rickets Classification and external resources |
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A family with rickets. Paris, 1900. | ||
ICD-10 | E55. | |
ICD-9 | 268 | |
DiseasesDB | 9351 | |
MedlinePlus | 000344 | |
eMedicine | ped/2014 | |
MeSH | D012279 |
Rickets is a softening of bones in children potentially leading to fractures and deformity. Rickets is among the most frequent childhood diseases in many developing countries. The predominant cause is a vitamin D deficiency, but lack of adequate calcium in the diet may also lead to rickets (due to this deficiency, cases of severe diarrhoea and vomiting may occur). 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.[1] The origin of the word "rickets" is probably from the Old English dialect word 'wrickken', to twist. The Greek derived word "rachitis" (meaning "inflammation of the spine") was later adopted as the scientific term for rickets, due chiefly to the words' similarity in sound.
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Those at higher risk for developing rickets include:
Individuals with red hair have been speculated to have a decreased risk for rickets due to their greater production of vitamin D in sunlight.
Vitamin D is required for proper calcium absorption from the gut. In the absence of vitamin D, dietary calcium is not properly absorbed, resulting in hypocalcemia, leading to skeletal and dental deformities and neuromuscular symptoms, e.g. hyperexcitability.
A rare X-linked dominant form exists called Vitamin D resistant rickets.
Signs and symptoms of rickets include:
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.
A doctor may diagnose rickets by:
The treatment and prevention of rickets is known as antirachitic.
Treatment involves increasing dietary intake of HGH, phosphates and vitamin D. Exposure to ultraviolet B light (sunshine when the sun is highest in the sky), cod liver oil, halibut-liver oil, and viosterol are all sources of vitamin D.
A sufficient amount of ultraviolet B light 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 therapy and medicine.
Recommendations are for 400 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.
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. Note that in July in New York City at noon with the sun out, a white male in tee shirt and shorts will produce 20,000 I.U Vitamin D from 20 minutes of non-sunscreen 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.[2] This requirement for supplemental vitamin D is not a defect in the evolution of human breastmilk but is instead a result of the modern-day infant's decreased exposure to sunlight.
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