Eight naturally occurring compounds have vitamin E activity. The most active of these, α-tocopherol, accounts for 90% of the vitamin E present in human tissues and is commercially available as an acetate or succinate. Vitamin E acts as a biologic antioxidant by inhibiting the peroxidation of polyunsaturated fatty acids present in cell membranes. It scavenges free radicals generated by the reduction of molecular oxygen and by the action of oxidative enzymes.
Vitamin E deficiency occurs in children with fat malabsorption secondary to liver disease, untreated celiac disease,cystic fibrosis, and abetalipoproteinemia. In these children, without vitamin E supplementation, a syndrome of progressive sensory and motor neuropathy develops; the first signof deficiency is loss of deep tendon reflexes. Deficient preterminfants at 1 to 2 months of age have hemolytic anemia characterized by an elevated reticulocyte count, an increased sensitivity of the erythrocytes to hemolysis in hydrogen peroxide,peripheral edema, and thrombocytosis. All the abnormalities are corrected after oral, lipid, or water-soluble vitaminE therapy.
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Cholecalciferol (vitamin D3) is the mammalian form of vitamin D and is produced by ultraviolet irradiation of inactive precursors in the skin. Ergocalciferol (vitamin D2) is derived from plants. Vitamin D2 and vitamin D3 require further metabolism to become active. They are of equivalent potency. Clothing, lack of sunlight exposure, and skin pigmentation decrease generation of vitamin D in the epidermis and dermis.
Vitamin D (D2 and D3) is metabolized in the liver to calcidiol, or 25-hydroxyvitamin D (25-[OH]-D); this metabolite, which has little intrinsic activity, is transported by a plasma-binding globulin to the kidney, where it is converted to the most active metabolite calcitriol, or 1,25-dihydroxyvitamin D (1,25-[OH]2-D). The action of 1,25-(OH)2-D results in a decrease in the concentration of messenger RNA (mRNA) for collagen in bone and an increase in the concentration of mRNA for vitamin D–dependent calcium-binding protein in the intestine (directly mediating increased intestinal calcium transport). The antirachitic action of vitamin D probably is mediated by provision of appropriate concentrations of calcium and phosphate in the extracellular space of bone and by enhanced intestinal absorption of these minerals. Vitamin D also may have a direct anabolic effect on bone. 1,25-(OH)2-D has direct feedback to the parathyroid gland and inhibits secretion of parathyroid hormone.
Vitamin D deficiency appears as rickets in children and as osteomalacia in postpubertal adolescents. Inadequate direct sun exposure and vitamin D intake are sufficient causes, butother factors, such as various drugs (phenobarbital, phenytoin) and malabsorption, may increase the risk of developmentof vitamin-deficiency rickets. Breastfed infants, especiallythose with dark-pigmented skin, are at risk for vitamin Ddeficiency.
The pathophysiology of rickets results from defective bone growth, especially at the epiphyseal cartilage matrix, which fails to mineralize. The uncalcified osteoid results in a wide, irregular zone of poorly supported tissue, the rachitic metaphysis. This soft, rather than hardened, zone produces many of the skeletal deformities through compression and lateral bulging or flaring of the ends of bones.