BOSTON — To differentiate definitively between acute gout and pseudogout, look at the crystals.
On UV light microscopy, fluid aspirated from the inflamed joint of a patient with pseudogout will be teeming with rhomboid-shaped calcium pyrophosphate dihydrate (CPPD) crystals, which are morphologically different from the needle-shaped monosodium urate (MSU) crystals implicated in the pain and swelling of acute gout, Dr. Dwight R. Robinson said at a meeting on rheumatology sponsored by Harvard Medical School. “[CPPD] crystals are less well formed and show more variation in size and shape than [MSU] crystals.”
Like MSU crystals in gout patients, the deposition of CPPD crystals in pseudogout causes acute pain and swelling the joints. The acute attacks can last from 1 day to 4 weeks and may be accompanied by fever, leukocytosis, and elevated acute-phase reactants, said Dr. Robinson, a rheumatologist and professor of medicine at Harvard Medical School, Boston. The latter signs also may be indicative of septic arthritis, so sepsis first must be excluded by Gram stain and culture of synovial fluid.
CPPD crystals have a predilection for depositing in articular and fibrocartilage, said Dr. Robinson. In pseudogout, this process commonly involves the knee or wrist joint but also may involve the first metatarsophalangeal joint, as occurs in gout, or almost any other joint. Radiographically, the diagnosis of pseudogout often can be confirmed by evidence of chondrocalcinosis in the affected joint.
In addition to mimicking the clinical patterns of gout, CPPD joint disease symptoms may overlap with other inflammatory conditions. It may be asymptomatic in many patients.
CPPD disease develops in patients older than age 50. In younger patients, “it's more likely to be a complication of osteoarthritis, a late consequence of joint trauma or knee meniscectomy, or related to an underlying metabolic disease.” There also may be a familial component.
The exact mechanism for the development of CPPD deposition disease is uncertain, but an overactivity of enzymes that break down nucleoside triphosphates has been implicated, as have genetic defects.
Acute attacks can be treated effectively with nonsteroidal anti-inflammatory drugs, said Dr. Robinson. Given the risks of gastrointestinal and renal toxicities associated with NSAIDs, particularly in elderly patients, intra-articular corticosteroid injection into the affected joint is a reasonable treatment option, he said.