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The latest on gout

Discussion in 'General Issues and Discussion Forum' started by Admin2, Dec 28, 2005.

  1. NewsBot

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    Articles:
    1
    The importance of urgent cytological examination of synovial fluids in differentiation inflammatory and non-inflammatory joint diseases.
    Ostović KT, Kaić G, Ostović I, Skoro M, Novak NP, Morović-Vergles J.
    Coll Antropol. 2010 Mar;34(1):145-52.
     
  2. NewsBot

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    Treatment of acute gouty arthritis by blood-letting cupping plus herbal medicine.
    Zhang SJ, Liu JP, He KQ.
    J Tradit Chin Med. 2010 Mar;30(1):18-20.
     
  3. NewsBot

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    Patients and providers view gout differently: a qualitative study.
    Harrold LR, Mazor KM, Velten S, Ockene IS, Yood RA.
    Chronic Illn. 2010 Jul 30. [Epub ahead of print]
     
  4. NewsBot

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    Articles:
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    Coffee consumption and risk of incident gout in women: the Nurses' Health Study.
    Choi HK, Curhan G.
    Am J Clin Nutr. 2010 Aug 25. [Epub ahead of print]
     
  5. NewsBot

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    Articles:
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    Development of a computed tomography method of scoring bone erosion in patients with gout: validation and clinical implications.
    Dalbeth N, Doyle A, Boyer L, Rome K, Survepalli D, Sanders A, Sheehan T, Lobo M, Gamble G, McQueen FM.
    Rheumatology (Oxford). 2010 Nov 8. [Epub ahead of print]
     
  6. NewsBot

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    Articles:
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    The pathogenesis of bone erosions in gouty arthritis.
    Schlesinger N, Thiele RG.
    Ann Rheum Dis. 2010 Nov;69(11):1907-12. Epub 2010 Aug 12.
     
  7. NewsBot

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    Comparison of measures of functional disability in patients with gout.
    Ten Klooster PM, Oude Voshaar MA, Taal E, van de Laar MA.
    Rheumatology (Oxford). 2010 Dec 2. [Epub ahead of print]
     
  8. NewsBot

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    Articles:
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    Quality of Care in Patients with Gout: Why is Management Suboptimal and What Can Be Done About It?
    Edwards NL.
    Curr Rheumatol Rep. 2010 Dec 14. [Epub ahead of print]
     
  9. NewsBot

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    Articles:
    1
    Compliance in gout patients.
    Silva L, Miguel ED, Peiteado D, Villalba A, Mola M, Pinto J, Ventura FS.
    Acta Reumatol Port. 2010 Out-Dez;35(5):466-474.
     
  10. NewsBot

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    Articles:
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    The Nail Plate Biopsy May Pick up Gout Crystals and Other Crystals.
    Tirado-González M, González-Serva A
    Am J Dermatopathol. 2011 Mar 11;
     
  11. Mart

    Mart Well-Known Member

    Re: Gout


    Extending this idea

    Editorial

    Immunology and Cell Biology (2010) 88, 13–14; doi:10.1038/icb.2009.99
    Out with gout: opening the door on acute inflammation

    Jacquie L Harper1
    1Malaghan Institute of Medical Research, Wellington, New Zealand
    Correspondence: Jacquie L Harper, E-mail: jharper@malaghan.org.nz

    Gout is a form of autoinflammatory arthritis driven by the innate immune response to the deposition of monosodium urate (MSU) crystals in the joint and periarticular tissues. Once considered to be the ‘disease of kings’, the prevalence of gout is increasing worldwide, establishing gout as a common disease in the western world.1, 2, 3
    Historically, gout research has played the reluctant bridesmaid to other arthritides; however, recent developments in the field have placed MSU crystal-induced inflammation back on the radar and have opened up a new understanding of the physiological relevance of MSU crystal-induced inflammation. A number of studies have now identified MSU crystals as a native adjuvant that is capable of enhancing antigen-specific immune responses.4 In this Special Feature of ICB, several key aspects of gouty arthritis are reviewed. In their Special Feature review, Liu-Bryan and colleagues discuss how the MSU crystal-induced inflammatory pathway begins with the activation of the NALP3 inflammasome5 in monocyte/macrophages, leading to engagement of the innate arm of the immune system.
    Low-level, local MSU crystal-induced inflammation may be advantageous in boosting adaptive immunity when tightly regulated. However, excessive, physiologically irrelevant, MSU crystal deposition results in an attack of acute gout. Innate cells of the monocyte/macrophage lineage are implicated as having a key role in initiating and driving inflammation in gout, but have also been implicated in resolving a gout attack.6, 7 In their contribution to the Special Feature, Martin and Harper put forward a working model of the progression of an acute gout attack in vivo that focuses on the contribution of resident macrophages and infiltrating monocytes, and outlines cellular and molecular interactions at the site of inflammation that dictate pro-inflammatory versus anti-inflammatory function.
    A characteristic feature of gout inflammation is the infiltration of large numbers of neutrophils. This has made neutrophil inflammatory responses to MSU crystals a significant focus of gout research to date. In their Special Feature review, Popa-Nita and colleagues present the current understanding of the early events involved in the activation of human neutrophils, providing insight into the nature of the strong inflammatory response of neutrophils to MSU crystals.
    Neutrophil activation triggers the production of a number of immune mediators that are generally associated with proinflammatory functions and/or killing. One such family of proteins are the calgranulins, S100A8, S100A9 and S100A12. These proteins are also produced by monocytes and macrophages and are found to be elevated in the synovial fluid of acute and chronic gout patients.8 However, the presence of calgranulins within inflamed joints may not necessarily indicate inflammation. In their Special Feature review, Perera et al. discuss the involvement of calgranulins in inflammation and present emerging evidence to support a potential regulatory role for S100 proteins in inflammatory arthritides, including gout.
    To date, the majority of gout research has concentrated around macrophage, monocyte and neutrophil responses to MSU crystals. As such the involvement of other cell types has been largely ignored. It appears that this is about to change. Although activation of innate immunity by MSU has been shown to enhance adaptive immune responses, it has now been shown that T cells may play a part in shutting down the NALP3 inflammasome, thereby providing a feedback loop to ameliorate innate inflammation.9 Another cell present in gouty joints is the natural killer (NK) cell. These cells have been reported to influence adaptive immune responses through their interactions with dendritic cells and T cells.10 Following along from this, Empson and co-workers, in their contribution to the Special Feature, discuss the potential for NK cells to undertake a similar modulatory role in gouty inflammation.
    Gout research is emerging out of the shadows and is delivering new insights into the intricacies of acute inflammation. The collective reviews in this issue highlight some of the recent advances in the field and illustrate the broad application of previous and future findings to the wider field of immunology and our understanding of gouty inflammation. The challenge is to think outside the square. Can inflammatory cells and mediators orchestrate their own end? Are innate and adaptive immunity co-dependent for effective immune regulation? Can we use adaptive immune therapy to treat innate inflammation? Answers to these and many as yet unidentified questions could be just around the corner.
    Top of page References

    1. Klemp P, Stansfield SA, Castle B, Robertson MC. Gout is on the increase in New Zealand. Ann Rheum Dis 1997; 56: 22–26. | Article | PubMed | ISI | ChemPort |
    2. Mikuls TR, Farrar JT, Bilker WB, Fernandes S, Schumacher Jr HR, Saag KG. Gout epidemiology: results from the UK General Practice Research Database, 1990–1999. Ann Rheum Dis 2005; 64: 267–272. | Article | PubMed | ISI | ChemPort |
    3. Kim KY, Ralph Schumacher H, Hunsche E, Wertheimer AI, Kong SX. A literature review of the epidemiology and treatment of acute gout. Clin Ther 2003; 25: 1593–1617. | Article | PubMed
    4. Shi Y, Evans JE, Rock KL. Molecular identification of a danger signal that alerts the immune system to dying cells. Nature 2003; 425: 516–521. | Article | PubMed | ISI | ChemPort |
    5. Martinon F, Petrilli V, Mayor A, Tardivel A, Tschopp J. Gout-associated uric acid crystals activate the NALP3 inflammasome. Nature 2006; 440: 237–241. | Article | PubMed | ISI | ChemPort |
    6. Yagnik DR, Evans BJ, Florey O, Mason JC, Landis RC, Haskard DO. Macrophage release of transforming growth factor beta1 during resolution of monosodium urate monohydrate crystal-induced inflammation. Arthritis Rheum 2004; 50: 2273–2280. | Article | PubMed | ChemPort |
    7. Martin WJ, Walton M, Harper J. Resident macrophages initiating and driving inflammation in a monosodium urate monohydrate crystal-induced murine peritoneal model of acute gout. Arthritis Rheum 2009; 60: 281–289. | Article | PubMed
    8. Rouleau P, Vandal K, Ryckman C, Poubelle PE, Boivin A, Talbot M et al. The calcium-binding protein S100A12 induces neutrophil adhesion, migration, and release from bone marrow in mouse at concentrations similar to those found in human inflammatory arthritis. Clin Immunol 2003; 107: 46–54. | Article | PubMed | ISI | ChemPort |
    9. Guarda G, Dostert C, Staehli F, Cabalzar K, Castillo R, Tardivel A et al. T cells dampen innate immune responses through inhibition of NLRP1 and NLRP3 inflammasomes. Nature 2009; 460: 269–273. | Article | PubMed | ChemPort |
    10. Gerosa F, Baldani-Guerra B, Nisii C, Marchesini V, Carra G, Trinchieri G. Reciprocal activating interaction between natural killer cells and dendritic cells. J Exp Med 2002; 195: 327–333. | Article | PubMed | ISI | ChemPort |
     
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    Press Release:
    Novartis data shows ACZ885 for severe gouty arthritis provided better pain relief and reduced risk of new attacks by up to 68% vs. steroid

     
  13. NewsBot

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    Articles:
    1
    Gender-specific risk factors for incident gout: a prospective cohort study.
    Chen JH, Yeh WT, Chuang SY, Wu YY, Pan WH.
    Clin Rheumatol. 2011 Jul 15. [Epub ahead of print]
     
  14. Don ESWT

    Don ESWT Active Member

    As a sufferer of the gout I was given a new anti inflammatory Arcoxia - (etoricoxib) 1* 120mg tablet.
    I like this drug

    Don
     
  15. NewsBot

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    Articles:
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    Prevalence of gout and hyperuricemia in the US general population.
    Zhu Y, Pandya BJ, Choi HK.
    Arthritis Rheum. 2011 Jul 28. doi: 10.1002/art.30520.
     
  16. NewsBot

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    Press Release:
    Medication For Severe, Chronic Gout Associated With Improvement in Symptoms
     
  17. NewsBot

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    The diagnostic value of the proposal for clinical gout diagnosis (CGD).
    Vázquez-Mellado J, Hernández-Cuevas CB, Alvarez-Hernández E, Ventura-Rios L, Peláez-Ballestas I, Casasola-Vargas J, García-Méndez S, Burgos-Vargas R.
    Clin Rheumatol. 2011 Oct 7. [Epub ahead of print]
     
  18. NewsBot

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    Articles:
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    Foot pain, impairment and disability in patients with acute gout flares; a prospective observational study.
    Rome K, Frecklington M, McNair P, Gow P, Dalbeth N.
    Arthritis Care Res (Hoboken). 2011 Oct 17.

     
  19. NewsBot

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    Illness perceptions in patients with gout and the relationship with progression of musculoskeletal disability.
    Dalbeth N, Petrie KJ, House M, Chong J, Leung W, Chegudi R, Horne A, Gamble G, McQueen FM, Taylor WJ.
    Arthritis Care Res (Hoboken). 2011 Nov;63(11):1605-12.
     
  20. MJJ

    MJJ Active Member

  21. NewsBot

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    Articles:
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    PS2-16: Patient Knowledge and Beliefs Concerning Gout and Its Treatment.
    Harrold L, Mazor K, Peterson D, Firneno C, Yood R.
    Clin Med Res. 2011 Nov;9(3-4):155.
     
  22. NewsBot

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    Articles:
    1
    Identification of ABCG2 Dysfunction as a Major Factor Contributing to Gout.
    Matsuo H, Takada T, Ichida K, Nakamura T, Nakayama A, Takada Y, Okada C, Sakurai Y, Hosoya T, Kanai Y, Suzuki H, Shinomiya N.
    Nucleosides Nucleotides Nucleic Acids. 2011 Dec;30(12):1098-104.
    ABCG2/BCRP Dysfunction as a Major Cause of Gout.
    Matsuo H, Takada T, Ichida K, Nakamura T, Nakayama A, Suzuki H, Hosoya T, Shinomiya N.
    Nucleosides Nucleotides Nucleic Acids. 2011 Dec;30(12):1117-28.
    ABCG2 is a High-Capacity Urate Transporter and its Genetic Impairment Increases Serum Uric Acid Levels in Humans.
    Nakayama A, Matsuo H, Takada T, Ichida K, Nakamura T, Ikebuchi Y, Ito K, Hosoya T, Kanai Y, Suzuki H, Shinomiya N.
    Nucleosides Nucleotides Nucleic Acids. 2011 Dec;30(12):1091-7.
     
  23. METaylor

    METaylor Active Member

    Celery seed tabs 6/day work as well or better than Indocid and colchicine and have no known side effects - some very grateful patients. And it works quickly - improvement is seen in less than a week. Nb not celery and juniper, must be celery seed.
     
  24. NewsBot

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    Press Release:
    Clinical trial demonstrates that rilonacept significantly reduces gout flares
    Drug appears to be well tolerated by patients
     
  25. METaylor

    METaylor Active Member

    How come drug companies are allowed to talk on this forum?
     
  26. admin

    admin Administrator Staff Member

  27. NewsBot

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    Disability due to gouty arthritis.
    Ten Klooster PM, Vonkeman HE, van de Laar MA.
    Curr Opin Rheumatol. 2012 Jan 5.
     
  28. NewsBot

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    Mechanisms of joint damage in gout: evidence from cellular and imaging studies.
    McQueen FM, Chhana A, Dalbeth N.
    Nat Rev Rheumatol. 2012 Jan 10.
     
  29. NewsBot

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    Rilonacept (Interleukin-1 Trap) for prevention of gout flares during initiation of uric acid-lowering therapy: Results of the presurge-1 trial.
    Schumacher HR Jr, Evans RR, Saag KG, Clower J, Jennings W, Weinstein SP, Yancopoulos GD, Wang J, Terkeltaub R.
    Arthritis Care Res (Hoboken). 2012 May 1.
     
  30. NewsBot

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    Press Release:
    U.S. drug advisers unanimously voted against Regeneron Pharmaceuticals Inc's experimental drug to prevent gout flares, based on studies that tested the drug for only 16 weeks.
     
  31. NewsBot

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    Challenges Associated with the Management of Gouty Arthritis in Patients with Chronic Kidney Disease: A Systematic Review.
    Curiel RV, Guzman NJ.
    Semin Arthritis Rheum. 2012 May 2
     
  32. NewsBot

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    Comorbidities of Gout and Hyperuricemia in the US General Population: NHANES 2007-2008.
    Zhu Y, Pandya BJ, Choi HK.
    Am J Med. 2012 May 23.
     
  33. NewsBot

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    Purine-rich foods intake and recurrent gout attacks.
    Zhang Y, Chen C, Choi H, Chaisson C, Hunter D, Niu J, Neogi T.
    Ann Rheum Dis. 2012 May 30. [Epub ahead of print]
     
  34. NewsBot

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    Female Gout: Age and Duration of the Disease Determine Clinical Presentation.
    García-Méndez S, Beas-Ixtláhuac E, Hernández-Cuevas C, Mendoza-Torres JM, Melo-Centeno C, Rull-Gabayet M, Alvarez-Hernández E, Vázquez-Mellado J.
    J Clin Rheumatol. 2012 Jul 24.
     
  35. NewsBot

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    Gout: why is this curable disease so seldom cured?
    Doherty M, Jansen TL, Nuki G, Pascual E, Perez-Ruiz F, Punzi L, So AK, Bardin T.
    Ann Rheum Dis. 2012 Aug 3. [Epub ahead of print]
     
  36. NewsBot

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    Patients' knowledge and beliefs concerning gout and its treatment: a population based study.
    Harrold LR, Mazor KM, Peterson D, Naz N, Firneno C, Yood R.
    BMC Musculoskelet Disord. 2012 Sep 21;13(1):180
     
  37. NewsBot

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  38. NewsBot

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    Cherry consumption and the risk of recurrent gout attacks.
    Zhang Y, Neogi T, Chen C, Chaisson C, Hunter D, Choi HK.
    Arthritis Rheum. 2012 Sep 28.
     
  39. NewsBot

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    Press Release:
    Gout Guidelines Arm Patients and Physicians with Tools to Fight Painful Disease
     
  40. NewsBot

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    Economic Burden of Gouty Arthritis Attacks for Employees with Frequent and Infrequent Attacks.
    Lynch W, Chan W, Kleinman N, Andrews LM, Yadao AM.
    Popul Health Manag. 2012 Oct 31.
     
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