Scientists from the University of California San Diego have uncovered a new cause of gout that could lead to more effective ways to prevent and treat the condition.
Their research reveals a previously unknown molecular pathway involving a protein called lubricin, which is essential for joint health and could be a key factor in both preventing and treating gout.
Gout is a painful form of arthritis caused by a buildup of urate, a substance produced from purine-rich foods like meat and alcohol. When urate levels rise, it can form sharp crystals in and around joints, typically starting in the foot.
This buildup triggers severe pain, swelling, and joint tenderness, which can eventually lead to chronic joint damage, limiting movement and reducing quality of life.
Until now, high urate levels in the blood, known as hyperuricemia, were thought to be the main cause of gout. However, many people with high urate levels don’t develop the disease.
In fact, asymptomatic hyperuricemia (high urate without symptoms) is four times more common than gout. Additionally, gout patients often show higher urate levels in their joint fluid than in their blood, a phenomenon that has puzzled researchers.
In this study, scientists focused on a unique case: a patient with gout who had urate crystal buildup and joint damage without high blood urate levels.
This case led researchers to explore the genetic and molecular factors that might cause urate to form crystals within the joints, even when blood levels are normal.
They discovered that the patient had a disruption in a molecular pathway involving lubricin. Lubricin, a protein found in joint fluid, helps keep joint tissues lubricated and protected. It also regulates a type of white blood cell that promotes inflammation within joints.
Under normal conditions, lubricin prevents urate and xanthine oxidase (an enzyme responsible for urate production) from increasing in joint fluid, which also helps stop urate crystals from forming.
Further experiments confirmed that lubricin plays a critical role in protecting joints from urate crystals.
The researchers then examined additional gout patients and found that they, too, had low levels of lubricin, suggesting that this deficiency could be a common factor in gout development.
These findings suggest that whether a person with high urate levels develops gout may depend on specific gene variations that influence lubricin production or breakdown.
This discovery points to lubricin as a promising therapeutic target, potentially leading to treatments that could prevent gout from occurring or progressing to more severe joint damage.
This study, conducted by Dr. Robert Terkeltaub and colleagues, was published in Arthritis & Rheumatology and could pave the way for new approaches to managing and preventing gout.
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