A drug used today to treat rheumatoid arthritis might be effective in treating asthma symptoms after two genetic variants have been found to increase asthma susceptibility, researchers from the Queensland Institute of Medical Research, Brisbane, Australia and others from around the world reported in The Lancet. The scientists found that cytokines - genes associated with signalling molecules that are involved in how the immune system functions - are involved in the development of asthma.

The authors explained that the causes of asthma have for long been poorly understood, in spite of several attempts to locate the genetic variants. Some recent GWAS (genome-wide associated studies) have only managed to locate some candidate genes which appear to have a slight effect on asthma risk. They have not fully explained the heritability of asthma, which leads doctors and scientists to believe that many genetic variations are involved.

Manuel Ferreira and an international team of experts set out to determine what genetic variations might be responsible for higher asthma risk by carefully examining all current GWAS and expanding on them.

They compared the genomes of thousands of asthma patients with individuals who do not have asthma across several populations and identified two genetic mutations that were strongly linked to asthma risk.

The genetic variants were:
  • rs4129267 in the interleukin-6 receptor (IL6R) gene, and
  • rs7130588 on chromosome 11q13.5
Interleukin 6 (IL-6) is a cytokine. A cytokine is any substance that is secreted by some immune system cells that have an effect on other cells. Interferon, interleukin, and growth factors are examples of cytokines. Interleukin 6 (IL-6) plays a major role in immunity response and inflammation - it is involved in the way diseases develop (pathogenesis), including rheumatoid arthritis. The expression of the IL-6 receptor is increased by the rs4129267 risk variant. Consequently, the researchers believe that medications that inhibit the receptor should be tested in clinical trials to see how effective they are at reducing asthma-associated airway inflammation.

The drug tocilizumab is an example of a medication that blocks the receptor. It is already approved for rheumatoid arthritis treatment.

A high proportion of atopic (allergic) asthma patients were found to have the rs7130588 variant on chromosome 11q13.5. Interestingly, it was correlated with a nearby variant which has been recently associated with atopic dermatitis risk.

The authors believe that a gene in this region is involved in the development of allergic sensitisation, which raises allergic asthma risk.

The authors wrote:

"At this stage it is unclear which gene underlies the association with 11q13.5. Given that no specific gene in this region has been directly implicated in allergic disease previou. sly, further characterisation of this region of association is likely to discover novel molecular mechanisms involved in the causality of eczema, atopy, and asthma."


So far, no single genetic cause has been located which is responsible for over 1% of asthma heritability, the authors added. Their findings demonstrate that asthma is a complex condition, and most likely several genes of small effect combine and interact with environmental risk factors in driving asthma risk.

The scientists concluded:

"Our results are consistent with the contribution of hundreds or potentially thousands of variants with weak effects on asthma risk, which can be identified through larger GWAS as already shown with other diseases."


Kathleen Barnes, from Johns Hopkins University, Baltimore, USA, in a Comment in the same journal wrote:

"Success in the validation of various candidates (and their pathways) that are already on the asthma shortlist of potential causal genes, and the biological insight to be gained from the novel findings in this report are grounds for optimism in the continuation of the GWAS approach. Combination of GWAS with next-generation technologies will undoubtedly further help to disentangle the molecular underpinnings of complex traits such as asthma."


Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

  • Additional
  • References
  • Citations

New research shows that chondroitin sulfate significantly decreased pain and improved hand function in patients with osteoarthritis (OA) of the hand compared with those in the placebo group. Results of the clinical trial available today in Arthritis & Rheumatism, a journal published by Wiley-Blackwell on behalf of the American College of Rheumatology (ACR), also report that chondroitin sulfate improves grip strength and relieves morning stiffness.

The ACR estimates that OA—the most common form of arthritis—affects more than 27 million adults in the U.S., causing joint pain and stiffness. Approximately 10% of the world population, 60 years and older, have symptomatic osteoarthritis according to the Global Burden of Disease 2000 report from the World Health Organization (WHO). Prior studies have found that 20% to 30% of adults have OA of the hand, with the prevalence rising to more than 50% after 60 years of age.

"Although hand OA is highly prevalent among adults and can significantly impact the quality of life for suffers, therapeutic options are still limited," said Cem Gabay, M.D., with University Hospitals of Geneva in Switzerland and lead investigation of the Finger osteoArthritis Chondroitin Treatment Study (FACTS). "There are few trials examining therapeutic approaches specific to hand OA and much of the available evidence has been extrapolated from studies investigating other forms of OA."

The single-center, placebo-controlled FACTS trial included 162 patients with radiographic hand OA who met inclusion criteria—spontaneous hand pain on the visual analogue scale (VAS) of 40 mm (scale 0-100) or more and Functional Index for Hand OA (FIHOA) level of 6 (scale 0-30). Participants received either 800 mg of chondroitin sulfate (80 patients) or placebo (82 patients) once daily for 6 months.

Results showed that patients in the chondroitin sulfate group had significant decrease in global hand pain compared with the placebo group, reflecting an 8.7 decrease on the VAS. Hand function also improved significantly for those taking chondroitin sulfate, decreasing more than 2 points on the FIHOA. Researchers also reported significantly improved hand function and reduction in morning stiffness for participants taking chondroitin sulfate versus placebo.

"Our findings show chondroitin sulfate is a safe and effective treatment for patients with hand OA," concluded Dr. Gabay. "Alternative therapies, such as nonsteroidal anti-inflammatory drugs (NSAIDs), provide similar pain reducing effects, but with considerably more long-term toxicities." Chondroitin sulfate is a naturally occurring molecule and a main component of joint cartilage. The chondroitin sulfate agent used in this study (Chondrosulf®) is licensed as a drug in Europe and not as a nutripharmaceutical; in the U.S. chondroitin sulfate is sold as a supplement and often paired with glucosamine.

More information: Symptomatic Effect of Chondroitin Sulfate 4&6 in Hand Osteoarthritis: The Finger osteoArthritis Chondroitin Treatment Study (FACTS): A Randomized Double-Blind Placebo Controlled Clinical Trial." Cem Gabay, Carole Medinger-Sadowski, Danielle Gascon, Frank Kolo, Axel Finckh. Arthritis & Rheumatism; Published Online: September 6, 2011. DOI:10.1002/art.30574

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. It's pretty funny to me that when we were growing up, she'd cry because she wasn't allowed to play football with us.There is a subcategory of folk art paintings since I was a child. It is done in vibrant colors and also depicts the buildings in the market like an ice cream parlor and the Hotel Van Nuys. I have a friend who collects these and I found one of a woman reclining in a hammock. It's called First Trolley to Van Nuys and shows the center of a town filled.....

" Cem Gabay, Carole Medinger-Sadowski, Danielle Gascon, Frank Kolo, Axel Finckh. Approximately 10% of the world population, 60 years and older, have symptomatic osteoarthritis according to the Global Burden of Disease 2000 report from the World Health Organization (WHO)., causing joint pain and stiffness.1002/art. More information: Symptomatic Effect of Chondroitin Sulfate 4&6 in Hand Osteoarthritis: The Finger osteoArthritis Chondroitin Treatment Study (FACTS). The chondroitin sulfate agent used in this study (Chondrosulf®) is licensed as a drug in Europe and not as a nutripharmaceutical; in the U. The expression of the IL-6 receptor is increased by the It's too bad my parents didn't let her play football with us. Still, they are a joy to behold. Now we're very close. It was painted in 1988 by Reverend Howard Finster and is done in enamel.My sister also shares my love for folk art. She looked so relaxed, that I could imagine what it felt like to lie there myself. I personally don't have any of these in my collection, since I like to collect pieces that I can relate to. If she could kick the ball they way she liked to kick me in the knee, I'd see to it she played for my team every time.Another painting that I admire is called Howard in 1944. When she died, she left me the painting and it hangs in a place of honor over my fireplace mantle.I have loved folk art paintings since I was a child. I don't know whose smile is bigger, the one in the painting or the one on my face every time I look at it. It's called First Trolley to Van Nuys and shows the center of a town filled with people. I spent a lot of time playing in my tree house, that the trees in the picture appealed to me so much.. I'll find someone to give it to.The painting that has touched me the most features a sad little girl and is called A Letter From My Mother. It's pretty funny to me that when we were growing up, she'd cry because she wasn't allowed to play football with the boys and I used to tease her relentlessly and pull her pigtails whenever I got the chance. She favors animal prints, and I found one that depicts leopards and gave it to her for her birthday.One of my favorite

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A drug used today to treat rheumatoid arthritis might be effective in treating asthma symptoms after two genetic variants have been found to increase asthma susceptibility, researchers from the Queensland Institute of Medical Research, Brisbane, Australia and others from around the world reported in The Lancet. The scientists found that cytokines - genes associated with signalling molecules that are involved in how the immune system functions - are involved in the development of asthma.

The authors explained that the causes of asthma have for long been poorly understood, in spite of several attempts to locate the genetic variants. Some recent GWAS (genome-wide associated studies) have only managed to locate some candidate genes which appear to have a slight effect on asthma risk. They have not fully explained the heritability of asthma, which leads doctors and scientists to believe that many genetic variations are involved.

Manuel Ferreira and an international team of experts set out to determine what genetic variations might be responsible for higher asthma risk by carefully examining all current GWAS and expanding on them.

They compared the genomes of thousands of asthma patients with individuals who do not have asthma across several populations and identified two genetic mutations that were strongly linked to asthma risk.

The genetic variants were:

  • rs4129267 in the interleukin-6 receptor (IL6R) gene, and
  • rs7130588 on chromosome 11q13.5
Interleukin 6 (IL-6) is a cytokine. A cytokine is any substance that is secreted by some immune system cells that have an effect on other cells. Interferon, interleukin, and growth factors are examples of cytokines. Interleukin 6 (IL-6) plays a major role in immunity response and inflammation - it is involved in the way diseases develop (pathogenesis), including rheumatoid arthritis. The expression of the IL-6 receptor is increased by the rs4129267 risk variant. Consequently, the researchers believe that medications that inhibit the receptor should be tested in clinical trials to see how effective they are at reducing asthma-associated airway inflammation.

The drug tocilizumab is an example of a medication that blocks the receptor. It is already approved for rheumatoid arthritis treatment.

A high proportion of atopic (allergic) asthma patients were found to have the rs7130588 variant on chromosome 11q13.5. Interestingly, it was correlated with a nearby variant which has been recently associated with atopic dermatitis risk.

The authors believe that a gene in this region is involved in the development of allergic sensitisation, which raises allergic asthma risk.

The authors wrote:

"At this stage it is unclear which gene underlies the association with 11q13.5. Given that no specific gene in this region has been directly implicated in allergic disease previou. sly, further characterisation of this region of association is likely to discover novel molecular mechanisms involved in the causality of eczema, atopy, and asthma."


So far, no single genetic cause has been located which is responsible for over 1% of asthma heritability, the authors added. Their findings demonstrate that asthma is a complex condition, and most likely several genes of small effect combine and interact with environmental risk factors in driving asthma risk.

The scientists concluded:

"Our results are consistent with the contribution of hundreds or potentially thousands of variants with weak effects on asthma risk, which can be identified through larger GWAS as already shown with other diseases."


Kathleen Barnes, from Johns Hopkins University, Baltimore, USA, in a Comment in the same journal wrote:

"Success in the validation of various candidates (and their pathways) that are already on the asthma shortlist of potential causal genes, and the biological insight to be gained from the novel findings in this report are grounds for optimism in the continuation of the GWAS approach. Combination of GWAS with next-generation technologies will undoubtedly further help to disentangle the molecular underpinnings of complex traits such as asthma."


Written by Christian Nordqvist
Copyright: Medical News Today
Not to be reproduced without permission of Medical News Today

  • Additional
  • References
  • Citations

New research shows that chondroitin sulfate significantly decreased pain and improved hand function in patients with osteoarthritis (OA) of the hand compared with those in the placebo group. Results of the clinical trial available today in Arthritis & Rheumatism, a journal published by Wiley-Blackwell on behalf of the American College of Rheumatology (ACR), also report that chondroitin sulfate improves grip strength and relieves morning stiffness.

The ACR estimates that OA—the most common form of arthritis—affects more than 27 million adults in the U.S., causing joint pain and stiffness. Approximately 10% of the world population, 60 years and older, have symptomatic osteoarthritis according to the Global Burden of Disease 2000 report from the World Health Organization (WHO). Prior studies have found that 20% to 30% of adults have OA of the hand, with the prevalence rising to more than 50% after 60 years of age.

"Although hand OA is highly prevalent among adults and can significantly impact the quality of life for suffers, therapeutic options are still limited," said Cem Gabay, M.D., with University Hospitals of Geneva in Switzerland and lead investigation of the Finger osteoArthritis Chondroitin Treatment Study (FACTS). "There are few trials examining therapeutic approaches specific to hand OA and much of the available evidence has been extrapolated from studies investigating other forms of OA."

The single-center, placebo-controlled FACTS trial included 162 patients with radiographic hand OA who met inclusion criteria—spontaneous hand pain on the visual analogue scale (VAS) of 40 mm (scale 0-100) or more and Functional Index for Hand OA (FIHOA) level of 6 (scale 0-30). Participants received either 800 mg of chondroitin sulfate (80 patients) or placebo (82 patients) once daily for 6 months.

Results showed that patients in the chondroitin sulfate group had significant decrease in global hand pain compared with the placebo group, reflecting an 8.7 decrease on the VAS. Hand function also improved significantly for those taking chondroitin sulfate, decreasing more than 2 points on the FIHOA. Researchers also reported significantly improved hand function and reduction in morning stiffness for participants taking chondroitin sulfate versus placebo.

"Our findings show chondroitin sulfate is a safe and effective treatment for patients with hand OA," concluded Dr. Gabay. "Alternative therapies, such as nonsteroidal anti-inflammatory drugs (NSAIDs), provide similar pain reducing effects, but with considerably more long-term toxicities." Chondroitin sulfate is a naturally occurring molecule and a main component of joint cartilage. The chondroitin sulfate agent used in this study (Chondrosulf®) is licensed as a drug in Europe and not as a nutripharmaceutical; in the U.S. chondroitin sulfate is sold as a supplement and often paired with glucosamine.

More information: Symptomatic Effect of Chondroitin Sulfate 4&6 in Hand Osteoarthritis: The Finger osteoArthritis Chondroitin Treatment Study (FACTS): A Randomized Double-Blind Placebo Controlled Clinical Trial." Cem Gabay, Carole Medinger-Sadowski, Danielle Gascon, Frank Kolo, Axel Finckh. Arthritis & Rheumatism; Published Online: September 6, 2011. DOI:10.1002/art.30574

Provided by Wiley (news : web)