Gout and pseudogout are both forms of inflammatory arthritis, conditions where the joints become painful, swollen, and red. They are often grouped together because they both arise from the body depositing microscopic, irritating crystals within the joint space, a group of diseases known as crystalline arthropathies. The underlying causes, specific joint involvement, and long-term management strategies are fundamentally different.
The Specific Crystals Driving Inflammation
The core difference between these two conditions lies entirely in the chemical composition of the crystals that accumulate in the joints. Gout is caused by the buildup of monosodium urate (MSU) crystals, which are the solid form of excess uric acid in the body. This accumulation is a direct result of hyperuricemia, a condition where the concentration of uric acid in the blood is too high.
Pseudogout, in contrast, is caused by crystals made of calcium pyrophosphate (CPP), which is why the condition is formally termed Calcium Pyrophosphate Deposition Disease (CPPD). These CPP crystals form when pyrophosphate binds with calcium in the joint cartilage, triggering an inflammatory immune response. Unlike gout, the formation of CPP crystals is not linked to elevated levels of a substance in the blood that can be easily managed, which creates a significant difference in treatment approaches.
How Symptoms and Joint Locations Differ
The clinical presentation of both conditions involves a sudden onset of joint pain, swelling, and warmth, but the typical locations and severity often provide initial clues. Gout attacks are known for their rapid onset, often waking an individual in the middle of the night with intense, burning pain. The joint most commonly affected is the metatarsophalangeal joint at the base of the big toe, a pattern of involvement known as podagra, which occurs in about half of all first-time attacks.
While gout can affect other areas like the ankle, knee, and wrist, the attacks are typically confined to a single joint in the early stages of the disease. In chronic, untreated cases, MSU crystals can form hard deposits under the skin called tophi, which can lead to joint deformation and severe bone erosion.
Pseudogout flares, while also painful and sudden, often target larger joints such as the knee, wrist, shoulder, or hip. Unlike gout, pseudogout rarely involves the big toe and frequently affects multiple joints simultaneously, or one after the other. A pseudogout episode may also last longer than a gout attack, potentially persisting for days or weeks. In some individuals, the presence of CPP crystals in the cartilage, a phenomenon called chondrocalcinosis, may be asymptomatic or present as a chronic arthritis that mimics osteoarthritis.
Confirming the Diagnosis
Because the symptoms of gout and pseudogout can overlap significantly, a definitive diagnosis cannot be made based on symptoms alone. The gold standard for confirming the diagnosis is a medical procedure called arthrocentesis, where a small sample of synovial fluid is drawn from the affected joint and analyzed under a specialized polarized light microscope. Under the microscope, the specific shape and light-polarizing properties of the crystals definitively identify the condition.
Monosodium urate crystals from gout appear as thin, sharp, needle-shaped structures that exhibit strong negative birefringence. In contrast, the calcium pyrophosphate crystals responsible for pseudogout are typically shorter and have a rhomboid or rod-like shape, displaying a weaker positive birefringence.
X-rays can also offer supporting evidence, though they are not sufficient for a definitive diagnosis. In pseudogout, X-rays may reveal chondrocalcinosis, which appears as thin lines of calcification in the joint cartilage. Advanced gout, on the other hand, can be identified by characteristic, punched-out bone erosions near the joint.
Managing Gout Versus Pseudogout
The difference in the underlying crystal is the primary reason why the long-term management of these two conditions diverges significantly. For acute attacks of both conditions, the immediate treatment involves reducing inflammation and pain using nonsteroidal anti-inflammatory drugs (NSAIDs), colchicine, or corticosteroids. These medications suppress the body’s inflammatory reaction to the presence of crystals.
The approach to long-term prevention varies considerably due to the ability to target the root cause of gout. Because gout is caused by high uric acid levels, preventative therapy focuses on urate-lowering medications like allopurinol or febuxostat. These drugs work by either reducing the production of uric acid or increasing its excretion, with the goal of dissolving the MSU crystals and preventing future attacks.
For pseudogout, there are currently no medications that effectively prevent the formation or accumulation of calcium pyrophosphate crystals. Therefore, the long-term management strategy for pseudogout focuses on managing the acute flares and treating any underlying metabolic conditions that may contribute to CPPD.