Vertebral gout and ambulatory dysfunction.

To the Editor: A 77-year-old male with a history of hypertension presented with progressively worsening bilateral leg weakness and difficulty walking, along with right knee pain and severe back pain for a week. Outpatient medications included hydrochlorothiazide. He had occasional alcohol intake. Physical examination was significant for effusion in the right knee along with marked hyporeflexia and decreased power in both lower extremities. Laboratory values were remarkable for an erythrocyte sedimentation rate of 160 mm/h, serum uric acid of 10.7 and leukocytosis of 14,000/[mm.sup.3]. Magnetic resonance imaging of the spine showed erosive bone changes around the facet joints of the L5 and S1 vertebrae. CT-guided aspiration recovered small amounts of fluid positive for monosodium urate crystals, and with negative Gram staining and culture growth. Synovial fluid analysis from both knees revealed the same findings. He was placed on prednisone and colchicine. His ambulatory status improved quite remarkably over the next 2 days. Upon discharge, he was able to walk out of the hospital and was placed on allopurinol. There were no recurrences.

Tophaceous gout of the spine can occasionally be the disease's primary presentation. Urate crystal deposition in the vertebral joints may be considered an extension of the articular involvement of the peripheral joints, and frequency of its occurrence is still unknown. Spinal involvement by tophi has ranged from the level of C1 to S1, with varying presentation throughout various segments. (1) Involvement of the cervical vertebrae may produce bony erosion and ligament softening, quite similar to the involvement of the peripheral joints, with the added complication of potential subluxation and spinal cord compression. (2) Thoracic vertebrae have been noted to develop distinctive right-sided osteophytosis with thoracic lipping. In the lumbar region, the facet joints, lamina and pedicles have all been involved by the extradural intraspinal tophi that eventually erode or compress these structures. (3)

Our patient presented with tophaceous gout of the spine in the absence of peripheral tophi and without a previous history of gouty arthritis. He had been on chronic antihypertensive therapy with hydrochlorothiazide for a few years. Although the rapid decline in his ambulatory status may not be explained completely by the chronicity of tophaceous gout, it does perhaps suggest that the tophus was undergoing a phase of acute inflammation, with cellular infiltration and inflammatory exudate formation, producing pain and resulting in a critical size increase, which was sufficient enough to produce clinical evidence of cord compression. It is postulated that in the spine, extradural tophaceous gout results from crystal deposition and acute inflammatory changes and causes symptoms varying from radicular pain to quadriparesis due to mass effect. (4) Although this phenomenon is not completely unheard of, it certainly is rare. Its presentation in this manner definitely adds to the old adage that there is more to it than meets the eye!

Humaira Naseem Adenwalla, MD

Mohammed Haris Umer Usman, MD

Department of Internal Medicine

Mercy Catholic Medical Center

Drexel University College of Medicine

Darby, PA

Misbah Baqir, MD

Department of Internal Medicine

St. Anthony's Central Hospital

Denver, CO

Muhammad Zulqarnain Ali

Haider Shah, MB, BS

Department of Medicine

King Abdul Aziz Specialist Hospital

Taif, Saudi Arabia

References

1. Varga J, Giampaolo C, Goldenberg DL. Tophaceous gout of the spine in a patient with no peripheral tophi: case report and review of the literature. Arthritis Rheum 1985;28:1312-1315.

2. Tkach S. Gouty arthritis of the spine. Clin Orthop Relat Res 1970;71:81-86.

3. King JC, Nicholas C. Gouty arthropathy of the lumbar spine: a case report and review of the literature. Spine 1997;22:2309-2312.

4. Sabharwal S, Gibson T. Cervical gout. Br J Rheumatol 1988;27:413-414.