According to researchers at the Mayo Clinic in Rochester, Minnesota, rheumatoid arthritis (RA) appears to be increasing in women after 40 years of decline.

In a report that was published earlier this year, researchers from the National Arthritis Data Workgroup stated that an estimated 1.3 million adults in the U.S. are affected by RA. This compares to the estimate of 2.1 million in 1995.

However, the group decided to take a look at more recent data than that used for the Workgroup study. To this end, they recruited 350 patients with RA in Olmstead County, Minnesota that were diagnosed between 1995 and 2005 and then looked at the population as a whole to determine the incidence rate.

Based on this more recent data, Dr. Hilal Maradit-Kremers, associate professor of epidemiology at the Mayo Clinic, and colleagues, found that 54 women out of every 100,000 develop rheumatoid arthritis each year as compared to 36 out of every 100,000 10 years earlier.

The incidence for men remained the same at 29 per 100,000.

“These rates would apply to the entire U.S. population,” Kremers says. “Based on this new data, the estimated number of people with RA in the U.S. is probably higher than 1.2 million.”

It is believed that the increase in the incidence rate is a result of environmental, and possibly hormonal, causes.

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Rheumatoid arthritis (RA) is an autoimmune disease that causes the body’s immune system to attack itself. Many treatments have been investigated that would control or suppress the body’s immune system. Anti tumor necrosis factor (TNF) drugs are immune system suppressants that are widely used to treat RA.

A new study conducted by researchers at the Medical Research Council’s Laboratory of Molecular Biology in Cambridge has resulted in a breakthrough in the understanding of how autoimmune responses can be controlled.

In a normal immune system, the body develops immune cells to recognize foreign material, like bacteria. Once encountered, the immune cells respond to eliminate the foreign material. Any rogue immune cells that would attack the body itself are destroyed during development or are regulated by special cell. A key gene in these regulatory cells is called Foxp3. Those people that either lack the Foxp3 gene or have a mutated version of the gene have dysfunctional immune regulation which can result in autoimmune diseases.

As a part of the study, scientists created a genetically engineered form of Foxp3 that can change developing immune cells into regulatory cells that have the ability to suppress immune response. They then injected the engineered gene into animals that were missing the Foxp3 gene.

Said group leader Dr. Alexander Betz: “When administered to and activated in animal models of arthritis, the modified cells inhibit or even reverse the disease process.”

The scientists are now working on determining the molecular mechanisms involved in the functioning of the Foxp3 gene and applying that to human cells. In that research they need to ensure that the human form of the gene does not negatively impact the body’s immune system.

“If Foxp3 functions as a key developmental switch in human immune cells, there is potential for a new avenue of therapy development that could transform arthritis treatment” — Dr. Betz.

The study was published in the current issue of the journal PLoS Biology.

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Many in the medical community still believe that fibromyalgia is a psychological condition since there have been no distinct causes found for the condition. In fact it has been called the “invisible syndrome” because it cannot be diagnosed using X-ray or lab tests. But a new brain scan study has found a common factor in fibromyalgia patients.

Researchers from the Centre Hospitalo-Universitaire de la Timone, in Marseille, France, took brain scans of 20 female fibromyalgia patients and 10 without the condition. They also had the participants provide information to measure anxiety, disability pain and depression.

The brain scan technique used in this research is called single photon emission computed tomography (SPECT). This type of scan uses gamma rays to create a true 3-dimensional image and can help detect functional abnormalities deep in the brain.

The researchers correlated the data and discovered that patients with fibromyalgia have abnormalities in the blood flow in the brain, which is called perfusion. More, the abnormalities are directly related to the severity of the condition. An increase in perfusion (hyperperfusion) was noted in the area of the brain that measures pain intensity and a decrease in perfusion was noted in the area thought to be involved in the emotional response to pain.

“Fibromyalgia may be related to a global dysfunction of cerebral pain-processing. This study demonstrates that these patients exhibit modifications of brain perfusion not found in healthy subjects and reinforces the idea that fibromyalgia is a ‘real disease/disorder.’” - Eric Guedj, M.D, lead author

The researchers also found that the functional abnormalities had no relationship to depression of anxiety.

The study was reported in the November issue of The Journal of Nuclear Medicine.

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On Wednesday’s post I reported on a study that indicated that people with rheumatoid arthritis (RA) were more likely to have cardiac problems that people without RA. In that study the researchers believed the increased cardiac risk was related to a condition known as diastolic dysfunction. Diastolic dysfunction is a condition where the there is stiffening in the heart which leads to problems with proper circulation of blood. Blood can actually spill backwards through the heart and into the lungs.

In a third study reported on at last week’s American College of Rheumatology’s (ACR) annual meeting in San Francisco, a team led Dr. Kimberly Liang, assistant professor at the University of Pittsburgh, found additional evidence that there is a link between RA and diastolic dysfunction.

“Diastolic dysfunction occurred in 38.9 percent, compared to 28.8 percent in the non-rheumatoid arthritis group. We also found that patients in the rheumatoid arthritis group had higher average pulmonary arterial pressure, which is high blood pressure in the lungs and the right side of the heart. This is consistent with the impaired filling of the heart seen in diastolic dysfunction.” - Dr. Kimberly Liang

According to Dr. Liang, increased usage of electrocardiography in rheumatoid arthritis patients may improve detection of heart problems before there are clinical signs.

The chief science officer for the Arthritis Foundation, Dr. John Hardin, says that these studies highlight the impacts that RA can have on the cardiovascular system.

“These studies are consistent with the idea that systemic inflammation promotes cardiovascular disease,” Hardin said. “Rheumatoid arthritis creates a general state of inflammation within the body.”

Dr. Hardin also pointed out that there are some arthritis drugs that can increase the risk of heart failure in RA patients with already damaged hearts.

“For example, Enbrel (etanercept) can, in fact, in some people, potentiate heart failure, which can be a complication of myocardial infarction. To prevent a heart attack, patients with rheumatoid arthritis need to pay particular attention to cholesterol, blood pressure and maintaining a healthy lifestyle. If you have rheumatoid arthritis, the things you do to protect yourself against cardiovascular disease become doubly important.” - Dr. John Hardin.

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I wrote on Monday about a study presented at the American College of Rheumatology’s (ACR) annual meeting in San Francisco. In that research study, a graduate student from Sweden found that people with rheumatoid arthritis (RA) had nearly twice the risk of heart attack and death from heart attack of those without RA.

Another research study presented at ACR meeting also indicates that people with RA have an increased risk of heart problems as those without RA.

The researchers in this study, led by Dr. Hilal Maradit Kremers, found that a condition known as diastolic dysfunction can lead to heart failure. Diastolic dysfunction is an abnormality in the left ventricle of the heart which causes blood returning from the lungs to spill back into the left atrium and eventually back into the lungs. This condition results in stiffness of the heart and can lead to heart failure.

The team followed 38 RA patients who had suffered a heart attack. They compared these patients to patients with RA who had not had a heart attack.

The team’s analysis showed that the patients with rheumatoid arthritis were 45% more likely to develop heart failure after a heart attack compared with the general population. They also found that RA patients had a 75% greater risk of dying from heart failure.

“Rheumatoid arthritis patients not only have more heart attacks and heart failures, but they also have worse prognosis once they have a cardiovascular event,” said Dr. Kremers.

Dr. Kremers is an epidemiologist at the Mayo Clinic in Rochester, Minnesota.

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