The clinical manifestations of rickets are most common during the first 2 years of life and may become evident only after several months of a vitamin D–deficient diet. Craniotabes is caused by thinning of the outer table of the skull, which when compressed feels like a Ping-Pong ball to the touch. Enlargement of the costochondral junction (rachitic rosary) and thickening of the wrists and ankles may be palpated. The anterior fontanelle is enlarged, and its closure may be delayed. In advanced rickets, scoliosis and exaggerated lordosis may be present. Bowlegs or knock-knees may be evident in older infants, and greenstick fractures may be observed in long bones.
The diagnosis of rickets is based on a history of poor vitamin D intake and little exposure to direct ultraviolet sunlight.The serum calcium usually is normal but may be low; the serum phosphorus level usually is reduced, and serum alkaline phosphatase activity is elevated. When serum calciumlevels decline to less than 7.5 mg/dL, tetany may occur. Levelsof 24,25-(OH)2-D are undetectable, and serum 1,25-(OH)2-Dlevels are commonly less than 7 ng/mL, although 1,25-(OH)2-D levels also may be normal. The best measure of vitamin D status is the level of 25-(OH)-D. Characteristic radiographicchanges of the distal ulna and radius include widening; concavecupping; and frayed, poorly demarcated ends. The increasedspace seen between the distal ends of the radius and ulna andthe metacarpal bones is the enlarged, nonossified metaphysis.
Breastfed infants born of mothers with adequate vitamin D stores usually maintain adequate serum vitamin D levels for at least 2 months, but rickets may develop subsequently if these infants are not exposed to the sun or do not receive supplementary vitamin D. The American Academy of Pediatrics recommends vitamin D supplementation of all breastfed infants in the amount of 400 IU/day, started soon after birth and given until the infant is taking more than 1000 mL/day of formula or vitamin D–fortified milk (for age >1 year). Toxic effects of excessive chronic vitamin D may include hypercalcemia, muscle weakness, polyuria, and nephrocalcinosis.
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The plant form of vitamin K is phylloquinone, or vitamin K1. Another form is menaquinone, or vitamin K2, one of a series of compounds with unsaturated side chains synthesized by intestinal bacteria. Plasma factors II (prothrombin), VII, IX, and X in the cascade of blood coagulation factors depend on vitamin K for synthesis and for post-translational conversion of their precursor proteins. The post-translational conversion of glutamyl residues to carboxyglutamic acid residues of a prothrombin molecule creates effective calcium-binding sites, making the protein active.
Other vitamin K–dependent proteins include proteins C, S, and Z in plasma and γ-carboxyglutamic acid–containing proteins in several tissues. Bone contains a major vitamin K–dependent protein, osteocalcin, and lesser amounts of other glutamic acid–containing proteins.
Phylloquinone is absorbed from the intestine and transported by chylomicrons. The rarity of dietary vitamin K deficiency in humans with normal intestinal function suggests that the absorption of menaquinones is possible. Vitamin K deficiency has been observed in subjects with impaired fat absorption caused by obstructive jaundice, pancreatic insufficiency, and celiac disease; often these problems are combined with the use of antibiotics that change intestinal flora.