Chapter 071. Vitamin and Trace Mineral Deficiency and Excess (Part 10)

ToxicityAcute toxicity of vitamin A was first noted in Arctic explorers who ate polar bear liver and has also been seen after administration of 150 mg in adults or 100 mg in children. Acute toxicity is manifested by increased intracranial pressure, vertigo, diplopia, bulging fontanels in children, seizures, and exfoliative dermatitis; it may result in death. In children being treated for vitamin A deficiency according to the protocols outlined above, transient bulging of fontanels occurs in 2% of infants, and transient nausea, vomiting, and headache occur in 5% of preschoolers. Chronic vitamin A intoxication is largely a concern in...
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Chapter 071. Vitamin and Trace Mineral Deficiency and Excess (Part 10) Chapter 071. Vitamin and Trace Mineral Deficiency and Excess (Part 10) Toxicity Acute toxicity of vitamin A was first noted in Arctic explorers who atepolar bear liver and has also been seen after administration of 150 mg in adults or100 mg in children. Acute toxicity is manifested by increased intracranialpressure, vertigo, diplopia, bulging fontanels in children, seizures, and exfoliativedermatitis; it may result in death. In children being treated for vitamin Adeficiency according to the protocols outlined above, transient bulging offontanels occurs in 2% of infants, and transient nausea, vomiting, and headacheoccur in 5% of preschoolers. Chronic vitamin A intoxication is largely a concernin industrialized countries and has been seen in normal adults who ingest 15 mg/dand children who ingest 6 mg/d of vitamin A over a period of several months.Manifestations include dry skin, cheilosis, glossitis, vomiting, alopecia, bonedemineralization and pain, hypercalcemia, lymph node enlargement,hyperlipidemia, amenorrhea, and features of pseudotumor cerebri with increasedintracranial pressure and papilledema. Liver fibrosis with portal hypertension andbone demineralization may result from chronic vitamin A intoxication. Whenvitamin A is provided in excess to pregnant women, congenital malformationshave included spontaneous abortions, craniofacial abnormalities, and valvularheart disease. In pregnancy, the daily dose of vitamin A should not exceed 3 mg.Commercially available retinoid derivatives are also toxic, including 13-cis-retinoic acid, which has been associated with birth defects. As a result,contraception should be continued for a least 1 year, and possibly longer, inwomen who have taken 13-cis retinoic acid. High doses of carotenoids do not result in toxic symptoms but should beavoided in smokers due to an increased risk of lung cancer. Carotenemia, which ischaracterized by a yellowing of the skin (creases of the palms and soles) but notthe sclerae, may be present after ingestion of >30 mg of β-carotene daily.Hypothyroid patients are particularly susceptible to the development ofcarotenemia due to impaired breakdown of carotene to vitamin A. Reduction ofcarotenes from the diet results in the disappearance of skin yellowing andcarotenemia over a period of 30–60 days Vitamin D See Chap. 346, Fig. 71-1, and Table 71-1 Vitamin E Vitamin E is a collective name for all stereoisomers of tocopherols andtocotrienols, although only the 2R tocopherols meet human requirements. VitaminE acts as a chain-breaking antioxidant and is an efficient pyroxyl radicalscavenger, which protects low-density lipoproteins (LDLs) and polyunsaturatedfats in membranes from oxidation. A network of other antioxidants (e.g., vitaminC, glutathione) and enzymes maintains vitamin E in a reduced state. Vitamin Ealso inhibits prostaglandin synthesis and the activities of protein kinase C andphospholipase A2. Absorption and Metabolism After absorption, vitamin E is taken up from chylomicrons by the liver, anda hepatic αtocopherol transport protein mediates intracellular vitamin E transportand incorporation into very low-density lipoprotein (VLDL). The transport proteinhas particular affinity for the RRR isomeric form of αtocopherol; thus this naturalisomer has the most biologic activity. Requirement Vitamin E is widely distributed in the food supply and is particularly highin sunflower oil, safflower oil, and wheat germ oil; γtocotrienols are notablypresent in soybean and corn oils. Vitamin E is also found in meats, nuts, and cerealgrains, and small amounts are present in fruits and vegetables. Vitamin E pillscontaining doses of 50–1000 mg are ingested by a large fraction of the U.S.population. The RDA for vitamin E is 15 mg/d (34.9 µmol or 22.5 IU) for alladults. Diets high in polyunsaturated fats may necessitate a slightly higherrequirement for vitamin E. Dietary deficiency of vitamin E does not exist. Vitamin E deficiency is seenin only severe and prolonged malabsorptive diseases, such as celiac disease, orafter small-intestinal resection. Children with cystic fibrosis or prolongedcholestasis may develop vitamin E deficiency characterized by areflexia andhemolytic anemia. Children with abetalipoproteinemia cannot absorb or transportvitamin E and become deficient quite rapidly. A familial form of isolated vitaminE deficiency also exists; it is due to a defect in the αtocopherol transport protein.Vitamin E deficiency causes axonal degeneration of the large myelinated axonsand results in posterior column and spinocerebellar symptoms. Peripher ...