A recent study conducted by scientists from the University of California San Diego and other institutions has uncovered a surprising new cause of gout, a painful form of arthritis.
The research reveals a previously unknown molecular pathway that contributes to the development and progression of gout, leading to joint damage.
This discovery suggests that a protein called lubricin, found in joint fluid, could be a promising target for new treatments to prevent and manage the disease.
Gout is the most common type of inflammatory arthritis. It occurs when urate, a substance produced from the breakdown of purine-rich foods like red meat and alcohol, accumulates in the body. This excess urate can form needle-like crystals in and around the joints, most often starting in the foot.
These crystal deposits cause sudden and intense pain, along with joint swelling and tenderness. Over time, if left untreated, gout can lead to chronic joint damage, severely impacting a person’s mobility and quality of life.
Traditionally, the primary cause of gout has been thought to be hyperuricemia, which is a condition where there is too much urate in the blood. However, it’s puzzling that most people with high urate levels never actually develop gout.
In fact, the condition known as asymptomatic hyperuricemia, where urate levels are high but no symptoms are present, is about four times more common than gout itself.
Another mystery in gout research has been the observation that patients with gout often have higher levels of urate in their joint fluid than in their blood.
In this study, researchers aimed to understand why some people with high urate levels develop gout while others do not. They focused on the genetic factors that specifically lead to urate production and crystal formation within the joints, rather than just high urate levels in the blood.
To do this, they examined a rare case where a patient developed urate crystal deposits and joint erosion without having elevated urate levels in her blood.
The researchers discovered that this patient had a significant reduction in lubricin, a mucinous protein that plays a critical role in protecting and lubricating joint tissues. Lubricin also helps regulate the activity of certain white blood cells that promote inflammation in the joints.
Under normal conditions, lubricin prevents urate from crystallizing in the joints by controlling the secretion of urate and the enzyme xanthine oxidase, which produces urate.
Further experiments confirmed that in healthy joints, lubricin helps suppress urate production and crystal formation. However, in patients with gout, levels of lubricin were found to be significantly lower.
This reduction in lubricin may contribute to the development of gout in individuals with hyperuricemia, depending on their genetic makeup and how their bodies produce or degrade lubricin.
The researchers believe that whether a person with high urate levels will develop gout could be influenced by the specific variants of genes responsible for the production and regulation of lubricin.
This finding opens up new avenues for treating and preventing gout by targeting lubricin and related molecular pathways.
The study, led by Dr. Robert Terkeltaub and published in Arthritis & Rheumatology, highlights the importance of lubricin in joint health and suggests that therapies aimed at increasing lubricin levels or improving its function could be effective in managing gout.
This research not only enhances our understanding of gout but also offers hope for new treatment strategies that could prevent the painful progression of this common condition.
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