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. 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.

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Linear sebaceous naevus syndrome and resistant rickets/Author's reply
From Journal of Bone and Joint Surgery, 1/1/04

Sir,

We read with interest the article in the May 2003 issue by Hosalker et al1 entitled 'Linear sebaceous naevus syndrome and resistant rickets'.

The first patient (case 1 ) is now being followed up at our hospital. The authors mentioned that when he was discharged after follow-up he was walking independently. Unfortunately, he is not doing as well as we had hoped.

He presented to us at 12 years of age having outgrown his Rush nail. He had a right tibia recurvatum deformity with extrusion of the Rush nail from the bone and a leg length discrepancy of 6 cm. Since then, he has undergone revision of the Rush nails in both tibiae and an epiphysiodesis of the upper left tibia. The bone quality of the tibiae has always been poor due to his disease and stress shielding. Despite bone grafting of the right tibia at the time of repeating nailing, the bone quality remains poor. he is now 16-years-old and prefers full-time use of a wheelchair. which is fortuitous because the management of fractures of his tibiae would be exceedingly complex. Needless to say, his compliance with medical treatment has been appalling.

B. GUHAN. Clinical Fellow

R. D. D. DUNCAN. Consultant Orthopaedic Surgeon

Royal Hospital for Sick Children

Glasgow. Scotland.

1. Hosalker HS, Jones DH, Offiah A, Hall C. Linear sebaceous naevus syndrome and resistant rickets. J Bone Joint Surg [Br] 2003: 85-B: 578-83.

Author's reply:

Sir,

We thank Messrs Guhan and Duncan for describing a finding, which is gradually becoming apparent to us. Their patient (our case 1) is deteriorating after initial good progress. The lack of compliance with medical treatment is also noted.

Case 3 in our series is generally doing well and is compliant with treatment because of his gastrostomy. he is also fully weight-bearing on his left lower limb. However, his right lower limb, now straight after nailing of the femur and tibia, has major shortening with growth plate disturbance. This could not be equalised surgically. We are therefore committed to an extension prosthesis with possible surgery to accommodate this.

The long-term outcome of the skeletal problems associated with linear sebaceous naevus syndrome (LSNS) is likely to be less optimistic than originally thought. Only longer term follow-up, continued hopefully with the experiences of others who have treated the condition, will give us more reliable information.

We would be very interested to hear of experiences of the skeletal problems associated with LSNS.

D. H. JONES. FRCS. FRCS Ed (Orth)

Great Ormond Street Hospital for Children

London, UK.

Copyright British Editorial Society of Bone & Joint Surgery Jan 2004
Provided by ProQuest Information and Learning Company. All rights Reserved

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