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[ New Diagnostic Method For Gout: Dual Energy Computed Tomography Instead Of Joint Aspiration ]

New Diagnostic Method For Gout: Dual Energy Computed Tomography Instead Of Joint Aspiration

The most reliable method of diagnosing gout is to aspirate the joint in order to obtain fluid to verify the presence of monosodiumurate crystals (uric acid). Up to now, computed tomography (CT) has played a limited role in the evaluation of gout, since conventional CT systems cannot reliably verify deposits of uric acid. However, a current study at the Vancouver General Hospital in Canada gives rise to speculation that dual-energy computed tomography (DECT) could radically change the management of this disease. DECT enables fast, noninvasive examinations and, based on initial evaluations, has the potential to surpass the clinical examination in terms of identifying subclinical disease. Investigations have confirmed the high sensitivity of the DECT method in detecting uric acid deposits.

Role For Innate, Not Adaptive, Immunity Revealed By Autoinflammatory Disease Model

Researchers at the University of California, San Diego School of Medicine have developed the first mouse model for auto-inflammatory diseases, disorders that involve the over-activation of the body's innate, primitive immune system. Their study, published early on-line in Cell Immunity on June 4, suggests that the innate - not adaptive - immune system drives auto-inflammatory diseases. The findings could open new therapeutic directions for research into disorders such as gout or inflammatory bowel disease. "Auto-inflammatory diseases are a relatively new classification of diseases that are different from autoimmune diseases or allergies, " said Hal Hoffman, MD, associate professor of medicine at UC San Diego School of Medicine. Hoffman studies a group of rare, inherited auto-inflammatory conditions called Cryopyrin-Associated Periodic Syndromes (CAPS), which includes Familial Cold Auto-inflammatory Syndrome (FCAS) and Muckle-Wells Syndrome (MWS).

Ardea Biosciences Announces Positive Interim Phase 2a Results For Lead Gout Drug, RDEA594

Ardea Biosciences, Inc. (Nasdaq:RDEA) announced positive interim results from an ongoing Phase 2a, proof-of-concept study of RDEA594, its lead product candidate for the treatment of hyperuricemia and gout, as well as additional positive results from completed Phase 1 studies of RDEA594 in normal, healthy volunteers. The Phase 1 results, along with additional preclinical data, were presented at the Annual European Congress of Rheumatology hosted by the European League Against Rheumatism (EULAR) in Copenhagen, Denmark. In late April 2009, the Company initiated a placebo- and active-controlled, proof-of-concept study of RDEA594 in gout patients with hyperuricemia (uric acid 8 mg/dL). This study is now fully enrolled and the majority of the 20 patients have completed the first week of dosing.

FDA Appointed Arthritis Advisory Committee Recommends U.S. Food And Drug Administration Approval For KRYSTEXXA TM For Refractory Chronic Gout

Savient Pharmaceuticals, Inc. (Nasdaq: SVNT) announced that the Arthritis Advisory Committee appointed by the U.S. Food and Drug Administration (FDA) recommended by a vote of 14 to 1 that KRYSTEXXA(TM) (pegloticase), a biologic PEGylated uricase enzyme, be granted marketing approval by the FDA for the treatment of refractory chronic gout. Refractory chronic gout or treatment failure gout (TFG) is gout in patients who have failed to normalize serum uric acid and whose signs and symptoms are inadequately controlled with conventional urate-lowering therapy at the maximum medically appropriate dose or for whom conventional urate-lowering therapy is contraindicated. The current target Prescription Drug User Fee (PDUFA) action date for the FDA's decision as to whether to grant marketing approval for KRYSTEXXA is August 1, 2009.

Johns Hopkins Scientists Out A Gene For Gout

Having partnered last year with an international team that surveyed the genomes of 12, 000 individuals to find a genetic cause for gout, Johns Hopkins scientists now have shown that the malfunctioning gene they helped uncover can lead to high concentrations of blood urate that forms crystals in joint tissue, causing inflammation and pain - the hallmark of this disease. The ABCG2 gene, they found, makes a protein that normally transports urate out of the kidney and into urine before the waste product does any harm. In studies using frog egg cells genetically engineered with human DNA, the Hopkins researchers established the role of the ABCG2 gene as a cause of gout, lending credence to suspicions that metabolic deficiencies, in addition to too much rich food and alcohol, are mostly to blame for this painful type of arthritis that affects 3 million Americans.

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