Pseudogout is a type of arthritis that occurs with deposition of Calcium Pyrophosphate Dihydrate crystals. It is important to diagnose it and differentiate from other kinds of arthritis to initiate proper treatment.
It is asymptomatic in most cases and the cause of calcium pyrophosphate dihydrate deposition is uncertain.
A great proportion of people have preexisting joint damage from other conditions. It might be possible that aging cartilage favors favor crystal nucleation.
The deposition of calcium pyrophosphate dihydrate crystals in articular cartilage, synovium, and periarticular ligaments and tendons is most common in the elderly, affecting 10 to 15 percent of persons 65 to 75 yeas old.
A minority of patients with calcium pyrophosphate dihydrate arthropathy have metabolic abnormalities or hereditary calcium pyrophosphate dihydrate disease.
Variety of different metabolic products may enhance calcium pyrophosphate dihydrate deposition. Included conditions are
- Hyper-parathyroidism
- Hemochromatosis
- Gout
- Hypophosphatasia
- Hypomagnesemia
- Ochronosis
- Hemochromatosis
- Hyperparathyroidism.
Investigation should include inquire for evidence of familial aggregation and evaluation of serum calcium, phosphorus, alkaline phophatase, magnesium, serum ferritin, and transferritin saturation.
Clinical Manifestation
Calcium pyrophosphate dihydrate arthropathy may be asymptomatic, acute, subacute, or chronic or cause acute synovitis superimposed on chronically involved joints. Clinical sequelae of calcium pyrophosphate dihydrate deposition include
- Induction of peculiar forms of osteoarthritis
- Induction of severe resorptive disease
- Symmetric proliferative synovitis, clinically similar to rheumatoid arthritis
- Intervertebral disk and ligament calcification with restriction of spine mobility, mimicking ankylosing spondylitis
- Spinal stenosis (most commonly seen in the elderly)
The knee is the joint most affected in calcium pyrophosphate dihydrate arthropathy. Other sites include the wrist, shoulder, ankle, elbow, and hands, the temporaomandibular joint and ligamentum flavum of the spinal canal.
Disease is polyarticular in at least two-thirds of patients.
Diagnosis is made by identification of rod-shaped or rhomboid crystals with weak positive birefringence in synovial fluid.
If radiographs reveal punctuate and/or linear radiodense deposits in fibrocartilaginous jont menisci or articular hyaline cartilage (chondrocalcinosis), the diagnosis certainty of calcium pyrophosphate dihydrate is further enhanced.
Acute attacks of calcium pyrophosphate dihydrate arthritis may be precipitated by trauma, such as physical injury to an extremity, joint surgery, a sprain, or even a long walk.
Rapid diminution of serum calcium concentration, as may occur in severe medical illness or after surgery, also can lead to pseudogout. the mechanism is unclear may facilitate calcium pyrophosphate dihydrate release is unclear.
Synovial fluid in acute calcium pyrophosphate dihydrate gout has inflammatory qualities, a feture that can be used to rule out infection
The white blood cell (WBC) count cis generally raised. Polarization microscopy usually reveals crystals with weak positive birefringence in the extracellular fluid and in neutrophils.
Treatment
- Joint aspiration to decrease intraarticular pressure
- Nonsteroidal and-inflammatory agents
- Intraarticular glucocorticoid injection
- Oral corticosteroids.
- Low doses of colchicines may be helpful in decreasing the frequency of the attacks.
- Patients with progressive destructive large joint arthropathy usually require joint replacement.
There is no effective way to remove calcium pyrophosphate dihydrate deposits from cartilage and synovium.
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