Rickets

Although rarely seen in the UK, rickets is still a problem in many parts of the world. It is currently ranked among the top five childhood diseases in developing countries. Inadequate vitamin D, from dietary sources or sunlight, has long been thought to be the cause of rickets.

Rickets is the inadequate osteoid mineralization in the growing skeleton as in osteomalacia, osteoid production is normal. It is due to a deficiency of calcium, phosphorus, or both. The deficiency may be secondary to:

• inadequate intake in the diet;

• problems with absorption from the gut - diseases of the bowel or pancreas which restrict absorption of fat-soluble vitamins;

Figure 22.39. CT scan of lumbar spine: axial views showing spinal canal stenosis.

• diseases of the kidney with failure of conservation of calcium and phosphorus or enzymatic disturbances involving the vitamin D pathway.

Rickets is characterized by softening of the skeleton resulting in characteristic deformities. Rickets is rare nowadays and is most obvious in the first

3 years of life. The clinical features are:

• frontal bossing;

• kyphoscoliosis of the spine;

• acetabular protrusion;

• bowing of lower limbs, especially the tibiae;

• shortness of stature due to stunted growth;

• rachitic rosary due to enlargement of the costochondral junctions;

• 'Harrison's groove' due to the traction from the diaphragm and softening of the thoracic margins.

Biochemically, the serum calcium is normal due to maintenance from the skeleton. Parathyroid hormones release calcium from the bone to keep this serum calcium normal and this may result in hyperplasia of the parathyroid glands (see Chapter 15). There is excessive loss of phosphate from the kidney and therefore the serum phosphate level is low. Radiographical changes include:

• widening of the epiphyseal growth plates;

• cupping of the end of long bones;

• widening of cranial sutures;

• green stick fractures;

• bowing, especially of long bone of lower limbs. Treatment is directed at the cause of the condition: that is dietary supplementation, correction of malabsorption or renal disease, or bypassing the defective step in the metabolic pathway with supplements of the required metabolite for the next step.

Figure 22.40. Renal rickets before (a) and after (b) treatment.
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