Occasionally a patient may present with a solitary bone lesion where gout is not suspected such as the young man whose navicular bone is shown in the CT at right. When the patient has no history of gout and is younger than average, concern about a bone tumor is raised. Simply remembering this diagnosis is enough to solve the puzzle, since the usual laboratory and pathological fingings are present and make confirming the diagnosis a simple matter.Gout is an inflammatory arthopathy that occurs as a result of hyperuricemia. It is the most common inflammatory arthritis in men over thirty years old. Hyperuricemia is generally secondary to under-excretion of uric acid. Only 10% of gout patients over produce uric acid and this may be a result of
myeloproliferative, lymphoproliferative or hemolytic disease. Uric acid is filtered at the glomerulus and is subject to tubular reabsorption. Drugs that interfere with tubular handling such as thiazides, cyclosporine, and salicylates can cause a gout crisis. Hyperuricemia is also correlated with obesity, alcohol use, and high protein intake. Gout primarily affects adult men and the peak incidence occurs in the fifth decade. The diagnosis of gout is dependent on the presence of urate cystals in joint fluid and the development of tophi,
not the presence of hyperuricemia.
Hyperuricemia causes the deposition of monosodium urate (MSU) crystals in the tissues. The crystals are consumed by neutrophils and then fused with a phagosome in an attempt to digest the crystal. The crystal causes lysosome lysis which releases protease enzymes within the cell causing cell death. This
process releases chemotactic factors which attracts more neutrophils and continues the cycle.
There are four stages of gout: asymptomatic hyperuricemia, acute gouty arthritis, intercritical gout and chronic tophaceous gout. Acute gouty arthritis is characterized by a rapid onset of severe pain, swelling and erythema most commonly in the metatarsal-phalangeal joint. Acute gout is normally
monoarticular and may also occur in the ankle or knee. Acute gout may be set off by trauma, illness or excess consumption of high protein food and alcohol and begins most commonly at night. Patients may have a low grade fever and leukocytosis. Untreated acute gout subsides in 3-10 days. Intercritical gout
refers to the asymptomatic periods between attacks. Chronic tophaceous gout occurs an average of 12 years after the first gout attack. Tophi occur within the synovium, subchondral bone, tendon and subcutaneous tissue resulting in osseous erosion, tendon rupture and carpal tunnel syndrome.
Patients with gout usually have a well known history and are not subject to extensive radiologic examination. Acute gout attacks may appear as soft tissue swelling, osteopenia or a-joint effusion on plain film. Signs of late gout include polyarticular involvement of asymmetric joints. Often the joint space will be decreased, osseus erosions may be present and lesions will have a well circumscribed, sclerotic margin. Intraosseous tophi and subchondral cysts will have local areas of trabeculae replacement. The radiologic differential includes psoriatic arthritis, rheumatoid arthritis, calcium pyrophosphate dihydrate (CPPD) and amyloidosis. Well circumscribed osteolytic lesions might resemble a neoplastic process.
On gross examination, tophi are chalky-white accumulations of urate crystals. Microscopically, tophi consist of MSU crystals surrounded by a protein matrix and fibrous tissue filled with lymphocytes, macrophages, fibroblasts and giant cells. Polarized light is used to examine synovial fluid as crystals within
neutrophils show negative birefringence.
Treatment for gout is largely medical. Colchicine inhibits the phagocytosis of urate crystals by polys and blocks the release of chemotactic factors. NSAIDs such as indomethacin can give patients relief of pain in two to four hours. Intra-articular steroid injections can also give relief of acute gout symptoms.
Colchicine and NSAIDS are used as prophylaxis only in patients who have had an attack of acute gout, not just hyperuricemi ,.'
References
l Bullough, Peter, Orthopaedic Pathologv (third edition), Times Mirror International Publishers Limited, London, 1997.
Huvos, Andrew. Bone Tumors: Diagnosis. Treatment and Prognosis,
W.B. Saunders Co., 1991.
Emmerson, BT, The Management of Gout, New England Journal of Medicine, 334(7) :445 -451, Feb. 15, 1996.
Uri, DS and MK Dalinka, Crystal Disease, Radiologic Clinics of
North America, 34(2):359-372, March, 1996.
1/6/98
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