Gout is one of those diseases that have stumbled doctors trying to find a cure. They know that it’s painful symptoms are caused by too much uric acid in the blood that cause crystals to form between joints, but aren’t sure what causes it.
A new study published in Arthritis and Rheumatology last December identified a novel molecular pathway thought to cause gout and lead to progression of erosion in the joint tissues. The international research team was led by the University of California San Diego School of Medicine.
The Findings
The study’s findings indicate that a protein in joint fluid called lubricin could be a novel therapeutic target that could both treat and prevent gout.
Even though high uric acid in the blood is to blame for the needle like crystals around the joints.
Gout symptoms typically start in the foot with flares amounting to severe pain and joint swelling. This can lead to chronic joint damage that diminishes the quality of life and limits movement.
However, many have high uric acid levels that don’t develop gout. Figures show that asymptomatic
hyperuricemia, the term to identify high levels of uric acid, affects four times more people than gout.
Gout patients also show higher uric acid levels in their joint fluid when you compare it to their blood levels.
That led researchers to believe that high uric acid levels can’t be the only thing causing gout.
The Gene Factor
Researchers wanted to look at other factors that could lead to gout other than high uric acid levels. That
includes looking at genetic elements.
Researchers used RNA sequencing, whole genome sequencing, and quantitative proteomic methods to find a molecular pathway that was disturbed in the patient and resulted in a reduction of lubricin.
Lubricin is what lubricates and protects joint tissues. It also regulates how a specific type of white blood cell functions in its promotion of joint inflammation.
Identifying the Risk
The idea from the study is that gene variants for lubricin and other molecules that manage its production are what determine which patients with high uric acid will develop gout.
That makes lubrican a biomarker and shows that future gout treatments should focus on drugs that affect
lubrican production.
