Deficiency of vitamin D can over a period of months cause rickets in children and osteomalacia in adults – a skeletal demineralization especially in the spine, pelvis, and lower extremities. Signs and symptoms of osteomalacia are burning in the mouth and throat, nervousness, diarrhea, and insomnia.
is a fat-soluble vitamin and while some is supplied by the diet, most of it is made in the body. To make vitamin D, cholesterol
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 ultraviolet light (sunlight). 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 within 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
. 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, kidneys, 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.
Causes and Development; Contributing Risk FactorsVitamin 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. It is thus possible to acquire vitamin D deficiency, even if you 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.Rickets
continues to be a problem in Africans and Asian Indians who migrate to Canada or Great Britain, especially where these immigrants do not consume fortified products.
Signs and Symptoms
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 and Tests
A vitamin D
deficiency diagnosis is confirmed by measuring the level of serum 25-hydroxy-vitamin D. The normal level or concentration of this form of the vitamin ranges from 25-50ng/ml. Deficiency occurs when this level decreases to about 12ng/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 through 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 and PreventionRickets
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.
Food fortification has almost completely eliminated rickets in the United States. Vitamin D deficiency can be prevented by acquiring the RDA through consuming fortified products or taking supplements in the form of pills. 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.
The prognoses for correcting vitamin D
, 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 generally persist throughout adult life.
The sequence of events that can lead to vitamin D
deficiency, and then 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.