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Rheumatology 2000; 39: 1415-1421
© 2000 British Society for Rheumatology

Grand Rounds in Rheumatology

Four cases of acquired hypophosphataemic (‘oncogenic’) osteomalacia. Problems of diagnosis, treatment and long-term management

G. P. R. Clunie, P. E. Fox and T. C. B. Stamp

Division of Bone and Mineral Metabolism, Royal National Orthopaedic Hospital, Brockley Hill, Stanmore, Middlesex HA7 4LP, UK

KEY WORDS: Acquired hypophosphataemic osteomalacia, Oncogenic hypophosphataemic osteomalacia (OHO).

The first 150 words of the full text of this article appear below.

The insidious development of progressive bone pains and muscle weakness are well-known features of osteomalacia which may have many causes [1]. Particular diagnostic difficulties are encountered in acquired hypophosphataemia, a condition associated with increased renal phosphate clearance [2] and low circulating 1,25dihydroxyvitamin D [1,25(OH)2D, calcitriol] [3, 4]. Many patients with this disease are shown to have benign tumours of mesenchymal origin with prominent fibrous and vascular characteristics [3, 4]. Cure is generally expected to follow surgical resection, with return of phosphate and 1,25(OH)2D levels to normal [3–5], indicating a likely causal relationship between tumour and both hypophosphataemia and 1,25(OH)2D production. Furthermore, experimental evidence supports a role for tumour products which influence both renal tubular cell phosphate transport and 1{alpha}-hydroxylase activity [6–9]. The term ‘oncogenic hypophosphataemic osteomalacia’ (OHO) is . . . [Full Text of this Article]

Case reports

Patient 1
Patient 2
Patient 3
Patient 4
Discussion
Delay in diagnosis of OHO and the search for tumours
Management of acquired hypophosphataemic osteomalacia and OHO
Relapse of osteomalacia
Long-term pharmacological management
Tumours in OHO

Concluding remarks


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