Another cause to a swollen joint? Pseudogout

Pseudogout (or calcium pyrophosphate dehydrate crystal deposition disease, CPPD) needs to be considered in an acutely inflamed joint and can often be mistaken for gout. There are a few ways to differentiate between the two however.

Pseudogout is a sudden joint inflammation due to calcium pyrophosphate crystals deposited in the joint. These are formed from the breakdown of ATP (adenosine triphosphate, which is an important molecule involved in energy) this results in increase pyrophosphate levels in the joints which can then react with calcium to form calcium pyrophosphate crystals, however the mechanism for pseudogout is poorly understood.

The differentiation can be both clinical and test based. Clinically it tends to occur in an older population than gout, over 60s. It also tends to affect more proximal joints (nearer the trunk of the body), such as the knee. In gout we discussed the use of synovial fluid (joint fluid) analysis in diagnosis and how in gout negatively birefringent monosodium urate crystals are seen using polarised light; this is important as positively birefringent crystals are seen in pseudogout and these are more rhomboid shaped crystals. Imagining is useful in pseudogout as cartilage calcifications can be seen to be affecting the joint, this is known as chondrocalcinosis. Imaging of the wrist needs to be carried out as pseudogout can result in a triangular fibrocartilage complex chondrocalcinosis which can result in chronic wrist pain. Chondrocalcinosis can also be seen in the meniscus of the knee.

Asymptomatic cases of pseudogout do not need to be treated unless there is an underlying condition. Sumpotomatic treatment of pseudogout is very similar to that of gout, with non-steroidal anti-inflammatories such as ibuprofen. Steroids injections can also be used as medical treatment and splints as conservative treatment. In chronic cases of pseudogout colchicine might be considered prior to more invasive treatment such as joint replacements. Colchicine is also used to acute gout treatment; it’s mechanism of action is to stop the influx of white blood cells into the joint. It does this by inhibiting microtubular polymerisation; these microtubules are involved in movements of cells therefore if inhibited the white cells can no longer move into the joint space as easily.

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