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The Merck Manual--Second Home Edition logo
 
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Chapter 154. Vitamins
Topics: Introduction | Vitamin A | Vitamin D | Vitamin E | Vitamin K | Vitamin B1 | Vitamin B2 | Niacin | Vitamin B6 | Vitamin B12 | Folic Acid | Vitamin C
 
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Vitamin D

Vitamin D exists in two forms that are important for nutrition. Vitamin D2 (ergocalciferol), which is produced by plants, is consumed in the diet. The most common food source of vitamin D2 is fortified foods, such as cereals and dairy products. Vitamin D2 is present in fish liver oils and fatty fish. Vitamin D3 (cholecalciferol) is formed in the skin when the skin is exposed to sunlight. Vitamin D is stored mainly in the liver. Vitamin D must be processed (metabolized) by the liver and kidneys before it is converted to the active form. The active form promotes the absorption of calcium and phosphorus from the intestine and thus is necessary for the formation and maintenance of bones.

Vitamin D Deficiency

In vitamin D deficiency, calcium and phosphate levels in the blood decrease because vitamin D is necessary for absorption of these minerals. The level of parathyroid hormone, which increases the calcium level in the blood, may increase as the body tries to compensate for the vitamin D deficiency. Because not enough calcium and phosphate are available to maintain healthy bones, vitamin D deficiency may result in a bone disorder called rickets in children or osteomalacia in adults.

Vitamin D deficiency can be caused by a lack of vitamin D in the diet or by inadequate exposure to sunlight. A pregnant woman with vitamin D deficiency may develop osteomalacia, and the newborn has a high risk of developing rickets. Because breast milk does not contain large amounts of vitamin D, breastfed infants who are not exposed to enough sunlight may develop rickets and usually require supplements. Vitamin D deficiency may occur in older people because their skin, when exposed to sunlight, produces less vitamin D. Also, older people tend to spend less time outdoors, and their diet may be deficient in vitamin D (because they tend to consume fewer fortified dairy products). Because people with kidney or liver disorders may be unable to convert vitamin D into a usable form, they are at risk of osteomalacia. Malabsorption disorders and the use of certain anticonvulsants increase the risk of vitamin D deficiency. Several rare hereditary forms of rickets develop because the body cannot process (metabolize) vitamin D normally.

Symptoms, Diagnosis, and Treatment

Muscle spasms caused by a low calcium level may be the first sign of rickets in infants. (However, spasms may occur at any age.) Older infants may be slow to sit and crawl, and the spaces between the skull bones (fontanelles) may be slow to close. In children aged 1 to 4 years, bone growth may be abnormal, causing an abnormal curve in the spine and bowlegs or knock-knees. These children may be slow to walk. For older children and adolescents, walking is painful. The pelvic bones may flatten, narrowing the birth canal in adolescent girls. In adults, the bones, particularly the spine, pelvis, and legs, weaken. Affected areas may be painful to touch, and fractures may occur.

The diagnosis of rickets or osteomalacia is based on symptoms, the appearance of bones on x-rays, and a low level of vitamin D by-products in the blood.

Treatment involves taking daily vitamin D and calcium supplements by mouth. People with a chronic liver or kidney disorder may require special formulations of vitamin D supplements.

Vitamin D Excess

Taking very high daily doses of vitamin D over several months can cause toxicity and a high calcium level in the blood (hypercalcemia (see Section 12, Chapter 155)).

Early symptoms are loss of appetite, nausea, and vomiting, followed by excessive thirst, weakness, nervousness, and high blood pressure. Because the calcium level is high, calcium may be deposited throughout the body, particularly in the kidneys, blood vessels, lungs, and heart. The kidneys may be permanently damaged and malfunction. As a result, urination increases, protein passes into the urine, and the level of urea (a waste product) increases in the blood. Kidney failure may result.

Vitamin D excess is usually diagnosed when blood tests detect a high calcium level in a person who takes high doses of vitamin D. The diagnosis is confirmed by measuring the level of vitamin D in the blood. Treatment consists of discontinuing vitamin D supplements, following a low-calcium diet for a while to offset the effects of a high calcium level in the body, and taking drugs to suppress the release of calcium from the bones.

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