Soon, simple blood test to spot arthritis early

Experts at the Karolinska Institute in Sweden and Johns Hopkins University School of Medicine in the United States discovered that certain genes and the "tags" that regulate them conspire together to promote the development of arthritis.

Separating the tags caused by the disease from those that help cause it led the team to find the specific DNA sequences vital for it to progress, the Daily Express reported.

They believe the discovery could be used in helping identify who will go on to suffer from arthritis and may also be used to predict other non-infectious conditions such as Type 2 diabetes and heart disease.

"Since rheumatoid arthritis is a disease in which the body's immune system turns on itself, current treatments often involve suppressing the entire immune system, which can have serious side effects," Dr Andrew Feinberg, professor of molecular medicine at Johns Hopkins' Institute for Basic Biomedical Sciences, said.

"The results of this study may allow clinicians to directly target the culpable genes and/or their tags," Feinberg said.

The researchers identified 10 DNA sites that were tagged differently in arthritis patients and which affected risk for developing the disease.

Nine sites were in a region known to play an important role in autoimmune diseases. The tenth was on a gene never before associated with the disease.

"Our method allows us to predict which tagging sites are most important in the development of a disease," Dr Yun Liu, lead researcher, said.

Several DNA mutations are known to increase risk for rheumatoid arthritis, but there appear to be additional factors that suppress or enhance that risk.

One of these involves chemical tags that attach to DNA sequences, part of an epigenetic system that helps regulate when and how DNA sequences are "read", how they are used to create proteins and how they affect the onset or progress of disease.

The researchers catalogued DNA sequences and their tagging patterns in the white blood cells of more than 300 people with and without arthritis.

They were able to identify DNA sequences that were more prevalent in patients with the disease, which could shed further light on how it operates.

"This could explain why risk genes assert themselves and cause disease and why some people are affected more easily than others," Tomas Ekstrom, professor of molecular cell biology at Karolinska Institute's Department of Clinical Neuroscience, said.