Posts
Saturday, March 14, 2009
Vitamin C reduces risk for gout
A publication in the Archives of Internal Medicine (Vitamin C Intake and the Risk of Gout in Men) suggests that Vitamin C may reduce the risk for Gout. This was a large prospective study. The BBC also picked up and reported this story (Vitamin C a 'gout preventer'). Interesting how the scientific study showed a "decreased risk" and the media publication called this "prevention".
Tuesday, January 6, 2009
Gout Protective for Parkinsons disease
If you have gout you are less likely than to develop parkinsons diseases than if you did not have gout! It is assumed that uric acid is the mechanism for the protective effect. (Ref: Gout and the risk of parkinson's disease: A cohort study Mary De Vera, M. Mushfiqur Rahman, James Rankin, Jacek Kopec, Xiang Gao, Hyon Choi Arthritis Care & Research; Volume 59 Issue 11, Pages 1549 - 1554 )
Variations in taking gout medication
A new study published inthe Annals of Rheumatic Diseases has found a large vairation in the uses of medication by those with gout. This suggests that there is considerable room for improvment in the management of gout. (Ref: Opportunities for improving medication use and monitoring in gout Jasvinder A Singh, James M Hodges and Steven M Asch Ann Rheum Dis)
Ardea Biosciences' Advances RDEA806 Into Phase 2a Proof-of-Concept Study for Gout
Press Release:
Ardea Biosciences, Inc. (Nasdaq: RDEA) today announced that it has received regulatory approval to begin a Phase 2a proof-of-concept clinical trial evaluating RDEA806 in gout patients with hyperuricemia. Gout, also known as metabolic arthritis, is a painful and debilitating disease caused by abnormally elevated levels of uric acid in the blood stream, and is the most common form of inflammatory arthritis in men over 40. The Company also announced that gout specialist, Dr. Fernando Perez-Ruiz in Spain, will be the newest member of its inflammatory disease scientific advisory board (SAB). Ardea previously announced the designation of RDEA594, a major metabolite of RDEA806, the Company's lead human immunodeficiency virus (HIV) development compound, as its lead development candidate for the treatment of patients with gout. RDEA594 does not have antiviral activity, but is believed to be responsible for essentially all of the uric acid lowering effects seen with RDEA806. Uric acid lowering effects have been observed following administration of RDEA806 in Phase 1 and Phase 2 clinical trials that included over 100 subjects. "The Phase 2a trial should allow us to confirm RDEA594's activity in the target population of patients with gout using its prodrug, RDEA806. Enrollment in the Phase 2a trial should begin shortly and we are on track to initiate a Phase 1 trial with RDEA594 in the second half of this year," said Barry D. Quart, PharmD, Ardea Biosciences' President and CEO. "We also are extremely pleased to add Dr. Fernando Perez-Ruiz to our inflammatory diseases SAB. Dr. Perez-Ruiz has extensive experience treating gout patients with drugs of the same class as RDEA594." The Phase 2a randomized, double-blind, dose ranging, efficacy and safety trial will be conducted in academic medical centers in Europe and Canada. In this trial, we plan to evaluate the serum uric acid (sUA) level, pharmacokinetics, safety and tolerability of two different dose regimens of RDEA806 versus placebo in establishing normal sUA concentrations in gout patients with hyperuricemia (greater than or equal to 8.0 mg/dl). The primary efficacy endpoint is the proportion of subjects whose sUA level is less than 6.0 mg/dl following four weeks of treatment. Dr. Fernando Perez-Ruiz is an Assistant Head of the Rheumatology Division at the Hospital de Cruces in Vizcaya, Spain. He received his medical degree from the Basque Country University in Bilbao, Spain, and a PhD from Barcelona University, Spain. Board-certified in Rheumatology, Dr. Perez-Ruiz is a member of the American College of Rheumatology and Spanish Society for Rheumatology and has collaborated with the European League Against Rheumatism (EULAR) Task Force for Gout and with the Outcome Measures for Rheumatic Arthritis Clinical Trials (OMERACT) group for chronic gout. He serves on the editorial boards of Arthritis Rheumatism (Care & Research), Bone Joint Spine, and Reumatologia Clinica and serves as a reviewer for more than 20 international journals. His research interests include crystal-induced arthritis, especially gout, but he has also investigated lupus, rheumatoid arthritis and fibromyalgia. Dr. Perez-Ruiz has published more than 80 articles on topics related to rheumatology, and most frequently to hyperuricemia and gout.
Ardea Biosciences, Inc. (Nasdaq: RDEA) today announced that it has received regulatory approval to begin a Phase 2a proof-of-concept clinical trial evaluating RDEA806 in gout patients with hyperuricemia. Gout, also known as metabolic arthritis, is a painful and debilitating disease caused by abnormally elevated levels of uric acid in the blood stream, and is the most common form of inflammatory arthritis in men over 40. The Company also announced that gout specialist, Dr. Fernando Perez-Ruiz in Spain, will be the newest member of its inflammatory disease scientific advisory board (SAB). Ardea previously announced the designation of RDEA594, a major metabolite of RDEA806, the Company's lead human immunodeficiency virus (HIV) development compound, as its lead development candidate for the treatment of patients with gout. RDEA594 does not have antiviral activity, but is believed to be responsible for essentially all of the uric acid lowering effects seen with RDEA806. Uric acid lowering effects have been observed following administration of RDEA806 in Phase 1 and Phase 2 clinical trials that included over 100 subjects. "The Phase 2a trial should allow us to confirm RDEA594's activity in the target population of patients with gout using its prodrug, RDEA806. Enrollment in the Phase 2a trial should begin shortly and we are on track to initiate a Phase 1 trial with RDEA594 in the second half of this year," said Barry D. Quart, PharmD, Ardea Biosciences' President and CEO. "We also are extremely pleased to add Dr. Fernando Perez-Ruiz to our inflammatory diseases SAB. Dr. Perez-Ruiz has extensive experience treating gout patients with drugs of the same class as RDEA594." The Phase 2a randomized, double-blind, dose ranging, efficacy and safety trial will be conducted in academic medical centers in Europe and Canada. In this trial, we plan to evaluate the serum uric acid (sUA) level, pharmacokinetics, safety and tolerability of two different dose regimens of RDEA806 versus placebo in establishing normal sUA concentrations in gout patients with hyperuricemia (greater than or equal to 8.0 mg/dl). The primary efficacy endpoint is the proportion of subjects whose sUA level is less than 6.0 mg/dl following four weeks of treatment. Dr. Fernando Perez-Ruiz is an Assistant Head of the Rheumatology Division at the Hospital de Cruces in Vizcaya, Spain. He received his medical degree from the Basque Country University in Bilbao, Spain, and a PhD from Barcelona University, Spain. Board-certified in Rheumatology, Dr. Perez-Ruiz is a member of the American College of Rheumatology and Spanish Society for Rheumatology and has collaborated with the European League Against Rheumatism (EULAR) Task Force for Gout and with the Outcome Measures for Rheumatic Arthritis Clinical Trials (OMERACT) group for chronic gout. He serves on the editorial boards of Arthritis Rheumatism (Care & Research), Bone Joint Spine, and Reumatologia Clinica and serves as a reviewer for more than 20 international journals. His research interests include crystal-induced arthritis, especially gout, but he has also investigated lupus, rheumatoid arthritis and fibromyalgia. Dr. Perez-Ruiz has published more than 80 articles on topics related to rheumatology, and most frequently to hyperuricemia and gout.
Saturday, January 3, 2009
More on the genetics of gout
Further to the previous post another study have found a link between 3 genetic loci and uric acid concentrations. (ref: Association of three genetic loci with uric acid concentration and risk of gout: a genome-wide association study The Lancet Early Online Publication, 1 October 2008 )
Serum uric acid levels not that useful
Serum uric acid levels have never been particularly useful when evaluating the patient with gout. Now we have a study of 339 patients with acute gouty arthritis whose serum urate levels were measured, 29% of individuals on chronic allopurinol had a true-normal serum urate level, defined as 6 mg/dL or less. Among patients not on the hypouricemic agent, 11% had a true-normal serum urate level during their acute episode of gout. (ref: Don't Be Fooled by Normal Serum Urate in Acute Gout Rheumatology News Volume 7, Issue 8, Page 22 (August 2008))
Thursday, January 1, 2009
Oral prednisolone and naproxen are equally effective
A new study in the Lancet has shown that oral prednisolone and naproxen were equally effective in the initial treatment of gout arthritis over 4 days. This suggests that systemic corticosteroids might be a viable alternative to NSAID's initially given the side effects of NSAID's.
Wednesday, December 31, 2008
Cardiovascular mortality and gout
Long-term Cardiovascular Mortality Among Middle-aged Men With Gout
Eswar Krishnan, MD, MPH; Kenneth Svendsen, MS; James D. Neaton, PhD; Greg Grandits, MS; Lewis H. Kuller, MD; for the MRFIT Research Group
Arch Intern Med. 2008;168(10):1104-1110.
Background: There are limited data available on the association of gouty arthritis (gout) in middle age with long-term cardiovascular disease (CVD) mortality.
Methods: We performed a 17-year follow-up study of 9105 men, aged 41 to 63 years and at above-average risk for coronary heart disease, who were randomized to the Multiple Risk Factor Intervention Trial and who did not die or have clinical or electrocardiographic evidence of coronary artery disease during the 6-year trial. Risk of CVD death and other causes subsequent to the sixth annual examination associated with gout was assessed by means of Cox proportional hazards regressions.
Results: The unadjusted mortality rates from CVD among those with and without gout were 10.3 per 1000 person-years and 8.0 per 1000 person-years, respectively, representing an approximately 30% greater risk. After adjustment for traditional risk factors, use of diuretics and aspirin, and serum creatinine level, the hazard ratio (gout vs no gout) for coronary heart disease mortality was 1.35 (95% confidence interval [CI], 1.06-1.72). The hazard ratio for death from myocardial infarction was 1.35 (95% CI, 0.94-1.93); for death from CVD overall, 1.21 (95% CI, 0.99-1.49); and for death from any cause, 1.09 (95% CI, 1.00-1.19) (P = .04). The association between hyperuricemia and CVD was weak and did not persist when analysis was limited to men with hyperuricemia without a diagnosis of gout.
Conclusion: Among middle-aged men, a diagnosis of gout accompanied by an elevated uric acid level imparts significant independent CVD mortality risk.
Eswar Krishnan, MD, MPH; Kenneth Svendsen, MS; James D. Neaton, PhD; Greg Grandits, MS; Lewis H. Kuller, MD; for the MRFIT Research Group
Arch Intern Med. 2008;168(10):1104-1110.
Background: There are limited data available on the association of gouty arthritis (gout) in middle age with long-term cardiovascular disease (CVD) mortality.
Methods: We performed a 17-year follow-up study of 9105 men, aged 41 to 63 years and at above-average risk for coronary heart disease, who were randomized to the Multiple Risk Factor Intervention Trial and who did not die or have clinical or electrocardiographic evidence of coronary artery disease during the 6-year trial. Risk of CVD death and other causes subsequent to the sixth annual examination associated with gout was assessed by means of Cox proportional hazards regressions.
Results: The unadjusted mortality rates from CVD among those with and without gout were 10.3 per 1000 person-years and 8.0 per 1000 person-years, respectively, representing an approximately 30% greater risk. After adjustment for traditional risk factors, use of diuretics and aspirin, and serum creatinine level, the hazard ratio (gout vs no gout) for coronary heart disease mortality was 1.35 (95% confidence interval [CI], 1.06-1.72). The hazard ratio for death from myocardial infarction was 1.35 (95% CI, 0.94-1.93); for death from CVD overall, 1.21 (95% CI, 0.99-1.49); and for death from any cause, 1.09 (95% CI, 1.00-1.19) (P = .04). The association between hyperuricemia and CVD was weak and did not persist when analysis was limited to men with hyperuricemia without a diagnosis of gout.
Conclusion: Among middle-aged men, a diagnosis of gout accompanied by an elevated uric acid level imparts significant independent CVD mortality risk.
Sunday, December 28, 2008
Press Release on Adenuric (febuxostat)
Adenuric® (febuxostat) receives marketing authorisationin the European UnionAdenuric® represents the first major treatment of chronic hyperuricemiain gout for more than forty years
"Paris (France), 5 May 2008 – Ipsen (Euronext: FR0010259150; IPN) today announced thatthe European Commission granted marketing authorisation for Adenuric® (febuxostat) for thetreatment of chronic hyperuricaemia in gout. Adenuric® thus pioneers the first majortreatment alternative for gout, a severe debilitating disease, for more than 40 years."Recent surveys confirm that management of gout is often suboptimal, with less than half ofpatients receiving appropriate lifestyle advice or urate lowering treatment" said MichaelDoherty, Professor of Rheumatology at the University of Nottingham (UK) and Co-chair ofthe 2006 EULAR Task Force for the Recommendations on Diagnosis and Management ofGout. "Recent European (EULAR) Recommendations emphasise the aim of "cure" bylowering serum urate levels below the saturation point for crystal formation. For somepatients, the existing urate lowering therapies have limitations in terms of suitability or sideeffects. The availability of a new effective therapy that allows the therapeutic target to beachieved will improve the physicians armamentarium and ultimately benefit the population ofpatients with gout."Adenuric® (febuxostat) 80 mg and 120 mg tablets are indicated for the treatment of chronichyperuricaemia for conditions in which urate deposition has already occurred (including ahistory, or presence of, tophus and/or gouty arthritis).Adenuric® will be marketed by Ipsen in France. Outside France, the commercialisation of theproduct will be partnered. "
"Paris (France), 5 May 2008 – Ipsen (Euronext: FR0010259150; IPN) today announced thatthe European Commission granted marketing authorisation for Adenuric® (febuxostat) for thetreatment of chronic hyperuricaemia in gout. Adenuric® thus pioneers the first majortreatment alternative for gout, a severe debilitating disease, for more than 40 years."Recent surveys confirm that management of gout is often suboptimal, with less than half ofpatients receiving appropriate lifestyle advice or urate lowering treatment" said MichaelDoherty, Professor of Rheumatology at the University of Nottingham (UK) and Co-chair ofthe 2006 EULAR Task Force for the Recommendations on Diagnosis and Management ofGout. "Recent European (EULAR) Recommendations emphasise the aim of "cure" bylowering serum urate levels below the saturation point for crystal formation. For somepatients, the existing urate lowering therapies have limitations in terms of suitability or sideeffects. The availability of a new effective therapy that allows the therapeutic target to beachieved will improve the physicians armamentarium and ultimately benefit the population ofpatients with gout."Adenuric® (febuxostat) 80 mg and 120 mg tablets are indicated for the treatment of chronichyperuricaemia for conditions in which urate deposition has already occurred (including ahistory, or presence of, tophus and/or gouty arthritis).Adenuric® will be marketed by Ipsen in France. Outside France, the commercialisation of theproduct will be partnered. "
Saturday, December 27, 2008
Gene Linked to Gout
The BBC are reporting:
A rise in UK gout cases has been blamed on increasingly unhealthy lifestyles. However, genetic analysis of more than 12,000 people, published in the journal Nature Genetics, has found that a gene variant may also raise the risk. Researchers at the MRC Human Genetics Unit, in Edinburgh, said the gene, and the protein it controls, might one day be targeted by new gout drugs. In a healthy body, uric acid, a waste product found in the blood, is removed by the kidneys and passes out of the body in urine. However, in some people the kidney cannot get rid of it properly and it builds up in the blood, forming crystals in the joints, leading to inflammation, stiffness and pain. Various food types have been blamed, with the consensus that diets rich in refined sugars, protein and alcohol increase the risk. Many thousands of people have a diet which appears to increase the risk of gout, but far fewer actually develop the illness. Now scientists at the MRC Human Genetics Unit may have worked out why that is. The gene variation they found, in the SLC2A gene, appears to make it harder for the body to remove uric acid from the blood. Professor Alan Wright, who led the research, said: "The gene is a key player in determining the efficiency of uric acid transport across the membranes of the kidney." His colleague Harry Campbell said: "Some people will have higher or lower risk of gout depending on the form of the gene they inherited. "This discovery may allow better diagnostic tools for gout to be developed." At the moment, drug treatment for patients is limited. Although gout is a disease more usually found in a historical textbook, it is estimated that one million people in the UK suffer from it in some form. Professor Stuart Ralston, from the British Society for Rheumatology, said that he often came across patients whose lifestyles did not fit the traditional view of over-consumption. "Until recently you would associate gout with boozing and rich food, but there are plenty of other patients who are quite abstemious. This might be a genetic marker for gout risk. "What is exciting is that it could be a target for new gout drugs."
Full story from the BBC
A rise in UK gout cases has been blamed on increasingly unhealthy lifestyles. However, genetic analysis of more than 12,000 people, published in the journal Nature Genetics, has found that a gene variant may also raise the risk. Researchers at the MRC Human Genetics Unit, in Edinburgh, said the gene, and the protein it controls, might one day be targeted by new gout drugs. In a healthy body, uric acid, a waste product found in the blood, is removed by the kidneys and passes out of the body in urine. However, in some people the kidney cannot get rid of it properly and it builds up in the blood, forming crystals in the joints, leading to inflammation, stiffness and pain. Various food types have been blamed, with the consensus that diets rich in refined sugars, protein and alcohol increase the risk. Many thousands of people have a diet which appears to increase the risk of gout, but far fewer actually develop the illness. Now scientists at the MRC Human Genetics Unit may have worked out why that is. The gene variation they found, in the SLC2A gene, appears to make it harder for the body to remove uric acid from the blood. Professor Alan Wright, who led the research, said: "The gene is a key player in determining the efficiency of uric acid transport across the membranes of the kidney." His colleague Harry Campbell said: "Some people will have higher or lower risk of gout depending on the form of the gene they inherited. "This discovery may allow better diagnostic tools for gout to be developed." At the moment, drug treatment for patients is limited. Although gout is a disease more usually found in a historical textbook, it is estimated that one million people in the UK suffer from it in some form. Professor Stuart Ralston, from the British Society for Rheumatology, said that he often came across patients whose lifestyles did not fit the traditional view of over-consumption. "Until recently you would associate gout with boozing and rich food, but there are plenty of other patients who are quite abstemious. This might be a genetic marker for gout risk. "What is exciting is that it could be a target for new gout drugs."
Full story from the BBC
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