Osteomalacia

Definition

Vitamin D deficiency exists when the concentration of 25-hydroxy-vitamin D (25-OH-D) in the blood serum occurs at 12 ng/ml (nanograms/milliliter), or less. The normal concentration of 25-hydroxy-vitamin D in the blood serum is 25-50 ng/ml. When vitamin D deficiency continues for many months in growing children, the disease commonly referred to as rickets will occur. A prolonged deficiency of the vitamin in adults results in osteomalacia. Both diseases involve defects in bones.

Description

Vitamin D is a fat-soluble vitamin, meaning it is able to be dissolved in fat. While some vitamin D is supplied by the diet, most of it is made in the body. To make vitamin D, cholesterol, a sterol that is widely distributed in animal tissues and occurs in the yolk of eggs, as well as in various oils and fats, is necessary. Once cholesterol is available in the body, a slight alteration in the cholesterol molecule occurs, with one change taking place in the skin. This alteration requires the energy of sunlight (or ultraviolet light). Vitamin D deficiency, as well as rickets and osteomalacia, tends to occur in persons who do not get enough sunlight and who fail to eat foods that are rich in vitamin D.

Once consumed, or made in the body, vitamin D is further altered to produce a hormone called 1,25-dihydroxy-vitamin D (1,25-diOH-D). The conversion of vitamin D to 1,25-diOH-D does not occur in the skin, but in the liver and kidney. First, vitamin D is converted to 25-OH-D in the liver; it then enters the bloodstream, where it is taken-up by the kidneys. At this point, it is converted to 1,25-diOH-D. Therefore, the manufacture of 1,25-diOH-D requires the participation of various organs of the body--the liver, kidney, and skin.

The purpose of 1,25-diOH-D in the body is to keep the concentration of calcium at a constant level in the bloodstream. The maintenance of calcium at a constant level is absolutely required for human life to exist, since dissolved calcium is required for nerves and muscles to work. One of the ways in which 1,25-diOH-D accomplishes this mission is by stimulating the absorption of dietary calcium by the intestines.

The sequence of events that can lead to vitamin D deficiency, then to bone disease, is as follows: a lack of vitamin D in the body creates an inability to manufacture 1,25-diOH-D, which results in decreased absorption of dietary calcium and increased loss of calcium in the feces. When this happens, the bones are affected. Vitamin D deficiency results in a lack of bone mineralization (calcification) in growing persons, or in an increased demineralization (decalcification) of bone in adults.

Causes & symptoms

Vitamin D deficiency can be caused by conditions that result in little exposure to sunlight. These conditions include: living in northern countries; having dark skin; being elderly or an infant, and having little chance to go outside; and covering one's face and body, such as for religious reasons. Many Arab women cover the entire body with black cloth, and wear a veil and black gloves when they go outside. These women may acquire vitamin D deficiency, even though they live in a sunny climate.

Most foods contain little or no vitamin D. As a result, sunshine is often a deciding factor in whether vitamin D deficiency occurs. Although fortified milk and fortified infant formula contain high levels of vitamin D, human breast milk is rather low in the vitamin. The term fortified means that vitamins are added to the food by the manufacturer.

To say that a food is high or low in vitamin D means how much of that food needs to be eaten in order to prevent vitamin deficiency and maintain good health. An exact meaning can be provided by comparing the Recommended Dietary Allowance of vitamin D with the amount of vitamin D supplied by a particular food per day. The Recommended Dietary Allowance, also referred to as RDA, is a recommendation based on data derived from different population groups and ages. The RDA for vitamin D for adults is 200 International Units (IU) per day, and can be supplied by eating approximately 1.5 kg of beef, 2.0 kg of corn oil, or 100 kg of cabbage. Few people, though, would want to eat a kilogram of beef in one day, and no human being is capable of eating 100 kg of cabbage in a day; therefore, these foods are poor sources of vitamin D. However, saltwater fish such as salmon, herring, and sardines are rich in vitamin D, supplied from the oils produced by these fish. The RDA can also be supplied by eating roughly 50 g of salmon or 2.0 g of cod liver oil, and since fortified milk contains 400 IU per quart, half a quart of milk provides the RDA. For comparison, human breast milk contains only 4 to 60 IU per quart.

No harm is likely to result from vitamin D deficiency that occurs for only a few days a year. If the deficiency occurs for a period of many months or years, however, rickets or osteomalacia may develop. The symptoms of rickets include bowed legs and bowed arms. The bowed appearance is due to the softening of bones, and their bending if the bones are weight-bearing. Bone growth occurs through the creation of new cartilage, a soft substance at the ends of bones. When the mineral calcium phosphate is deposited onto the cartilage, a hard structure is created. In vitamin D deficiency, though, calcium is not available to create hardened bone, and the result is soft bone. Other symptoms of rickets include particular bony bumps on the ribs called rachitic rosary (beadlike prominences at the junction of the ribs with their cartilages) and knock-knees. Seizures may also occasionally occur in a child with rickets, because of reduced levels of dissolved calcium in the bloodstream.

Although osteomalacia is rare in the United States, symptoms of this disease include reduced bone strength, an increase in bone fractures, and sometimes bone pain, muscle weakness, and a waddling walk.

Diagnosis

Vitamin D deficiency is diagnosed by measuring the level of 25-hydroxy-vitamin D in the blood serum. The normal level or concentration of this form of the vitamin ranges from 25-50 ng/ml. Deficiency occurs when this level decreases to about 12 ng/ml or less. As mentioned previously, 25-OH-D is not the active form of the vitamin. It must be converted to 1,25-diOH-D in order to cause responses in various organs of the body. However, the levels of vitamin D, or of 1,25-dihydroxy-vitamin D in the blood, do not give a reliable picture of whether a person is deficient in the vitamin. For this reason, they are not measured when testing for vitamin D deficiency.

Rickets is diagnosed by x-ray examination of leg bones. A distinct pattern of irregularities, abnormalities, and a coarse appearance can be clearly seen with rickets. Osteomalacia is also diagnosed with x-ray examination. Measurements of blood plasma 25-OH-D, blood plasma calcium, and blood plasma parathyroid hormone must also be obtained for the diagnosis of these diseases. Parathyroid hormone and 1,25-diOH-D work together in the body to regulate the levels of calcium in the blood.

Treatment

Rickets heals promptly with 4000 IU of oral vitamin D per day administered for approximately one month. During this treatment, the doctor should monitor the levels of 25-OH-D in the plasma to make certain they are raised to a normal value. The bone abnormalities (visible by x ray) generally disappear gradually over a period of 3-9 months. Parents are instructed to take their infants outdoors for approximately 20 minutes per day with their faces exposed. Children should also be encouraged to play outside. Foods that are good sources of vitamin D include cod liver oil, egg yolks, butter, and oily fish. Some foods, including milk and breakfast cereals, are also fortified with synthetic vitamin D.

Osteomalacia is treated by eating 2500 IU per day of vitamin D for about three months. Measurements of 25-OH-D, calcium, and parathyroid hormone should be obtained after the treatment period to make sure the therapy did, in fact, result in normal blood values.

Care must be taken in treating vitamin D deficiency, since high doses of vitamin D are toxic and can result in the permanent deposit of minerals in the heart, lungs, and kidneys. Symptoms of toxicity are nausea, vomiting, pain in joints, and lack of interest in eating food. In adults, vitamin D toxicity occurs with eating 50,000 IU or more per day. In infants, toxicity occurs with 1000 IU per day. The continued intake of toxic doses results in death.

Rickets and osteomalacia are almost always treated with oral supplements of vitamin D, with the recommendation to acquire daily exposure to direct sunlight. An alternative to sunlight is the use of an ultraviolet (UV) lamp. When using UV lamps, the eyes must be covered to protect them against damage. Many types of sunglasses allow UV light to pass through, so only those that are opaque to UV light should be used. Attempts to acquire sunlight through glass windows fail to help the body make vitamin D. This is because UV light does not pass through window glass.

Rickets may also occur with calcium deficiency, even when a child is regularly exposed to sunshine. This type of rickets has been found in various parts of Africa. The bone deformities are similar to, or are the same as, those that occur in typical rickets; however, calcium deficiency rickets is treated by increasing the amount of calcium in the diet. No amount of vitamin D can cure the rickets of a child with a diet that is extremely low in calcium. For this reason, it is recommended that calcium be given in conjunction with vitamin D supplementation.

Prognosis

The prognoses for correcting vitamin D deficiency, rickets, and osteomalacia are excellent. Vitamin D treatment results in the return of bone mineralization to a normal rate, the correction of low plasma calcium levels, the prevention of seizures, and a recovery from bone pain. On the other hand, deformities such as bowed legs and the rachitic rosary persist throughout adult life.

Prevention

Food fortification has almost completely eliminated rickets in the United States. Vitamin D deficiency can be prevented by acquiring the RDA through drinking fortified milk and eating fortified cereals. For those who cannot drink milk, supplements of pills might be considered. In some older people, a 400 IU supplement may not be enough to result in the normal absorption of calcium; therefore, daily doses of 10,000 IU per day may be needed. For infants who are fed only breast milk (and rarely exposed to sunshine), a daily supplement of 200-300 IU is recommended.

Rickets continues to be a problem in Africans and Asian Indians who migrate to Canada or Great Britain, especially where these immigrants do not drink fortified milk. Prevention of rickets in these populations is attempted through educational programs sponsored by the government.

Key Terms

25-hydroxy-vitamin D

This is the form of vitamin D that is measured in order to assess vitamin D deficiency.

Cholesterol

A fat-soluble steroid alcohol (sterol) found in animal fats and oils, and in egg yolks. The human body needs cholesterol to produce vitamin D.

Fat-soluble vitamin

A vitamin that dissolves easily in fat or oil, but not in water. The fat-soluble vitamins are vitamins D, E, A, and K.

International unit (IU)

A measurement of biological activity in which one IU is equal to one mg (milligram).

Osteomalacia

Osteomalacia is a bone disease that occurs in adults and is caused by a prolonged period of vitamin D deficiency.

Rachitic rosary

Beadlike bumps present at the junction of the ribs with their cartilages--often seen in children with rickets.

Recommended Dietary Allowance (RDA)

The amount of nutrients, including vitamins, that should be supplied by foods on a daily basis to maintain normal health. Recommendations are based on data obtained from different population groups and ages.

Rickets

Rickets is a bone disease that occurs in infants and growing children and is caused by a prolonged period of vitamin D deficiency.

Further Reading

For Your Information

Books

• Brody, Tom. "Vitamin D." In Nutritional Biochemistry. San Diego, CA: Academic Press, 1994.
• Collins, E.D. and Anthony Norman. "Vitamin D." In Handbook of Vitamins, edited by Lawrence Machlin. New York: Marcel Dekker, Inc., 1991.
• Feldman, D. Vitamin D. San Diego, CA: Academic Press, 1997.
• Food and Nutrition Board. "Vitamin D." In Recommended Dietary Allowances. 10th Edition. Washington, D.C.: National Academy Press, 1989.

  Periodicals

• Binet, A. and S.W. Kooh. "Persistence of Vitamin D-Deficiency Rickets in Toronto in the 1990s." Cancer Journal of Public Health (July-Aug. 1996): 227-230.
• El-Sonbaty, M.R. and N. Abdul-Ghaffar."Vitamin D Deficiency in Veiled Kuwaiti Women." European Journal of Clinical Nutrition 50(1996): 315-318.
• Kinyamu, H., et al. "Serum Vitamin D Metabolites and Calcium Absorption in Normal Young and Elderly Free-Living Women and in Women Living in Nursing Homes." American Journal of Clinical Nutrition 65(1997): 790-797.

Gale Encyclopedia of Medicine. Gale Research, 1999.