Pseudo-gout is a painful form of inflammatory arthritis that mimics the symptoms of true gout. It is more accurately called Calcium Pyrophosphate Dihydrate (CPPD) crystal deposition disease, which describes the underlying cause. This disease involves the accumulation of tiny, sharp crystals within joint structures. When these crystals suddenly shed, they trigger intense episodes of pain, swelling, and warmth.
Understanding CPPD Crystal Accumulation
The foundation of pseudo-gout is the chronic deposition of Calcium Pyrophosphate Dihydrate (CPPD) crystals within the joints. These microscopic crystals embed themselves in the cartilage and the synovial lining, a process known as chondrocalcinosis. This buildup is often asymptomatic for years and is frequently observed in older adults due to the aging and degeneration of joint cartilage.
Crystal formation is linked to an elevated concentration of inorganic pyrophosphate (PPi) within the joint space. PPi combines with calcium to form CPPD crystals. While the precise reason for the increase in PPi is unclear, aging cartilage is believed to release more of this substance. A symptomatic flare only occurs when the crystals are released from the cartilage matrix into the synovial fluid.
Identifying Triggers for Sudden Flare Ups
A symptomatic flare-up, or acute CPPD arthritis, is precipitated by an event that causes the release of accumulated crystals into the joint fluid. The immune system recognizes these crystals as foreign invaders, initiating a vigorous inflammatory response that leads to severe pain and swelling. These acute attacks often come on suddenly and can last for days or weeks.
Mechanical Stress and Trauma
Physical trauma or injury to a joint is a common mechanical trigger. Even minor events, such as a fall, heavy strain, or repetitive overuse, can disrupt the crystal-laden cartilage. This mechanical stress causes microscopic fragments of CPPD deposits to break off and enter the joint space, starting the inflammatory cascade.
Systemic Stress
Major surgery, even if unrelated to the joints, is a well-documented cause of an attack. The body experiences significant systemic stress during and after surgery, leading to rapid metabolic and hormonal shifts. This upheaval destabilizes the crystal deposits, prompting their release. Acute illness or infection, such as pneumonia or a severe flu, can also trigger a flare-up. These conditions produce systemic inflammation, raising levels of pro-inflammatory chemicals throughout the body.
Metabolic and Fluid Changes
Sudden changes in the body’s fluid and electrolyte balance are also potent triggers.
- Dehydration, often seen in hospitalized patients, can concentrate the joint fluid, making crystals more likely to shed.
- Rapid shifts in calcium levels, such as those following parathyroid surgery, can stimulate the release of CPPD crystals.
- A joint procedure like arthrocentesis can mechanically disturb the crystals and inadvertently provoke an acute inflammatory reaction.
Medical Conditions Associated with Higher Risk
Certain underlying medical conditions significantly increase the long-term risk of CPPD crystal formation by altering the body’s metabolic environment. These conditions promote chronic crystal accumulation, making a person more susceptible to acute flares. Screening for these metabolic and endocrine disorders is often standard for younger patients with pseudo-gout.
Endocrine and Metabolic Disorders
Hyperparathyroidism, which results in an overactive parathyroid gland, is a strong risk factor. This condition causes abnormally high levels of calcium in the blood, providing more raw material for CPPD crystal formation. Correcting this endocrine imbalance is an important step in managing the disease.
Hemochromatosis, an inherited disorder leading to excessive iron absorption and storage, is also closely linked to CPPD. The iron overload is thought to promote crystal deposition within joint tissues. Hypothyroidism, a disorder affecting the thyroid, has similarly been associated with an increased prevalence of CPPD.
Low magnesium levels (hypomagnesemia) can also promote crystal formation. Magnesium regulates enzymes involved in pyrophosphate metabolism, and a deficiency may contribute to the buildup of PPi, the CPPD crystal precursor. Addressing these underlying systemic issues helps reduce the rate of new crystal formation and potentially decreases the frequency of flare-ups.