Abstract
A 73-year-old woman with chronic tophaceous gout presented with acute right-sided sciatica. Conventional radiology and CT scan of the lumbar spine revealed severe degenerative changes at the level of L3/4 and L4/5 disc and tophaceous deposits around the facet joints bilaterally. Investigations revealed a raised acute phase response (C reactive protein 97 mg/l, erythrocyte sedimentation rate >100 mm/h), leucocytosis and thrombocytosis. Because of non-steroidal anti-inflammatory drug-induced gastrointestinal toxicity and intolerance to colchicine, a local steroid infiltration of the L4–5 facet joint was administered with a partial response. The patient was treated with anakinra 100 mg daily administered for 3 days. The treatment led to rapid clinical improvement of sciatica as well as normalisation of the acute phase response. She was subsequently maintained on anakinra 100 mg three times weekly with total resolution of sciatic pain.
BACKGROUND
Spinal tophaceous deposits are infrequently seen in gouty patients and are often diagnosed only after surgery for suspected infection. Our case illustrates that gout can elicit an inflammatory response in unusual sites, in this case the spine, leading to sciatic pain. Prompt treatment, in this case by local steroid injection and an interleukin 1 inhibitor, can rapidly control the signs and symptoms of inflammation and avoid unnecessary surgery.
CASE PRESENTATION
The patient was a 73-year-old woman with a 15 year history of chronic tophaceous gout. Over the years, she was unable to tolerate nearly all the treatments she had received: she developed a perforating peptic ulcer on non-steroidal anti-inflammatory drugs (NSAIDs), diarrhoea with low-dose colchicine, severe toxidermic reaction with allopurinol, renal stones with benzbromarone, and low back pain with rasburicase. Her usual serum urate level was between 600 and 800 μmol/l.
She presented with a sudden onset of severe, progressive right low back and leg pains that markedly limited her mobility. On clinical examination, numerous tophaceous deposits were present on her hands, elbows and feet, and around the knees. There was marked limitation of lumbar spine movements in flexion and extension without any neurological deficits. Straight leg raising test was positive on the right side.
INVESTIGATIONS
Laboratory findings showed raised estimated sedimentation rate >110 mm/h (normal value <20), C reactive protein 196 mg/l (normal value <10), leucocytosis of 10.2 g/l (normal value <10) and serum urate of 581 μmol/l (normal value <339). Latent tuberculosis was excluded by a T-spot ELISA assay that was negative.
CT scan of the lumbar spine and knee (see fig 1) revealed severe degenerative changes at L3/4 and L4/5 disc levels with numerous bony erosions of the L4–5 facet joint. Numerous low density periarticular deposits of 160 Hounsfield units, corresponding to the density of monosodium urate crystal deposits,1 were seen around the facet joints and the spine (see arrow in fig 1).
Figure 1.
CT scan of the lumbar spine. Transverse L4/5 (upper scan) and sagittal (lower scan) views of the lumbar spine showing extensive cystic changes in the facet joints, and the presence of material that has a radiological density of 170 Hounsfield units (arrows) characteristic of tophaceous gout.
DIFFERENTIAL DIAGNOSIS
Lumbar disc herniation, lumbar spinal stenosis, Piriformis syndrome, neoplasia, spondylodiscitis.
TREATMENT
The patient responded partially to a local steroid infiltration of 40 mg methylprednisone of the L4–5 facet joint with a reduction of the pain from the leg to the buttocks. These symptoms regressed almost totally after the second of three subcutaneous injections of anakinra (100 mg).
OUTCOME AND FOLLOW-UP
The treatment by anakinra led to rapid clinical improvement of sciatica as well as reduction in the acute phase response. She was subsequently maintained on anakinra 100 mg three times weekly with total resolution of sciatic pain.
DISCUSSION
Gouty inflammation due to monosodium urate (MSU) crystals is the end result of chronic hyperuricaemia. The precipitation of MSU crystals occurs mostly in peripheral joints and soft tissues such as tendons and the joint capsule, but it can include the spine.1 Tophaceous gout affecting the spine is increasingly recognised, but often diagnosis is delayed and is made on histological grounds after surgery.2,3 Tophaceous deposits can be diagnosed radiologically, but, as they are radiotranslucent, the diagnosis is often missed. On CT, tophaceous gout has a characteristic radiodensity of around 170 Hounsfield units and this has facilitated diagnosis of tophaceous gout in non-osseus sites such as the joint capsule and tendons.1
MSU deposits induce a strong local inflammatory response mediated by the so-called “inflammasome”,4,5 which is a protein complex that is formed within monocytes and macrophages after phagocytosis of urate crystals. This complex activates the caspase-1 pro-enzyme and leads to the release of mature interleukin 1(IL1)β by leucocytes. The crucial role of IL1β in MSU-induced inflammation is supported by the results of treating acute gout with an IL1 inhibitor, anakinra.6,7 Our patient presented with right-sided sciatica due to tophaceous gout of the lumbar spine, in particular deposits around the L4–5 facet joint. Her symptoms responded partially to a facet joint infiltration with local steroids but her symptoms persisted. Following treatment with anakinra, the sciatica and acute phase response responded rapidly. This case highlights the usefulness of anakinra in the management of acute gouty inflammation that has not responded to standard treatments
LEARNING POINTS
Spinal tophaceous gout can cause inflammatory nerve root pain.
Targetted treatment of interleukin 1β can be useful in acute gouty inflammation that fails to respond to standard therapies.
Footnotes
Competing interests: none.
Patient consent: Patient/guardian consent was obtained for publication.
REFERENCES
- 1.Gerster JC, Landry M, Dufresne L, et al. Imaging of tophaceous gout: computed tomography provides specific images compared with magnetic resonance imaging and ultrasonography. Ann Rheum Dis 2002; 61: 52–4 [DOI] [PMC free article] [PubMed] [Google Scholar]
- 2.Suk KS, Kim KT, Lee SH, et al. Tophaceous gout of the lumbar spine mimicking pyogenic discitis. Spine J 2007; 7: 94–9 [DOI] [PubMed] [Google Scholar]
- 3.Hou LC, Hsu AR, Veeravagu A, et al. Spinal gout in a renal transplant patient: a case report and literature review. Surg Neurol 2007; 67: 65–73 [DOI] [PubMed] [Google Scholar]
- 4.So A. Avancées récentes dans la physiopathologie de l’hyperuricémie et de la goutte. Revue Médicale Suisse 2007: 103. [PubMed] [Google Scholar]
- 5.Pétrilli V, Martinon F. The inflammasome, autoinflammatory diseases and gout. Joint Bone Spine 2007; 74: 571–6 [DOI] [PubMed] [Google Scholar]
- 6.So A, Th De Smedt, Revaz S, et al. A pilot study of IL–1 inhibition by anakinra in acute gout. Arthritis Res Ther 2007; 9: R28. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 7.McGonagle D, Tan AL, Shankaranarayana S, et al. Management of treatment resistant inflammation of acute on chronic tophaceous gout with anakinra. Ann Rheum Dis 2007; 66: 1683–4 [DOI] [PMC free article] [PubMed] [Google Scholar]
