The mechanism of CPPD deposition in articular cartilage is not yet fully understood but may, in part, relate to genetically determined activity of phosphate transporters. Serum calcium, phosphate, and alkaline phosphatase levels are normal, as is urinary calcium excretion. The synovitis of pseudogout is induced by crystals of CPPD in synovial fluid, and trauma to the joint and surgery are two factors that can provoke an attack. Attacks are particularly common after parathyroidectomy as therapy for hyperparathyroidism. Conditions strongly associated with CPPD deposition disease include osteoarthritis, trauma, gout, hyperparathyroidism, hemochromatosis, hypophosphatasia, and hypomagnesemia. Other conditions have weaker associations, including hypothyroidism, Wilson disease, and acromegaly. The crystals may induce inflammation by similar mechanisms to the urate crystal–induced synovitis of gout (see Plates 5-38 and 5-39).
Clinical Manifestations/Radiographic Findings. Pseudogout affects men and women, and patients are generally middle-aged or elderly. One or a few joints of the limbs, most often the knee and wrist, are involved. A self-limiting disorder, an episode of pseudogout lasts from 1 or 2 days to a few weeks. Between attacks, the patient may be asymptomatic.
However, in some patients a subacute or chronic polyarthritis occurs that resembles rheumatoid arthritis. This manifestation occurs either with or without the attacks of acute synovitis typical of pseudogout.
About half of older patients with chondrocalcinosis (mostly women) also exhibit progressive degenerative changes in many joints (osteoarthritis). The knee joint is the most common site of involvement, followed by the wrist, metacarpophalangeal, hip, shoulder, elbow, and ankle joints. Most joints with radiographic signs of chondrocalcinosis are asymptomatic, even in patients with synovitis in other joints. Thus, articular chondrocalcinosis does not necessarily imply the existence of pseudogout. Documentation of synovial fluid crystals remains the gold standard for diagnosis.
On radiographs of the joint, chondrocalcinosis appears as a fine line of CPPD crystals arranged parallel to the cartilage surface. Diagnosis of pseudogout should be suspected in cases of acute synovitis in a large joint of an older person whose serum uric acid level is normal. Diagnosis requires the radiographic demonstration of chondrocalcinosis and the finding of CPPD crystals on microscopic examination of aspirated joint fluid.
Treatment. Aspiration of fluid from the inflamed joint, coupled with intra-articular injection of a corticosteroid, is often sufficient to relieve symptoms of acute pseudogout arthritis. Oral administration of an NSAID is helpful. The response to treatment with colchicine is unpredictable but occasionally dramatic; the efficacy of low-dose colchicine is not as well tested in pseudogout as it is in gout. Some patients may benefit from a short-term course of oral corticosteroid therapy. Treatment of chronic arthritis associated with chondrocalcinosis is the same as that for osteoarthritis. It is not possible to halt the progressive deposition of CPPD crystals in articular cartilage or to remove CPPD crystals that have already been deposited.
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