Gout is the most prevalent form of inflammatory arthritis.
It occurs when urate (a byproduct of purine-rich foods like meat and alcohol) accumulates in the body, forming needle-like crystals in and around the joints.
This typically starts in the foot, causing severe pain, joint swelling, and tenderness, which can progress to chronic joint damage.
Although excess urate in the blood (hyperuricemia) has long been considered the primary cause of gout, most people with high urate levels don’t develop the disease.
Also, gout patients often have mysteriously higher levels of urate in their joint fluid compared to their blood.
In the study, the researchers aimed to understand the genetic factors that lead to urate production and crystal deposition within joints.
They studied a unique case of gout where the patient developed urate crystal deposits and joint erosion, but didn’t have high urate levels in the blood.
The researchers identified a major disrupted molecular pathway in the patient, centered around a significant reduction in lubricin, a protein that lubricates and protects joint tissues.
Lubricin also regulates the function of specific white blood cells that promote joint inflammation.
Additional experiments showed that, under normal conditions, lubricin suppresses the secretion of urate and xanthine oxidase (an enzyme that produces urate) by activating white blood cells and prevents urate from crystallizing in the joint.
The researchers confirmed that several patients with the common form of gout also had markedly decreased levels of lubricin.
They suggested that whether a hyperuricemia patient develops gout could be influenced by the gene variants they have for lubricin and other molecules controlling its production or degradation in the joint.
Implications and Future Directions
The findings could have significant implications for the prevention and treatment of gout. Targeting the lubricin pathway could offer a new therapeutic strategy.
However, more research will be required to confirm these findings and explore the potential for interventions targeting lubricin.
The study, conducted by a team led by Robert Terkeltaub, was published in the journal Arthritis & Rheumatology.
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