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2 Chondrocalcinosis & Pseudogout
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Chondrocalcinosis is the presence of calcium-containing salts in articular cartilage Diagnosed radiologically, it may be familial and is commonly associated with a wide variety of metabolic disorders, eg, hemochromatosis, hyperparathyroidism, ochronosis, diabetes mellitus, hypothyroidism, Wilson s disease, and gout Pseudogout (also called calcium pyrophosphate dihydrate [CPPD] deposition disease) is most often seen in persons age 60 or older, is characterized by acute, recurrent and rarely chronic arthritis involving large joints (most commonly the knees and the wrists) and is almost always accompanied by chondrocalcinosis of the affected joints Other joints frequently affected are the MCPs, hips, shoulders, elbows, and ankles Involvement of the DIP and PIP joints is no more common in CPPD deposition disease than in other age-matched controls Pseudogout, like gout, frequently develops 24 48 hours after major surgery Identification of calcium pyrophosphate crystals in joint aspirates is diagnostic of pseudogout With light microscopy, the rhomboid-shaped crystals differ from the needle-shaped gout crystals A red compensator is used for positive identification, since pseudogout crystals are blue when parallel and yellow when perpendicular to the axis of the compensator Urate crystals give the opposite pattern X-ray examination shows not only calcification (usually symmetric) of cartilaginous structures but also signs of degenerative joint disease (osteoarthritis) Unlike gout, pseudogout is usually associated with normal serum urate levels Treatment of chondrocalcinosis is directed at the primary disease, if present NSAIDs (salicylates, indomethacin, naproxen, and other drugs) are helpful in the treatment of acute episodes Patients at increased risk for
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With rigorous medical compliance, allopurinol shrinks tophi and in time can lead to their disappearance Resorption of extensive tophi requires maintaining a serum uric acid below 5 mg/dL, which may be achievable only with concomitant use of allopurinol and a uricosuric agent Surgical excision of large tophi offers mechanical improvement in selected deformities
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E Gout in the Transplant Patient
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Hyperuricemia and gout commonly develop in many transplant patients because they have decreased renal function and require drugs that inhibit uric acid excretion (especially cyclosporine and diuretics) Treating these patients is challenging: NSAIDs are usually contraindicated because of renal impairment; intravenous colchicine is generally avoided for acute gout because of its narrow therapeutic index (particularly in renal dysfunction); and corticosteroids are already being used Often the best approach for monarticular gout after excluding infection is injecting corticosteroids into the joint (see above) For polyarticular gout, increasing the dose of systemic corticosteroid may be the only alternative Since transplant patients often have multiple attacks of gout, long-term relief requires lowering the serum uric acid with allopurinol (Renal impairment seen in many transplant patients makes uricosuric agents ineffective) Allopurinol should be started at a low dose in patients with renal dysfunction and then adjusted according to its effect on the serum uric acid level Allopurinol potentiates the effect of azathioprine If allopurinol cannot be avoided, the dose of azathioprine should be reduced by 75% before allopurinol is started
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objective finding Neurologic signs depend on the extent of compression of nerve roots or the spinal cord Compression of the spinal cord may cause paraparesis or paraplegia
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upper gastrointestinal bleeding may use a COX-2 inhibitor to treat acute attacks of pseudogout Long-term use of COX-2 inhibitors is not advised because of the association with increased risk of cardiovascular events Colchicine, 06 mg orally twice daily, is more effective for prophylaxis than for acute attacks Aspiration of the inflamed joint and intra-articular injection of triamcinolone, 10 40 mg, depending on the size of the joint, are also of value in resistant cases
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Molloy ES et al Calcium crystal deposition diseases: update on pathogenesis and manifestations Rheum Dis Clin North Am 2006 May;32(2):383 400 [PMID: 16716885]
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