Rickets

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Rickets is a vitamin deficiency disease of infancy and early childhood caused by lack of vitamin D. Rickets causes soft bones because vitamin D is not present to assist in calcium and phosphate uptake. Vitamin D is synthesised in the body on exposure to ultraviolet light and is supplemented in milk products. Some people who do not get enough sun exposure, milk products, or green vegetables may develop the disease, although this is rare today. Hereditary rickets is caused by an inherited defect which prevents the kidney from retaining phosphate. Rickets can also be caused by some other kidney and liver diseases.

Rickets causes bone pain, slowed growth in children, dental problems, muscle loss and increased risk of fractures. The classic image of advanced rickets sufferers is of bow legs and a deformed chest and skull, with prominent frontal and parietal bones causing a distinctive "square headed" appearance. These deformities persist into adult life.

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

Despite the name, rickets is not caused by Rickettsia infection. "Rickets" is a corruption of "rachitis", a disease of the "rachis", or spinal column.

Infantile osteomalacia, juvenile osteomalacia and rachitis are alternative names for rickets. Things seen in children with rickets are vitamin-D deficiency, skeletal deformity, growth disturbance, hypocalcemia, and tetany.

A sufficient amount of ultraviolet light or 10 micrograms (ÃÂÃÂµg) (400 U) PO each day and a dietary supply of calcium and phosphorus can prevent rickets. 20 min/d of ultraviolet light to the face of a less pigmented infant is adequate. Darker skinned babies need to be exposed longer to the ultraviolet rays. The replacement of Vitamin D may correct rickets using these methods of ultraviolet light and medicine.

Therapy for rickets may be administered steadily over several months or in one dayÃÂÃÂs dosage with 15,000 ÃÂÃÂµg (600,000 U) of vitamin D. A medicine can be taken to treat rickets. It is called Cholecalciferol (Delta-D). The replacement of insufficient calcium, phosphorus, or Vitamin D will get rid of most symptoms of rickets. Dietary sources of vitamin D include fish, liver, and processed milk. Exposure to moderate amounts of sunlight is encouraged. Positioning or bracing may be used to reduce or prevent deformities. Some skeletal deformities may need corrective surgery.

Rickets is caused by the inability of the osteoid to calcify, or harden, in an adult. The osteoid is the uncalcified bone matrix. Rickets occurs when the products of Vitamin D are scarce. Less frequently, nutritional shortage of calcium or phosphorus may produce rickets. Infants who are breastfed and obtain no Vitamin D are at risk.

There is also a form of rickets, called X-Linked Hypophosphatemia (XLH), or Familial Hypophosphatemic rickets, that results from a genetic disorder; no matter how much Vitamin D is provided to babies or people with this disorder, their bones may still bend or bow. This disorder used to be called Vitamin D Resistant Rickets because of this, and it is still probably the most common cause of rickets in the industrialized world today. It's estimated that perhaps 1 in 20,000 live births may have this metabolic bone disorder, which can occur spontaneously even if neither parent has been affected. A specific patient support network [1] exists to provide support and information about the forms of genetic rickets, and about possible treatments and management, as well as about current research. X-Linked Hypophosphatemia (XLH) is sometimes also called X-Linked Hypophosphatemic Rickets, Familial Hypophosphatemia, Vitamin D-Resistant Rickets (VDRR) or Genetic Rickets. Notable characteristics for patients with XLH are bowed legs, short stature, poor teeth formation and low blood phosphorus levels.