X-ray of the legs in a two-year-old child with rickets
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Osteomalacia

Osteomalacia (pronounced /ˌɑstioməˈleɪʃiə/),is also referred to as bow-leggedness or rickets - taken from the Greek word ῥάχις (rhákis), meaning "spine". It is a disorder which relates directly to Vitamin D deficiency, which causes a lack of calcium being absorbed. Because calcium is an essential nutrient which aids bone rigidity, the lack of it being absorbed into the body causes fragile or malformed bones, which are unable to support the weight of a growing body. more...

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Although osteomalacia can occur in adults, the majority of cases occur in children with poor nutrient intake usually resulting from famine or starvation during early stages of childhood.

Aetiology

Vitamin D is created by the body when it is exposed to UV light, which is more commonly known as being present in sunlight. In 1916, German medical research scientist and pediatrician Kurt Huldschinsky (1883-1940) discovered that exposing patients who had osteomalacia to artificially generated ultra-violet light, or by therapeutically exposing them to sunlight, he was able to yield quicker recovery than other methods, such as supplementation of dairy products within a patient's diet.

Vitamin D3 is produced naturally by the human body on exposure to UVB in sunlight. Vitamin D is also added to milk, milk products, and multi-vitamin pills through a process originally patented by Harry Steenbock. Some people who do not get enough sun exposure, milk products, or green vegetables may also develop the disease. Deficiency of calcium can also cause rickets, particularly in some developing countries where the intake of calcium-rich products such as leafy greens, nuts, and seeds is low.

Hereditary rickets is caused by an inherited disease that interferes with phosphate absorption in the kidney or by Renal tubular acidosis, in which calcium is taken from the bones to counteract acid produced in the kidneys. Rickets can also be caused by certain liver diseases.

Manifestations of disease

Rickets causes bone pain, slowed growth in children, dental problems, muscle loss and increased risk of fractures (easily broken bones). Medical problems seen in children with rickets are

  1. Vitamin D deficiency,
  2. Skeletal deformity,
  3. Growth disturbance,
  4. Hypocalcaemia (low level of calcium in the blood),
  5. Tetany (uncontrolled muscle spasms).

The X-ray, or radiograph, in the article is the classic image of advanced rickets sufferers: 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.

Treatment and prevention

Treatment involves increasing dietary intake of calcium, phosphates and Vitamin D. Exposure to sunshine, cod liver oil, halibut-liver oil, and viosterol are all sources of vitamin D.

Rickets is a severe and prolonged vitamin D deficiency that leads to softening and weakening of the bones in children. Vitamin D helps the body absorb calcium and phosphate, which children need to build strong bones. Good sources of dietary vitamin D are vitamin D-fortified formulas and milk.

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Higher doses of vitamin D needed for fracture prevention
From Townsend Letter for Doctors and Patients, 11/1/05 by Alan R. Gaby

A meta-analysis was performed of 5 randomized double-blind trials (n = 9,292) of vitamin D3 supplementation for hip fracture prevention and 7 randomized double-blind trials (n = 9,820) of vitamin D3 supplementation for prevention of non-vertebral fractures. All participants were at least 60 years of age. A dose of 700 to 800 IU/day reduced the relative risk (RR) of hip fracture by 26% (3 trials with 5,572 persons; pooled RR = 0.74; 95% confidence interval [CI], 0.61-0.88) and any non-vertebral fracture by 23% (5 trials with 6,098 persons; pooled RR = 0.77; 95% CI, 0.68-0.87) vs. calcium or placebo. No significant benefit was observed with 400 IU/day of vitamin D (2 trials with 3,722 persons; pooled RR for hip fracture = 1.15; 95% CI, 0.88-1.50; and pooled RR for any non-vertebral fracture = 1.03; 95% CI, 0.86-1.24).

Comment: Vitamin D plays a role in calcium absorption, and vitamin D deficiency causes bone abnormalities including osteoporosis or osteomalacia. In addition, vitamin D deficiency can result in poor balance and proximal muscle weakness, both of which increase the risk of falling. Several clinical trials have shown that supplementation of elderly people with 800 IU/day of vitamin D reduced the number of falls by nearly 50%. The reduction in fracture risk associated with vitamin D supplementation is probably due to a combination of stronger bones and less falling.

The Adequate Intake for vitamin D, as established by the Institute of Medicine of the National Academy of Sciences, is 400 IU/day for adults aged 51-70, and 600 IU/day for people aged 71 and older. Vitamin D requirements tend to increase with advancing age, because the capacity of the skin to synthesize vitamin D decreases as people get older. In addition, many elderly people are housebound, and fail to obtain adequate amounts of sunlight to protect against vitamin D deficiency. The results of the present study suggest that 400 IU/day of vitamin D is insufficient for elderly people, and that a dose of 800 IU/day is more effective for fracture prevention. The Institute of Medicine has set the "safe upper limit" for vitamin D at 2,000 IU/day, but some research suggests that as much as 4,000 IU/day is safe for the average person.

Bischoff-Ferrari HA, et al. Fracture prevention with vitamin D supplementation: a meta-analysis of randomized controlled trials. JAMA 2005; 293:2257-2264.

COPYRIGHT 2005 The Townsend Letter Group
COPYRIGHT 2005 Gale Group

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