Vitamin D deficiency, commonly called rickets, causes failure of normal bone calcification, which occurs through several mechanisms: decreased calcium and phosphorus (the major components of bone) from the intestines, increased excretion of calcium from renal tubules, and increased parathyroid secretion resulting in increased release of calcium from the bone. The deficiency results in rickets in infants and young children and osteomalacia in adults. With treatment, the prognosis is good. However, in rickets, bone deformities usually persist, while in osteomalacia, such deformities may disappear.
Vitamin D deficiency results from inadequate dietary intake of preformed vitamin D, malabsorption of vitamin D, or too little exposure to sunlight.
Once a common childhood disease, rickets is now rare in the United States but occasionally appears in breast-fed infants who don’t receive a vitamin D supplement or in infants receiving a formula with a nonfortified milk base. This deficiency may also occur in overcrowded urban areas in which smog limits sunlight penetration. Incidence is highest in black children who, because of their skin color, absorb less sunlight. (Solar ultraviolet rays irradiate 7-dehydrocholesterol, a precursor of vitamin D, to form calciferol.)
Osteomalacia, also uncommon in the United States, is most prevalent in Asia, among young multiparas who eat a cereal diet and have minimal exposure to sunlight. Other causes include:
❑ vitamin D–resistant rickets (refractory rickets, familial hypophosphatemia) from an inherited impairment of renal tubular reabsorption of phosphate (from vitamin D insensitivity)
❑ conditions that lower absorption of fat-soluble vitamin D, such as chronic pancreatitis, celiac disease, Crohn’s disease, cystic fibrosis, gastric or small bowel resections, fistulas, colitis, and biliary obstruction
❑ hepatic or renal disease, which interferes with the formation of hydroxylated calciferol, necessary to initiate the formation of a calcium-binding protein in intestinal absorption sites
❑ malfunctioning parathyroid gland (decreased secretion of parathyroid hormone), which contributes to calcium deficiency (normally, vitamin D controls calcium and phosphorus absorption through the intestine) and interferes with activation of vitamin D in the kidneys.
Early indications of vitamin D deficiency are profuse sweating, restlessness, and irritability. Chronic deficiency induces numerous bone malformations due to softening of the bones: bowlegs, knock-knees, rachitic rosary (beading of ends of ribs), enlargement of wrists and ankles, pigeon breast, delayed closing of the fontanels, softening of the skull, and bulging of the forehead. (See Recognizing bowlegs.)
Other rachitic features are poorly developed muscles (potbelly) and infantile tetany. Bone deformities may cause difficulty in walking and in climbing stairs, spontaneous multiple fractures, and lower back and leg pain.
Physical examination, dietary history, and laboratory tests establish the diagnosis. Test results that suggest vitamin D deficiency include plasma calcium serum levels less than 7.5 mg/dl, serum inorganic phosphorus levels less than 3 mg/dl, serum citrate levels less than 2.5 mg/dl, and alkaline phosphatase levels less than 4 Bodansky units/dl.
For osteomalacia and rickets — except when caused by malabsorption — treatment consists of oral doses of vitamin D or sources such as fish, liver, and processed milk. Exposure to sunlight is encouraged. For rickets refractory to vitamin D or in rickets accompanied by hepatic or renal disease, treatment includes 25-hydroxycholecalciferol, 1, 25-dihydroxycholecalciferol, or a synthetic analogue of active vitamin D. Replacement of deficient calcium and phosphorus also helps to eliminate most symptoms of rickets. Positioning or bracing may be used to reduce or prevent deformities; some skeletal deformities may require corrective surgery.
❑ Obtain a dietary history to assess the patient’s current vitamin D intake. Encourage him to eat foods high in vitamin D — fortified milk, fish liver oils, herring, liver, and egg yolks — and get sufficient sun exposure. If deficiency is due to socioeconomic conditions, refer the patient to appropriate community agencies.
❑ If the patient must take vitamin D for a prolonged period, tell him to watch for signs of vitamin D toxicity (headache, nausea, constipation and, after prolonged use, renal calculi).
❑ To prevent rickets, administer supplementary aqueous preparations of vitamin D for chronic fat malabsorption, hydroxylated cholecalciferol for refractory rickets, and supplemental vitamin D for breast-fed infants.
❑ Consider genetic counseling for a patient with a family history of inherited disorders that can cause rickets.
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Copyright notice for book excerpts: Copyright © 2008 Lippincott Williams & Wilkins. All rights reserved.
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Title: Professional Guide to Diseases (Eighth Edition)
Authors: Springhouse
Publisher: Lippincott Williams & Wilkins
Copyright: 2005
ISBN: 1-58255-370-X
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