Results of a recent research project, carried out by the University of Pittsburgh School of Medicine and published in the Archives of Internal [...] No related posts.]]> Gout is a form of arthritis that is caused by an excess of uric acid in the bloodstream. This causes crystals to form in the joints, typically in the big toe.

Results of a recent research project, carried out by the University of Pittsburgh School of Medicine and published in the Archives of Internal Medicine, indicates that people with existing risk factors for heart disease may have an increased risk for heart attack or stroke if they also develop gout.

The study involved over 9,000 men who were between 41 and 63 years old. They all had above average risk for heart disease, with factors such as high cholesterol, high blood pressure and smoking.

The researchers found that after 17 years the men who developed gout were 30% more likely to die from cardiac arrest or other cardiovascular disease than those without gout.

Not all men with elevated uric acid levels develop gout. Men in this study that had high levels of uric acid, but did not develop gout, did not have a higher risk of cardiovascular related death.

This study supports the findings in a 2004 study of 1,423 middle aged Finnish men. That research found that men with excess uric acid in the blood had a 250% greater risk of death from cardiovascular disease than those with normal levels.

One theory is that an excess of uric acid in the bloodstream causes “oxidative stress”, which results in the LDL cholesterol being oxidized. Oxidized LDL is viewed as more dangerous because it causes hardening and narrowing of the arteries.

Originally posted 2008-07-22 21:20:25. Republished by Blog Post Promoter

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Dr. Hallie Buckley, from Otago University’s Department of Anatomy and Structural Biology, has been studying bones from the oldest cemetery found in thePacific [...] No related posts.]]> Interesting story from New Zealand discussing the possibility that high rates of gout in Pacific Islanders may be a genetic trait passed to them by ancient voyagers across the Pacific Ocean.

Dr. Hallie Buckley, from Otago University’s Department of Anatomy and Structural Biology, has been studying bones from the oldest cemetery found in thePacific Islands. These remains are estimated to be 3000 to 3200 years old and were discovered on Efate Island in Vanuatu.

Dr. Hallie’s team examined the bones from 20 skeletons using radiography and other techniques and found damage to the joints in seven of them. Analysis of the damage, or erosive lesions, indicated that they were most likely caused by gouty arthritis, a build up of uric acid crystals in the joints.

The skeletons that were studied were from a people known as “Lapita”. They were named for the distinctive decorated pottery that has been found across the Pacific.

The Lapita’s diet would have consisted of plants and seafood, a diet that is rich in purines which are organic compounds that are a crucial part of DNA and RNA. This high purine diet may have set off attacks of gout in people that are susceptible.

There are scientists that have theorized that as the descendents of the Lapita people migrated across the Pacific they passed their genetic predisposition to gout on to their descendents. This is known as the “founder effect”, where a small number of people pass a genetic trait on to a large number of descendents. This could explain the high incidence of high uric acid levels and gout in many modern Pacific Island societies. The Maori of New Zealand have an incidence of gout of over 10%.

Dr. Hallie’s research was published in the publication Current Anthropolgy.

Originally posted 2007-12-27 19:54:50. Republished by Blog Post Promoter

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Arthritis Australia hopes that these activities will make all Australians aware that [...] No related posts.]]> Arthritis Awareness Week is March 29th to April 4th, an initiative of Arthritis Australia, and is a time of promotional and educational activities, held around the country, to raise awareness about arthritis, its effects, and the various treatment and management options available.

Arthritis Australia hopes that these activities will make all Australians aware that arthritis is not a natural part of ageing but a disease that affects many people of working age and also children.

Arthritis includes more than 100 different diseases such as osteoarthritis, rheumatoid arthritis, gout, ankylosing spondylitis, Reiter’s syndrome and systemic lupus erythematosus (SLE or lupus), that affect the musculoskeletal system.

Pain, stiffness, inflammation, and damage to the cartilage, bones and other structures within the joints are all common manifestations of arthritis. Although it cannot be cured, the symptoms and impacts of arthritis can be reduced through early diagnosis and appropriate treatment and management.

An estimated three million Australians – 15 per cent of the population – have some form of arthritis, the most common types being osteoarthritis (affecting more than 1.5 million Australians) and rheumatoid arthritis (affecting around 491,000 Australians).

Although the number of people who have arthritis increases with age, about one in every four Australians with arthritis are less than 50 years of age and there are an estimated 4600 Australians with arthritis who are less than 16 years.

In 2003, around 34 per cent of people with a disability reported that arthritis or another musculoskeletal condition was their main disabling condition.

In 2004-05, arthritis and musculoskeletal conditions accounted for the fourth highest amount of direct health expenditure at a total of $4 billion. Close to one-third of this amount was spent on osteoarthritis, with hospital inpatient costs accounting for a large proportion.

In cases of severe osteoarthritis, people may have their symptoms relieved and joint function improved through joint replacement. More than 17,000 total hip replacements and almost 25,000 total knee replacements for arthritis were performed in Australian hospitals in 2006-07, most of these for osteoarthritis.

Originally posted 2009-03-25 06:00:12. Republished by Blog Post Promoter

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The research was a trial involving 10 patients with chronic, active, gouty arthritis. They averaged 62 years of age [...] No related posts.]]> Gout has typically been treated with non-steroidal anti-inflammatory drugs (NSAIDs). But a report presented at the American College of Rheumatology on October 30, 2007 indicates that a new therapy may provide greater relief than NSAIDs.

The research was a trial involving 10 patients with chronic, active, gouty arthritis. They averaged 62 years of age and had gout for an average of 13 years. This trial was a multi-center, non-randomized, single-blind, placebo-controlled study.

Rilonacept is a potential new therapy being tested for treatment of inflammatory conditions. It acts by preventing interleukin-1 (IL-1) from attaching to cell-surface receptors. IL-1 is a protein secreted by many cells in the body and, if secreted in excess, can trigger activity in gout.

The participants in the study were given 2 weekly injections of a placebo followed by 6 weekly injections of rilonacept. The researchers assessed the patient’s gout activity by the degree of pain, number of joints with pain and C-reactive protein blood test used to measure inflammation in the body.

From the second through the eighth weeks of treatment, 70% of the patients experienced at least a 50% improvement in pain, and 60% had at least 75% improvement in pain. None of the patients reported improvements from the placebo.

In addition, by week 8 of treatment on the rilonacept, the inflammation levels in the blood had decreased by 59%.

The researchers reported that tolerance to the therapy was good, as there were no reported deaths or serious adverse events, and that this therapy may provide a better option for treatment than NSAIDs.

Originally posted 2007-11-23 17:48:38. Republished by Blog Post Promoter

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Normally, the kidneys remove uric acid from the blood and eliminate it in urine. But the kidneys in those with gout [...] No related posts.]]> Gout is a painful condition which results from high levels of uric acid in the blood. Over time the uric acid forms crystals in the joints which leads to inflammation, stiffness and pain.

Normally, the kidneys remove uric acid from the blood and eliminate it in urine. But the kidneys in those with gout do not keep up with the production of uric acid.

It has been believed that diets high in sugar, alcohol and protein lead to increased risk of gout. In fact, gout was known as the “Disease of Kings” due to its link to rich foods and alcohol.

This view may change as a result of a recent study of 12,000 people which revealed a genetic link to gout.

Scientists at the Medical Research Council Human Genetics Unit and the University of Edinburgh, along with researchers in Croatia, have found a gene variation that makes it harder for the body to remove uric acid from the blood.

That gene is responsible for coding a protein known as SLC2A9 which is responsible for transporting uric acid across the membranes of the kidney. Variations in the SLC2A9 gene cause some people to have higher levels of uric acid in the blood.

The researchers identified genetic variations in the SLC2A9 gene in different populations in Orkney, Tayside and Croatia. Further analysis has eliminated links between the genetic variations in SLC2A9 and increased risk of heart disease, obesity and elevated blood pressure.

Additional research in Germany demonstrated that the gene is associated with the capacity to remove uric acid from the body through urine.

The results of this study is published in the journal Nature Genetics.

Professor Alan Wright of the Human Genetics Unit, and one of the lead authors, says: “The discovery of this important new function for the SLC2A9 protein will aid the development of drugs which could lower blood uric acid levels and prevent or treat gout.”

Another lead author, Harry Campbell, Professor of Genetic Epidemiology and Public Health and the University of Edinburgh says: “This discovery may allow better diagnostic tools for gout to be developed.”

Originally posted 2008-03-31 19:06:43. Republished by Blog Post Promoter

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