rickets

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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.

rickets

 [rik´ets]
a condition of infancy and childhood caused by deficiency of vitamin D, which leads to altered calcium and phosphorus metabolism and consequent disturbance of ossification of bone. Because of the widespread use of vitamin D–fortified milk, and the giving of vitamin supplements to most infants, the disease is now uncommon in the United States. (A second disease, clinically indistinguishable from ordinary rickets but resistant to large doses of vitamin D, is called vitamin D–resistant rickets.)

Since the action of sunlight on the skin produces vitamin D in the human body, rickets often occurs in parts of the world where the winter is especially long, or where smoke and fog constantly intercept the sun. Black and other dark-skinned people are somewhat more susceptible to the disease if they live in areas with little sunlight, since the pigment in the skin blocks absorption of the sun's rays. When a vitamin D deficiency occurs in adults, it produces osteomalacia.
Symptoms. A major symptom of rickets is softening (decalcification) of the bones. In children, this can produce various degrees of deformity, including nodules on the ribs and flexibility and bending of bones. Bowleg and knock-knee and an improperly developed or misshapen skull of a squared or boxed appearance are typical. The ability of the bones to support the body is seriously impaired.
Prevention. A proper diet that includes vitamin D–fortified milk is usually sufficient to prevent rickets. Ordinary milk contains adequate amounts of calcium but is a poor source of vitamin D. Small amounts of the vitamin are present in eggs, and in such fish as cod, herring, tuna, sardines, and salmon. Sunlight and other sources of ultraviolet light are beneficial.
Treatment. Treatment of an active case of rickets involves the administration of vitamin D concentrate. The response to treatment usually is rapid.
anticonvulsant rickets rickets occurring in children receiving long-term anticonvulsant therapy; the drugs induce vitamin D deficiency (frequently compounded by dietary insufficiency of the vitamin) and hypocalcemia, hypophosphatemia, and secondary hyperparathyroidism by increasing the rate of conversion of the vitamin to inactive metabolites.
familial hypophosphatemic rickets any of several inherited disorders of proximal renal tubular function causing phosphate loss, hypophosphatemia, and skeletal deformities, including rickets and osteomalacia.
hypophosphatemic rickets any of a group of disorders characterized by rickets associated with hypophosphatemia, resulting from dietary phosphorus deficiency (antacid-induced osteomalacia) or due to defects in renal tubular function, either hereditary (familial hypophosphatemic rickets) or acquired. While skeletal deformities (e.g., bowleg, short stature) are present, neither hypocalcemia, myopathy, nor tetany occur, and serum parathyroid hormone is normal.
vitamin D–dependent rickets, type I an autosomal recessive disorder of rickets with myopathy, hypocalcemia, moderate hypophosphatemia, secondary hyperparathyroidism, and subnormal serum concentrations of 1,25-dihydroxyvitamin D. The disorder can be overcome by high doses of vitamin D or physiologic doses of calcitriol.
vitamin D–dependent rickets, type II an autosomal recessive disorder similar to type I but with elevated serum concentrations of 1,25-dihydroxyvitamin D. The disorder cannot be overcome by high levels of vitamin D or its metabolites and is believed to be due to defective receptor binding, absence of the receptors, or post-receptor defects. Multiple variants exist, subdivided as those with or without alopecia.
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.

rick·ets

(rik'ets),
A disease attributable to vitamin D deficiency, and characterized by overproduction and deficient calcification of osteoid tissue, with associated skeletal deformities, disturbances in growth, hypocalcemia, and sometimes tetany; usually accompanied by irritability, listlessness, and generalized muscular weakness; fractures are frequent.
[E. wrick, to twist]

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.
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 
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.

rickets

(rĭk′ĭts)
n. (used with a sing. or pl. verb)
A bone disease of children marked by bone demineralization and defective bone growth, caused usually by a deficiency of or an impaired metabolism of vitamin D. Also called rachitis.

rickets

[rik′əts]
Etymology: Gk, rachis, backbone, itis, inflammation
a condition caused by the deficiency of vitamin D, seen primarily in infancy and childhood and characterized by abnormal bone formation. Symptoms include soft, pliable bones causing such deformities as bowlegs and knock-knees; nodular enlargements on the ends and sides of the bones; muscle pain; enlarged skull; chest deformities; spinal curvature; enlargement of the liver and spleen; profuse sweating; and general tenderness of the body when touched. Prophylaxis and treatment include a diet rich in calcium, phosphorus, and vitamin D and adequate exposure to sunlight. Kinds of rickets include celiac rickets, renal rickets, and genetic forms of vitamin D-resistant rickets. See also osteodystrophy, osteomalacia, vitamin D. rachitic, adj.
observations Characteristic manifestations in infants and children include soft, pliable bones; softening of skull bones; enlargement of ribs at costochondral junctions; limb deformities; epiphyseal swelling (bowed legs and knock-knees); pigeon breast deformity; Harrison's groove; spinal deformities; and possible decrease in thoracic volume. Spleen and liver may be enlarged. Body is generally tender to touch. Bone deformities are seen on radiographs. Adults may have bone pain, fractures, weakness, weight loss, and malaise.
interventions Prevention and treatment are the same and include a diet rich in calcium, phosphorus, and vitamin D and adequate exposure to sunlight. Surgical intervention may be indicated for correction of a slipped femoral epiphysis in infants and young children. Deformities may need correction through bracing. The health care team should focus on prevention, with education about the importance of calcium and vitamin D in diet and prevention of complications associated with existing disease.
enlarge picture
Rickets

rickets

Osteomalacia in children, renal osteodystrophy, renal rickets, vitamin D deficiency Metabolism A rare condition caused by vitamin D deficiency, insufficiency or inefficiency, with interference of normal ossification in children, whose bones are poorly mineralized, accompanied by deficit of Ca2+ or PO4 from the bone and supportive matrix; the parathyroid ↑ PTH secretion in response to ↓ serum Ca2+, resulting in ↑ loss of Ca2+ and PO4, as it is reabsorbed from bone; bone cysts may develop in severe cases, especially during rapid growth when the body demands more Ca2+ and PO4; rickets is usually seen in young children 6 to 24 months old and is rare in newborns Etiology ↓ vitamin D in diet, especially in strict vegetarians or those who are lactose intolerant, malabsorption syndromes–eg, fat malabsorption, steatorrhea, sprue, short bowel syndrome; dietary lack of Ca2+ and PO4 is rare–both are present in milk and green vegetables; hereditary rickets is an X-linked vitamin D-resistant form of rickets caused when the kidney is unable to retain PO4, renal tubular acidosis–which dissolves Ca2+ in the bones, leaving them soft and weak bones; rickets may occur in children with disorders of the liver or biliary system, when fats and vitamin D are poorly absorbed or when the vitamin D is not converted to its active form. See Hepatic rickets, Vitamin D, Vitamin D deficiency, Vitamin D-dependent rickets, X-linked hypophosphatemic rickets.

rick·ets

(rik'ĕts)
A disease due to vitamin D deficiency characterized by overproduction and deficient calcification of osteoid tissue, with associated skeletal deformities, disturbances in growth, and hypocalcemia.
Synonym(s): infantile osteomalacia, juvenile osteomalacia, rachitis.
[E. wrick, to twist]

rickets

A disorder of bone mineralization in children caused by vitamin D deficiency, both nutritional and skin-synthesised, and the resulting failure of absorption of calcium from the intestine. As a result of diminished deposition of calcium and phosphorus in the bones there is weakening and softening. There may be bowing of the legs, curvature of the spine, squaring-off and flattening of the skull, delay in the eruption of teeth with softening of the enamel and an increased tendency to bone fracture. Rickets is essentially a problem of the developing world where its is promoted by cultural patterns involving covering of the female skin, over-long breast-feeding by vitamin-D deficient mothers, geberal nutritional deficiency and possibly genetic factors. The disease is treated with vitamin D and a calcium-rich diet. The equivalent disease in adults is OSTEOMALACIA.

rickets

a disease of young children and other mammals where faulty calcification of bones produces bowed limbs. Rickets is due to a diet deficient in VITAMIN D and low in calcium and phosphorus. At the beginning of the 20th century around 80% of urban children in Britain suffered from rickets to some degree. The condition is now rare in the UK, although it is still common in children of poorer countries.

rickets

childhood osteomalacia due to chronic deficiency of vitamin D; characterized by skeletal deformity, e.g. severe bowing of legs

rick·ets

(rik'ĕts)
Disease due to vitamin D deficiency, characterized by overproduction and deficient calcification of osteoid tissue, with associated skeletal deformities, disturbances in growth, hypocalcemia, and sometimes tetany; usually accompanied by irritability, listlessness, and generalized muscular weakness; fractures are frequent.
[E. wrick, to twist]

rickets (rik´əts),

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,
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.

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.

adult rickets
osteomalacia; a rickets-like disease affecting adults.
fetal rickets
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.
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