Tumour-induced osteomalacia: a curable condition
Abstract
Osteomalacia is a condition characterised by failure of bone
mineralisation. While abnormalities of vitamin D supply, metabolism or action are the most common and well-known causes, chronic phosphate deficiency, due to either insufficient input (intake or absorption) or renal losses are also important causes of rickets or osteomalacia.1 Hypophosphataemia also commonly co-exists with vitamin D deficiency, pursuant to secondary hyperparathyroidism.
Other causes include chronic calcium deficiency, hypophosphatasia, fluoride and aluminium excess.
In respect of chronic hypophosphataemia-associated rickets/ osteomalacia, the commonest aetiology is X-linked dominant
hypophosphataemia, XLH, (1:20000 births).1 Others include Fanconi syndrome, autosomal dominant hypophosphataemic rickets (ADHR) and tumour-induced osteomalacia (TIO).2
mineralisation. While abnormalities of vitamin D supply, metabolism or action are the most common and well-known causes, chronic phosphate deficiency, due to either insufficient input (intake or absorption) or renal losses are also important causes of rickets or osteomalacia.1 Hypophosphataemia also commonly co-exists with vitamin D deficiency, pursuant to secondary hyperparathyroidism.
Other causes include chronic calcium deficiency, hypophosphatasia, fluoride and aluminium excess.
In respect of chronic hypophosphataemia-associated rickets/ osteomalacia, the commonest aetiology is X-linked dominant
hypophosphataemia, XLH, (1:20000 births).1 Others include Fanconi syndrome, autosomal dominant hypophosphataemic rickets (ADHR) and tumour-induced osteomalacia (TIO).2