would require an ingestion of greater than 60 g of a typical ointment to result in vitamin A toxicity. Smaller amounts could also cause gastrointestinal disturbances such as diarrhea due to the emollient base. As much as... 

Ingestion of carotenes alone does not cause vitamin A toxicity, probably because of markedly decreased absorption at high doses and feedback inhibition of carotene conversion to retinaldehyde, but can cause harmless carotene-mia with yellowing of the skin, particularly on the palmar and plantar surfaces. Carotenemia can cause falsely elevated values for the icterus index or for other direct reading methods for estimating serum bilirubin (Chapter 29). 

Supplemental vitamin A is used in some neonatal treatment centers to reduce the risk of BPD and sepsis in preterm infants. However, concern over the risk of vitamin A toxicity (i.e., posthemorrhagic hydrocephalus or liver disease) and sequelae from repeated intramuscular injections of vitamin A prevent its widespread use. 

Vitamin A is needed to maintain healthy eyes, skin, and mucous membranes. It is stored in the bod/s fat cells, especially in the liver. Polar bears store huge quantities of vitamin A in their livers. In the 19th century, many Arctic explorers died from vitamin A toxicity after eating large amounts of polar bear liver. 

The client is taking vitamin A. Which assessment data would indicate to the nurse that the client is experiencing vitamin A toxicity ... 

Paresthesia is not a sign of vitamin A toxicity. It may be a sign of thiamine deficiency, along with neuralgia and progressive loss of feeling and reflexes. 

A. Chronic vitamin A toxicity is characterized by dry, peeling skin and signs of increased intracranial pressure (headache, altered mental status, and blurred vision pseudotumor cerebri). Bulging fontanelles have been described in infants. Liver injury may cause jaundice and ascites. 

B. Possible adjunctive agent in treating severe vitamin A toxicity associated with increased intracranial pressure (pseudotumor cerebri). 

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