Rickets

Rickets 

Definition

Rickets is a childhood condition caused by serious vitamin D deficiency. This lacking in vitamin D results in weak, soft bones, along with slowed growth and skeletal development. Rickets is, by definition, a disorder which begins in childhood. If this problem occurs only later in life it is known as osteomalacia.

Description

Rickets occurs when the body has a severe lack of vitamin D during the developmental years. Vitamin D is essential to the development of strong, healthy bones. A child with rickets can experience stunted growth and will most likely be short in stature as an adult. This is because, without proper vitamin D levels, decreased mineralization of the bones at the growth plate level affects the strength, size and shape of the bones. A related condition called osteomalacia can occur in adults with the same sort of vitamin D deficiency, but osteomalacia occurs only in adulthood after the growth plates of the bones have closed.

Most vitamin D is produced by the body, although some can be directly supplied by diet. In order to accomplish production of vitamin D, the body requires both cholesterol and ultraviolet light. Most often, the cholesterol comes from digesting animal tissue, oils, fats, and egg yolks. The ultraviolet light is usually supplied by direct sunlight. Only when this light is available can the skin alter the cholesterol molecule to make vitamin D. Children who do not receive enough sunlight are at greater risk of developing rickets, as are children with darker skin, which can block the ultraviolet rays. Vitamin D is found naturally in the foods listed above, but more often children receive vitamin D supplements through foods which have had the vitamin added, as in milk or infant formula.

Vitamin D is necessary in the body, because it can be converted into a hormone which stimulates calcium intake by the intestines. This conversion begins in the liver, where vitamin D becomes a hormone called 25-OH-D, and is completed when the kidneys convert 25-OH-D into a hormone called 1,25-diOH-D. This is the hormone that causes the intestines to absorb calcium from the person's diet. Without proper levels of vitamin D, there is not enough 1,25-diOH-D produced, which results in lower levels of calcium in the body. Adequate calcium is needed by the bones for both development and maintenance.

Causes and symptoms

Rickets is directly caused by insufficient calcium for bone mineralization during growth and development. This is caused by vitamin D deficiency which can be a result of too little cholesterol, ultraviolet light, or vitamin D supplement. During the Industrial Revolution, rickets was quite common in cities because pollution in the air blocked much of the sunlight needed for vitamin D production in the body. There is also a hereditary type of rickets, called X-linked hypophosphatemia, that causes the kidneys bo be unable to retain phosphate.

The most commonly recognized symptoms of rickets occur in the arms and legs, where stress on the underdeveloped bones can cause bowing. Children with rickets may feel pain or tenderness in the bones of their arms, legs, spine, pelvis, and ribs. The skull may develop an odd or asymmetrical shape. Calcium levels in the blood will be low and overall growth is often impaired.

Diagnosis

The initial approach to diagnosing rickets involves a musculoskeletal examination followed by an x ray is often. Affected children may have obviously widened spaces between their joints or bowing of the bones in their arms and legs. Some children may not experience normal dental development as well. A doctor may also assess levels of serum calcium, alkaline phosphatase and other indicator chemicals by using a blood test. While calcium levels can be normal or slightly low, alkaline phosphatase levels in a child with rickets can be high even compared to a normal adult. While x rays can prove misleading, diagnosis by chemical analysis is highly accurate.

Treatment

The treatment for rickets primarily involves corrections of the conditions which led to the disorder. This can be as simple as a change in diet to include foods high in vitamin D such as milk, fish, or liver. Treatment might also mean a gradual increase in the amount sunlight received by the child. In more severe cases, bracing or surgery may be necessary to aid in the correction and repair of bones. Treatment is usually mild and bone deformities usually reduce over time.

Alternative treatment

There is currently little known about any alternative method for treating rickets. Treatments which involve raising vitamin D levels and ultraviolet light exposure are usually simple and effective.

Prognosis

Children with rickets are likely to suffer from stunted growth, bone abnormalities and bone pain, however these symptoms often disappear with treatment. In women, deformation of the pelvic bone structure can prevent vaginal childbirth later in life. Most deformities correct with growth when proper levels of vitamin D are restored and normal bone calcification is maintained.

Prevention

Rickets caused by vitamin D deficiency is simple to prevent. Commercially available infant formula is usually fortified with more than enough vitamin D for infants. For parents who breastfeed their children, it is recommended by the U.S. Department of Health and Human Services that children also receive 400 international units (10 micrograms) of vitamin D supplement. This is because human breast milk contains little vitamin D. It is also important that children are allowed decent amounts of sunlight. As little as twenty minutes each day can be sufficient. For children living in cities, where pollution is likely to block ultraviolet light, and children with dark skin, which can block ultraviolet light, vitamin D supplement is especially important.

Resources

Books

Hochber, Ze'ev, ed. Vitamin D and Rickets New York: Karger 2003.

Periodicals

Spence, Jean, T. and Janet R. Serwint."Secondary Prevention of Vitamin D-Deficiency Rickets." Pediatrics. 113, no 5: (Jan 2004), 129.

Wharton, Brian and Nick Bishop. "Rickets." The Lancet 362 no9393: (Oct 2003). 1389.

Other

Finberg, Laurence. Rickets. E-Medicine December 18, 2003 [cited March 30, 2005]. http://www.emedicine.com/ped/topic2014.htm.

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.

Growth plate — The place in long bones where growth occurs during childhood.

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

Mineralization — The process by which the body uses minerals to build bone structure.

X-linked hypophosphatemia — A type of rickets caused by genetic factors which prevent the kidneys from retaining phosphate.

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rickets /rick·ets/ (rik´ets) a condition due to vitamin D deficiency, especially in infancy and childhood, with disturbance of normal ossification, marked by bending and distortion of the bones, nodular enlargements on the ends and sides of the bones, delayed closure of the fontanelles, muscle pain, and sweating of the head.

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adult rickets  osteomalacia.

familial hypophosphatemic rickets  any of several inherited disorders of proximal renal tubule function causing phosphate loss, hypophosphatemia, and skeletal deformities, including rickets and osteomalacia.

fetal rickets  achondroplasia.

hereditary hypophosphatemic rickets with hypercalciuria  a form of familial hypophosphatemic rickets; hypophosphatemia is accompanied by elevated serum 1,25-dihydroxyvitamin D, increased intestinal absorption of calcium and phosphate, and hypercalciuria.

hypophosphatemic rickets  any of a group of disorders characterized by rickets associated with hypophosphatemia, resulting from dietary phosphorus deficiency or due to defects in renal tubular function; skeletal deformities are present but hypocalcemia, myopathy, and tetany are absent and serum parathyroid hormone is normal.

oncogenous rickets  oncogenous osteomalacia occurring in children.

pseudovitamin D–deficiency rickets  vitamin D, sometimes specifically the type I form.

refractory rickets  vitamin D

vitamin D–dependent rickets  either of two (types I and II) inherited disorders characterized by myopathy, hypocalcemia, moderate hypophosphatemia, secondary hyperparathyroidism, and subnormal serum concentrations of 1,25-dihydroxyvitamin D; type I can be overcome by high doses of vitamin D, but type II cannot.

vitamin D–resistant rickets 

1. X-linked hypophosphatemia.

2. any of a group of disorders characterized by rickets but not responding to high doses of vitamin D; most are forms of familial hypophosphatemic rickets.

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rick·ets (rkts)

n.

A bone disease resulting in defective skeletal growth in children, analogous to osteomalacia in adults, characterized by bone demineralization caused by deficiency or impaired metabolism of vitamin D or phosphates. Also called infantile osteomalacia, juvenile osteomalacia, rachitis.

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rickets (rik´ts),

n a condition caused by deficiency of vitamin D or calcium in infants and children, with disturbance in the mineralization of osseous and dental tissues. Marked by bending and bowing of bones, nodular enlargements at the ends of bones, myalgia, delay in closure of fontanels, and other problems. See also osteomalacia.

rickets, adult,

n See osteomalacia.

rickets, refractory,

n See rickets, resistant.

rickets, renal,

n a disturbance marked by excessive excretion of phosphorus and calcium resulting from a lowered renal threshold of excretion of these mineral elements. See also osteodystrophy, renal.

rickets, resistant,

n (late rickets, refractory rickets), rickets that responds only to extremely large amounts of vitamin D.

Rickettsia

n a genus of microorganisms that combine aspects of both bacteria and viruses. Examples of rickettsial diseases are Rocky Mountain spotted fever and typhus.

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rickets

a disease of young growing animals caused by a nutritional deficiency of phosphorus or vitamin D. There is a failure of calcification of osteoid and cartilage of the bones which become bowed and a persistence with enlargement of the epiphyses so that the joints appear swollen. The animals are lame and dentition is delayed. Radiological examination shows a wider and thicker growth plate.

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adult rickets

osteomalacia; a rickets-like disease affecting adults.

fetal rickets

see achondroplasia.

hypervitaminosis D rickets

deposition of large amounts of osteoid matrix in the metaphyses with a delay in its mineralization occurs in feeding excessive amounts of vitamin D.

inherited rickets

affected piglets are normal at birth but develop rickets indistinguishable from classical rickets. There is a defect in calcium absorption.

renal rickets

see renal secondary hyperparathyroidism.

vitamin D-resistant rickets

a condition almost indistinguishable from ordinary rickets clinically but resistant to unusually large doses of vitamin D; it is often familial but may occur sporadically. In hypophosphatemic vitamin D-resistant rickets, hypophosphatemia is the main characteristic, while in hypocalcemic vitamin D-resistant rickets, the serum concentration of phosphate is within normal limits or nearly so, and the concentration of calcium is abnormally low.