Magnetic resonance imaging in non-infective destructive spondyloarthropathy (2024)

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Volume 61 Issue 726 1 June 1988
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B. Patel, MB, ChB

Renal Medicine, Manchester Royal Infirmary

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C. D. Mistry, MB, ChB, MRCP

Renal Medicine, Manchester Royal Infirmary

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E. Nanda Kumar, MB, BS, MD, FRCR

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C. D. Short, BSc, MB, ChB, MRCP

Renal Medicine, Manchester Royal Infirmary

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J. P. R. Jenkins, MRCP, DMRD, FRCR

Department of Diagnostic Radiology, University of Manchester

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    B. Patel, C. D. Mistry, E. Nanda Kumar, C. D. Short, J. P. R. Jenkins, Magnetic resonance imaging in non-infective destructive spondyloarthropathy, British Journal of Radiology, Volume 61, Issue 726, 1 June 1988, Pages 511–514, https://doi.org/10.1259/0007-1285-61-726-511

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In recent years a destructive arthropathy of the spine chas been recognized in patients with chronic renal cfailure on haemodialysis (Kuntz et al, 1984; Deramond cet al, 1987; Kaplan et al, 1987) which radiographically may mimic infective spondylitis. Conclusive diagnosis may be made by biopsy of the affected area and should include culture, crystal analysis and staining for amyloid of the biopsied material. We describe a patient with chronic renal failure on maintenance haemodialysis for 6 years, who developed such a condition and in whom magnetic resonance imaging was utilized as a non-invasive technique to exclude infection.

A 64-year-old man with chronic renal failure of unknown aetiology, on maintenance haemodialysis for 6 years, presented with a 12-month history of progressive leg weakness. Three months before his admission he developed pain in his neck and shoulders and swelling of the left arm.

On examination he was clinically anaemic, normotensive, apyrexial and had an oedematous left arm due to axillary vein thrombosis. Examination of the peripheral nervous system revealed evidence of cervical cord compression with tetraparesis, hyper-reflexia, hypertonia and extensor plantar responses. Laboratory investigations showed a normocytic, normochromic anaemia (haemoglobin (Hb) 11.6 g/dl) and no biochemical evidence of secondary hyperparathyroidism (serum calcium 2.31 mmol/1 and serum phosphate 2.36 mmol/1). A parathyroid hormone assay performed 4 years previously was normal (2.0 mg/ml).

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