Difference between revisions of "Rickets" - New World Encyclopedia
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| − | '''Rickets''' is a softening of the bones in | + | '''Rickets''' or '''rachitis''' is a childhood deficiency [[disease]] characterized by defective bone growth resulting from lack of [[vitamin D]] or [[calcium]]. Insufficient sunlight can be a contributing factor due to its role in the synthesis of vitamin D. |
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| + | Rickets is among the most frequent infant and childhood diseases in many developing countries. The softening of the bones in childen due to improper deposition of calcium in the [[bone]]s potentially can lead to fractures and deformity, such as stunting and curving of the bones. | ||
| + | Osteomalacia | ||
| + | Bender and Bender | ||
| + | ==Overview== | ||
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| + | ====Vitamin D==== | ||
| + | Vitamin D is a group of fat-soluble [[prohormones]]; that is, a substance that has no [[hormone]] activity itself, but is converted to a hormone. As a [[vitamin]], Vitamin D is an organic ([[carbon]]-containing) nutrient obtained through the diet and essential in small amounts for normal [[metabolism|metabolic]] reactions. While there are several forms, the two major forms are vitamin D<sub>2</sub> (or [[ergocalciferol]]) and vitamin D<sub>3</sub> (or [[cholecalciferol]]). (The term vitamin D also refers to [[metabolite]]s and other analogues of these substances.) Vitamin D<sub>2</sub> is derived from [[fungal]] and [[plant]] sources, and is not produced by the human body. Vitamin D<sub>3</sub> is derived from animal sources and is made in the skin upon exposure to sunlight (specfically when [[7-dehydrocholesterol]] reacts with UVB [[ultraviolet light]] at [[wavelengths]] between 270–290 nm) (Norman 1998). | ||
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| + | Among the several roles of vitamin D are (Merck 2005): | ||
| + | *Vitamin D regulates the [[calcium]] and [[phosphorus]] levels in the [[blood]] by promoting their absorption from food in the [[intestines]], and by promoting re-absorption of calcium in the [[kidney]]s. | ||
| + | *Vitamin D promotes [[bone]] formation and [[mineralization]] and is essential in the development of an intact and strong [[skeleton]]. | ||
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| + | ====Vitamin D deficiency==== | ||
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| + | Vitamin D deficiency can result from inadequate intake coupled with inadequate sunlight exposure; disorders that limit its absorption; conditions that impair conversion of vitamin D into active [[metabolite]]s, such as [[liver]] or kidney disorders; or, rarely, by a number of hereditary disorders (Merck 2005). Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and [[osteomalacia]] in adults, and possibly contributes to [[osteoporosis]] (Merck 2005). | ||
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| + | The role of diet in the development of [[rickets]] was determined by [[Edward Mellanby]] between [[1918]]–[[1920]].<ref name= History>{{cite journal |author=Rajakumar K |title=Vitamin D, cod-liver oil, sunlight, and rickets: a historical perspective |url=http://pediatrics.aappublications.org/cgi/content/full/112/2/e132 |journal=Pediatrics |volume=112 |issue=2 |pages=e132-5 |year=2003 |pmid=12897318 |issn=}}</ref> In 1921 Elmer McCollum identified an anti-rachitic substance found in certain fats could prevent rickets. Because the newly discovered substance was the fourth vitamin identified, it was called vitamin D.<ref name= History/> The 1928 Nobel Prize in Chemistry was awarded to [[Adolf Windaus]], who discovered the steroid, 7-dehydrocholesterol, the precursor of vitamin D. | ||
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| + | Vitamin D deficiency is known to cause several bone diseases<ref>{{cite journal | author=Grant WB, Holick MF | title=Benefits and requirements of vitamin D for optimal health: a review | journal=Altern Med Rev | year=2005 | pages=94-111 | volume=10 | issue=2 | id=PMID 15989379}}</ref> including: | ||
| + | *[[Rickets]], a childhood disease characterized by impeded growth, and deformity, of the [[long bones]]. | ||
| + | *[[Osteomalacia]], a bone-thinning disorder that occurs exclusively in adults and is characterised by [[proximal]] muscle weakness and bone fragility. | ||
| + | *[[Osteoporosis]], a condition characterized by reduced [[bone mineral density]] and increased bone fragility. | ||
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| + | Prior to the fortification of milk products with vitamin D, rickets was a major public health problem. In the United States, milk has been fortified with 10 micrograms (400 [[International unit|IU]]) of vitamin D per [[quart]] since the [[1930s]], leading to a dramatic decline in the number of rickets cases.<ref name= Sun/> | ||
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| + | A rare [[X-linked dominant]] form exists called Vitamin D resistant rickets. | ||
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| + | ====Calcium deficiency==== | ||
| + | The predominant cause of rickets is a [[vitamin D]] deficiency, but lack of adequate [[calcium]] in the diet may also lead to rickets. Although it can occur in adults, the majority of cases occur in children suffering from severe [[malnutrition]], usually resulting from [[famine]] or [[starvation]] during the early stages of childhood. | ||
[[Osteomalacia]] is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D.{{Fact|date=March 2007}} | [[Osteomalacia]] is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D.{{Fact|date=March 2007}} | ||
The word "rickets" comes from the word "rachitis," meaning wrist (and also spine), as wrist deformities are common and obvious in rickets. | The word "rickets" comes from the word "rachitis," meaning wrist (and also spine), as wrist deformities are common and obvious in rickets. | ||
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Individuals with [[red hair]] (who also generally have extremely pale skin that burns rather than tans) have a decreased risk for rickets due to their greater production of vitamin D in sunlight.<ref>[http://www.derm.med.ed.ac.uk/06_teaching/redhairgen.htm Red hair and genetics]</ref> | Individuals with [[red hair]] (who also generally have extremely pale skin that burns rather than tans) have a decreased risk for rickets due to their greater production of vitamin D in sunlight.<ref>[http://www.derm.med.ed.ac.uk/06_teaching/redhairgen.htm Red hair and genetics]</ref> | ||
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==Presentation== | ==Presentation== | ||
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== References == | == References == | ||
<references/> | <references/> | ||
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| + | <ref name= Merck>[http://www.merck.com/mmpe/sec01/ch004/ch004l.html#BABBBEAE Vitamin D] The Merck Manual of Diagnosis and Therapy. Last modified November 2005</ref> | ||
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| + | .<ref name= Norman> Norman, Anthony W. (1998) [http://www.ajcn.org/cgi/reprint/67/6/1108.pdf Sunlight, season, skin pigmentation, vitamin D, and 25-hydroxyvitamin D:integral components of the vitamin D endocrine system.] Am J Clin Nutr;67:1108–10.</ref> | ||
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== External links == | == External links == | ||
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[[Category:Life sciences]] | [[Category:Life sciences]] | ||
| − | {{credit|147329031}} | + | {{credit|Rickets|147329031|Vitamin_D|148289745}} |
Revision as of 15:38, 4 August 2007
| Rickets Classification and external resources | ||
 | ||
|---|---|---|
| A family with rickets. Paris, 1900. | ||
| ICD-10 | E55 | |
| ICD-9 | 268 | |
| DiseasesDB | 9351 | |
| MedlinePlus | 000344 | |
| eMedicine | ped/2014 | |
| MeSH | D012279 | |
Rickets or rachitis is a childhood deficiency disease characterized by defective bone growth resulting from lack of vitamin D or calcium. Insufficient sunlight can be a contributing factor due to its role in the synthesis of vitamin D.
Rickets is among the most frequent infant and childhood diseases in many developing countries. The softening of the bones in childen due to improper deposition of calcium in the bones potentially can lead to fractures and deformity, such as stunting and curving of the bones. Osteomalacia Bender and Bender
Overview
Vitamin D
Vitamin D is a group of fat-soluble prohormones; that is, a substance that has no hormone activity itself, but is converted to a hormone. As a vitamin, Vitamin D is an organic (carbon-containing) nutrient obtained through the diet and essential in small amounts for normal metabolic reactions. While there are several forms, the two major forms are vitamin D2 (or ergocalciferol) and vitamin D3 (or cholecalciferol). (The term vitamin D also refers to metabolites and other analogues of these substances.) Vitamin D2 is derived from fungal and plant sources, and is not produced by the human body. Vitamin D3 is derived from animal sources and is made in the skin upon exposure to sunlight (specfically when 7-dehydrocholesterol reacts with UVB ultraviolet light at wavelengths between 270–290 nm) (Norman 1998).
Among the several roles of vitamin D are (Merck 2005):
- Vitamin D regulates the calcium and phosphorus levels in the blood by promoting their absorption from food in the intestines, and by promoting re-absorption of calcium in the kidneys.
- Vitamin D promotes bone formation and mineralization and is essential in the development of an intact and strong skeleton.
Vitamin D deficiency
Vitamin D deficiency can result from inadequate intake coupled with inadequate sunlight exposure; disorders that limit its absorption; conditions that impair conversion of vitamin D into active metabolites, such as liver or kidney disorders; or, rarely, by a number of hereditary disorders (Merck 2005). Deficiency results in impaired bone mineralization, and leads to bone softening diseases, rickets in children and osteomalacia in adults, and possibly contributes to osteoporosis (Merck 2005).
The role of diet in the development of rickets was determined by Edward Mellanby between 1918–1920.[1] In 1921 Elmer McCollum identified an anti-rachitic substance found in certain fats could prevent rickets. Because the newly discovered substance was the fourth vitamin identified, it was called vitamin D.[1] The 1928 Nobel Prize in Chemistry was awarded to Adolf Windaus, who discovered the steroid, 7-dehydrocholesterol, the precursor of vitamin D.
Vitamin D deficiency is known to cause several bone diseases[2] including:
- Rickets, a childhood disease characterized by impeded growth, and deformity, of the long bones.
- Osteomalacia, a bone-thinning disorder that occurs exclusively in adults and is characterised by proximal muscle weakness and bone fragility.
- Osteoporosis, a condition characterized by reduced bone mineral density and increased bone fragility.
Prior to the fortification of milk products with vitamin D, rickets was a major public health problem. In the United States, milk has been fortified with 10 micrograms (400 IU) of vitamin D per quart since the 1930s, leading to a dramatic decline in the number of rickets cases.[3]
A rare X-linked dominant form exists called Vitamin D resistant rickets.
Calcium deficiency
The predominant cause of rickets is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets. Although it can occur in adults, the majority of cases occur in children suffering from severe malnutrition, usually resulting from famine or starvation during the early stages of childhood. Osteomalacia is the term used to describe a similar condition occurring in adults, generally due to a deficiency of vitamin D.[citation needed] The word "rickets" comes from the word "rachitis," meaning wrist (and also spine), as wrist deformities are common and obvious in rickets.
Epidemiology
Those at higher risk for developing rickets include:
- Dark-skinned children
- Breast-fed infants whose mothers are not exposed to sunlight
- Breast-fed infants who are not exposed to sunlight
- Individuals not consuming fortified milk, such as those who are lactose intolerant
Individuals with red hair (who also generally have extremely pale skin that burns rather than tans) have a decreased risk for rickets due to their greater production of vitamin D in sunlight.[4]
Presentation
Signs and symptoms of rickets include:
- Bone pain or tenderness
- dental problems
- muscle weakness (rickety myopathy or "floppy baby syndrome")
- increased tendency for fractures (easily broken bones), especially greenstick fractures
- Skeletal deformity
- Toddlers: Bowed legs (genu varus)
- Older children: Knock-knees (genu valgus) or "windswept knees"
- Cranial, spinal, and pelvic deformities
- Growth disturbance
- Hypocalcemia (low level of calcium in the blood), and
- Tetany (uncontrolled muscle spasms all over the body).
- Craniotabes (soft skull)
- Costochondral swelling (aka "rickety rosary" or "rachitic rosary")
- Harrison's groove
- Double malleoli sign due to metaphyseal hyperplasia [1]
An X-ray or radiograph of an advanced sufferer from rickets tends to present in a classic way: bow legs (outward curve of long bone of the legs) and a deformed chest. Changes in the skull also occur causing a distinctive "square headed" appearance. These deformities persist into adult life if not treated.
Long-term consequences include permanent bends or disfiguration of the long bones, and a curved back.
Diagnosis
A doctor may diagnose rickets by:
- Blood tests:
- Serum calcium may show low levels of calcium, serum phosphorus may be low, and serum alkaline phosphatase may be high.
- Arterial blood gases may reveal metabolic acidosis
- X-rays of affected bones may show loss of calcium from bones or changes in the shape or structure of the bones.
- Bone biopsy is rarely performed but will confirm rickets.
Treatment and prevention
Diet and sunlight
Treatment involves increasing dietary intake of calcium, phosphates and vitamin D. Exposure to ultraviolet in sunshine, cod liver oil, halibut-liver oil, and viosterol are all sources of vitamin D.
A sufficient amount of ultraviolet in sunlight each day and adequate supplies of calcium and phosphorus in the diet can prevent rickets. Darker-skinned babies need to be exposed longer to the ultraviolet rays. The replacement of vitamin D has been proven to correct rickets using these methods of ultraviolet light therapyand medicine.
Recommendations are for 200 international units (IU) of vitamin D a day for infants and children. Children who do not get adequate amounts of vitamin D are at increased risk of rickets. Vitamin D is essential for allowing the body to uptake calcium for use in proper bone calcification and maintenance.
Supplementation
Sufficient vitamin D levels can also be achieved through dietary supplementation. Vitamin D3 (cholecalciferol) is the preferred form since it is more readily absorbed than vitamin D2. Most dermatologists recommend vitamin D supplementation as an alternative to unprotected ultraviolet exposure due to the increased risk of skin cancer associated with sun exposure.
According to the American Academy of Pediatrics (AAP), infants who are breast-fed may not get enough vitamin D from breast milk alone. For this reason, the AAP recommends that infants who are exclusively breast-fed receive daily supplements of vitamin D from age 2 months until they start drinking at least 17 ounces of vitamin D-fortified milk or formula a day.[citation needed]
ReferencesISBN links support NWE through referral fees
- ↑ 1.0 1.1 Rajakumar K (2003). Vitamin D, cod-liver oil, sunlight, and rickets: a historical perspective. Pediatrics 112 (2): e132-5.
- ↑ Grant WB, Holick MF (2005). Benefits and requirements of vitamin D for optimal health: a review. Altern Med Rev 10 (2): 94-111. PMID 15989379.
- ↑ Cite error: Invalid
<ref>tag; no text was provided for refs namedSun - ↑ Red hair and genetics
.[2]
External links
- Dr. Susan Ott's website on osteomalacia
- Rickets - Symptoms, Causes, Treatment
- Dictionary.com - Osteomalacia
- Fluoride & Osteomalacia
- History of Vitamin D and the battle against Rickets
- Template:Chorus
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- ↑ Vitamin D The Merck Manual of Diagnosis and Therapy. Last modified November 2005
- ↑ Norman, Anthony W. (1998) Sunlight, season, skin pigmentation, vitamin D, and 25-hydroxyvitamin D:integral components of the vitamin D endocrine system. Am J Clin Nutr;67:1108–10.
