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


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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Are elderly Asians in Britain at a high risk of vitamin D deficiency and osteomalacia?
From Age and Ageing, 3/1/95 by T. Solanki


The elderly population is at particular risk of vitamin D deficiency and osteomalacia [1]. The two main sources of vitamin D are diet and sunlight exposure, the latter being more important [2]. The mean dietary intake of vitamin D in elderly British people is about one-fifth of the level recommended by the Department of Health [3]. In addition elderly people have less sunlight exposure and less efficient photosynthesis of vitamin D [4, 5]. Further, ageing is associated with a decline in renal function resulting in a decreased activity of 1[Alpha]-hydroxylase. This may also be a factor contributing to osteomalacia in elderly people [6]. Most of the research on vitamin D deficiency in the elderly has been performed in institutionalized individuals and suggests that this group is especially at risk [7, 8]. Community-based studies of elderly people have reported lower levels and diminished seasonal variation of vitamin D levels compared with younger subjects [9, 10]. Clinically this deficiency of vitamin D in elderly people may not only result in osteomalacia but may also be associated with muscle weakness (unpublished data R. H. Hyatt et al.).

The problem of rickets and osteomalacia in British Asians was first reported over 30 years ago by Dunnigan et al. [11]. Since this original report many studies have looked at the problem of vitamin D deficiency and osteomalacia in Asians. Elderly Asians living in Britain are likely to be at an even higher risk from vitamin D deficiency and osteomalacia than younger Asians. However, to date there are few data to confirm or refute this suspicion. The aim of the current study was to try to assess the prevalence of vitamin D deficiency and the risk of osteomalacia in apparently healthy elderly Asians living in the community.


Local ethical committee approval was obtained prior to approaching any subjects. Healthy, community-living elderly Asians (over 65 years old) were recruited from two sources: general practitioner lists and from a number of Asian day centres run by Birmingham Social Services Department. (In the context of this study 'Asians' implies people with an ethnic origin in the Indian subcontinent and adjacent territories.) Approval was obtained from Birmingham Social Services Department to approach clients in their day centres. Healthy elderly white controls were recruited from a local church day centre, while young Asian and white controls were made up from hospital staff. Written informed consent was obtained from all volunteers.

The study was performed in the last week of March and first week of April when vitamin D levels are likely to be at their lowest. It was not possible to match the sample and elderly control groups for age and sex because of the short time period and difficulties in recruiting elderly Asians. All elderly subjects and controls answered a questionnaire covering ethnic subgroup, religion, personal health (including [TABULAR DATA FOR TABLE I OMITTED] drug history), musculoskeletal symptoms and dietary habits. Heights, weights and demi-span were also measured by one of the authors (T.S.).

Blood samples were obtained for haematology and biochemistry including parathyroid hormone (PTH) and 25-hydroxyvitamin [D.sub.3] (25-OH[D.sub.3]). All samples were placed in an ice pack at 0 [degrees] C for transfer to the laboratory. The samples for PTH and 25-OH[D.sub.3] were centrifuged within 3 hours of collection and stored at -20 [degrees] C. Basic biochemical analysis was performed using a Kodak Ektachem 700 analyser. Intact PTH was assayed using the Nichols Institute Diagnostics kit and 25-OH[D.sub.3] was assayed using a modification of the method of Preece et al. [12].

Forty-one elderly Asians (23 men, 18 women), 20 elderly whites (5 men, 15 women), 24 young Asians (19 men, 5 women) and 21 young whites (6 men, 15 women) were recruited, though some of the data were incomplete in some cases due to insufficient samples for analysis. All data were analysed using SPSS. Groups were compared using the Mann-Whitney and [[Chi].sup.2] tests and analysis of variance (ANOVA).


The mean age of the groups was 72 years (range 67-91) for elderly Asians, 74 years (range 67-83) for elderly whites, 31 years (range 19-63) for young Asians and 30 years (range 20-64) for young whites. The elderly Asians had a lower body mass index (26.7 kg/[m.sup.2] [+ or -] 6.1) than their white counterparts (32.2kg/ [m.sup.2] [+ or -] 4.5, p [less than] 0.001).

COPYRIGHT 1995 Oxford University Press
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