A gout is a form of arthritis that has been around for a long time but is becoming more common. It is caused by the build-up of urate in the body, which forms crystals in and around the joints. These crystals can cause severe pain, swelling, and tenderness, and can lead to chronic joint damage. It is estimated that more than 10 million people in the United States have gout.
It is a type of arthritis that is caused by an excess of urate in the body. This substance, which is produced by the breakdown of purine-rich foods like meat and alcohol, forms needle-shaped crystals in the joints. This can result in severe pain, swelling, and tenderness, and can ultimately lead to chronic joint damage that can limit a person's movement and quality of life. It is the most common form of inflammatory arthritis, as per the Centers for Disease Control and Prevention (CDC).
This illness typically affects only one joint at a time, and the big toe is the most common location for a gout flare. Other common sites of gout include the lesser toe joints, the ankle, and the knee. A gout flare can start suddenly and last for days or weeks, followed by a period of remission without symptoms. This period of remission can last for weeks, months, or even years before another flare begins.
Basic Knowledge of Gout
Hyperuricemia, or excess urate in the blood, has traditionally been thought to be the main cause of gout. However, most people with high urate levels do not develop the disease. Asymptomatic hyperuricemia is more common than gout. Additionally, gout patients have higher levels of urate in their joint fluid than in their blood, suggesting that other factors may be involved in the development of the disease. It is not fully understood what these factors may be.
A new study by researchers from the University of California San Diego School of Medicine has identified a molecular pathway that causes gout and its progression to joint tissue erosion. The study suggests that lubricin, a protein found in joint fluid, could be a potential therapeutic target for preventing and treating the disease. These findings were published online in the journal Arthritis & Rheumatology.
The scientists in the study focused on investigating the genetic factors that cause not just high levels of circulating urate, but specifically the production of urate crystals and their deposition within joints. They examined a rare case of gout in which the patient had developed urate crystal deposits and joint erosion despite not having high levels of urate in their blood. This allowed the researchers to identify potential genetic factors that specifically contribute to the development of gout within joints.
The researchers involved in the study saw the rare disorder as a chance to study gouty arthritis in a new way, and to understand the molecular processes that contribute to the disease independently of high levels of circulating urate. Senior author Robert Terkeltaub, MD, professor at UC San Diego School of Medicine and section chief of Rheumatology at the Veterans Affairs San Diego Healthcare System, explained the significance of this unique opportunity.
James Gillray's 1799 painting illustrates the painful symptoms of gout. New developed methods in treating gouts reveals, ancient history of inflammatory arthritis, sheds new knowledge.
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New Methods in Treating Gout Inflammation
The team used a variety of techniques, including whole genome sequencing, RNA-sequencing, and quantitative proteomic methods, to identify a major molecular pathway that was disrupted in the patient. They found that the patient had significantly reduced levels of lubricin, a mucinous protein that provides lubrication and protection to joint tissues and regulates the function of certain white blood cells that promote inflammation in the joint. These findings suggest that lubricin could be a novel therapeutic target for the prevention and treatment of gout.
As reported by Medical Xpress, to further confirm the role of lubricin in gout, the researchers conducted additional experiments. These experiments showed that under healthy conditions, lubricin suppresses the secretion of urate and the enzyme xanthine oxidase, which produces urate, by activating white blood cells. It also blocks urate from crystallizing in the joint. The researchers also looked at several patients with the common form of gout and found that they too had reduced levels of lubricin.
These findings suggest that the likelihood of a hyperuricemia patient developing gout may be influenced by their genetic variants for lubricin and other molecules that control its production or degradation in the joint. The authors of the study propose that targeting these molecules could be a potential approach for preventing and treating gout.
According to Dr. Terkeltaub, the findings suggest that lubricin may be a potential biomarker for identifying patients at risk of developing gout and that drugs that maintain or increase lubricin levels could potentially prevent or slow the progression of gouty arthritis. These findings could pave the way for new therapeutic approaches for gout.
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