Vitamin B12 deficiency in children is rare. Early diagnosisand treatment of this disorder in childhood are importantbecause of the danger of irreversible neurologic damage.Most cases in childhood result from a specific defect inabsorption (see Table 31-2). Such defects include congenital pernicious anemia (absent intrinsic factor), juvenile pernicious anemia (autoimmune), and deficiency of transcobalamin II transport. Gastric or intestinal resection and smallbowel bacterial overgrowth also cause vitamin B12 deficiency. Exclusively breastfed infants ingest adequate vitaminB12 unless the mother is a strict vegetarian without supplementation.
Depression of serum vitamin B12 and the appearance of hypersegmented neutrophils and macrocytosis (indistinguishable from folate deficiency) are early clinical manifestations of deficiency. Vitamin B12 deficiency also causes neurologic manifestations, including depression, peripheral neuropathy, posterior spinal column signs, dementia, and eventual coma. The neurologic signs do not occur in folate deficiency, but administration of folate may mask the hematologic signs of vitamin B12 deficiency, while the neurologic manifestations progress. Patients with vitamin B12 deficiency also have increased urine levels of methylmalonic acid. Most cases of vitamin B12 deficiency in infants and children are not of dietary origin and require treatment throughout life. Maintenance therapy consists of repeated monthly intramuscular injections, although a form of vitamin B12 is administered intranasally.
Fat-soluble vitamins generally have stores in the body, and dietary deficiencies generally develop more slowly than for water-soluble vitamins. Absorption of fat-soluble vitamins depends on normal fat intake, digestion, and absorption. The complexity of normal fat absorption and the potential for perturbation in many disease states explains the more common occurrence of deficiencies of these vitamins.
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The basic constituent of the vitamin A group is retinol.Ingested plant carotene or animal tissue retinol estersrelease retinol after hydrolysis by pancreatic and intestinal enzymes. Chylomicron-transported retinol esters arestored in the liver as retinol palmitate. Retinol is transportedfrom the liver to target tissues by retinol-binding protein,releasing free retinol to the target tissues. The kidney thenexcretes the retinol-binding protein. Diseases of the kidneydiminish excretion of retinol-binding protein, whereas liverparenchymal disease or malnutrition lowers the synthesis ofretinol-binding protein. Specific cellular binding proteinsfacilitate the uptake of retinol by target tissues. In the eye, retinol is metabolized to form rhodopsin; the action of light onrhodopsin is the first step of the visual process. Retinol alsoinfluences the growth and differentiation of epithelia. Theclinical manifestations of vitamin A deficiency in humansappear as a group of ocular signs termed xerophthalmia. The earliest symptom is night blindness, which is followed by xerosis of the conjunctiva and cornea. Untreated, xerophthalmia can result in ulceration, necrosis, keratomalacia, and a permanent corneal scar. Clinical and subclinical vitamin A deficiencies are associated with immunodeficiency; increased risk of infection, especially measles; and increasedrisk of mortality, especially in developing nations. Xerophthalmia and vitamin A deficiency should be urgently treated.Hypervitaminosis A also has serious sequelae, includingheadaches, pseudotumor cerebri, hepatotoxicity, and teratogenicity.