Metabolic bone disease



This results from inadequate mineralization of the osteoid framework, leading to soft bones. It is thus usually caused by a defect in vitamin 0 availability or metabolism. The effect on bone is shown.



• Dietary plus inadequate sunlight exposure often seen in Asian immigrant females in Western countries. increased melanin in skin decreases vitamin 03 formantion  and as many Asians are vegans they do not benefit from the small amounts of dietary vitamin D.
• ElderIy people who are immobile and not exposed to right.
• Malabsorption: patients after gastric surgery, those with coeliac disease and those with deficient bile salt production.
• Renal disease leading to inadequate conversion of 25(OH)03 to 1,25(OH)203.

Diagrammatic representation of the effects of osteoporosis
Diagrammatic representation of the effects of

Less common causes are hepatic failure (reduced 25(OH)03 causes) and phenytoin or barbiturate therapy (which induce the mixed function oxidase system and affect vitamin 0 metabolism). Vitamin O-resistant rickets (familial hypophosphataemia) is an X-linked disorder with hypophosphataemia, phosphaturia and rickets:


Childhood rickets usually presents with bony deformity or failure of adequate growth. In the adult, osteomalacia may produce bone and muscle pain and tenderness, often due to subclinical fractures. There is often a marked proximal myopathy, with a characteristic ‘waddling’ gait, but a high degree of clinical suspicion is needed.


Certain diagnosis can only be made by bone biopsy with demonstration of increased unmineralized bone; undecalcified
bone must be used. The procedure is uncomfortable and clinically rarely necessary.
The biochemical  and radiological findings are characteristic:
• low serum phosphate
• increased serum alkaline phosphatase
• low or low-normal plasma calcium, corrected for albumin
• a low phosphate-calcium product is a useful screening test, but use the local laboratory normal ranges
• X-rays show defective mineralization, especially in the pelvis, long bones and ribs, often with Looser’s zone (linear areas of low density)


The simplest treatments are exposure to sunlight and oral vitamin O2 supplements (calciferol); 250/kg daily will cure rickets and osteomalacia and should be given until the serum alkaline phosphatase returns to normal. An adequate calcium intake is necessary. Vitamin D 1 mg (40000 units) daily should be given as a supplement to patients with chronic fat malabsorption. la-Hydroxycholecalciferol (alfacalcidol) (1 J.Lg daily) is the usual treatment for vitamin D deficiency in renal disease and other conditions. 1,25(OH)2D, (calcitriol) is also available for anephric patients.

Serum biochemical findings in some bone diseases.
Serum biochemical findings in some bone diseases.
A whole-life strategy to prevent osteoporosis.
A whole-life strategy to
prevent osteoporosis.

All patients receiving pharmacological doses of vitamin D should have their serum calcium measured regularly. Hypervitaminosis D presents with nausea and vomiting and other features of hypercalcaemia. REVENTION. Education to ensure a balanced diet,
exposure to sunlight and the taking of vitamin D supplements when necessary will prevent both rickets and osteomalacia.

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