Abstract
Gout is described as difficult in joint sore, uttermost ordinarily in the principal metatarsophalangeal joint, attend from formation of urate monosodium crystallization in a joint space. Analysis might be affirmed by recognizable proof of urate monosodium precious stones in synovial liquid of the influenced joint. There has been expanded enthusiasm for gout in common scholarly and clinical practice settings. The pervasiveness of both hyperuricemia and gout has ascended as most recent decade of time in created nations and in this way weight of gout as expanded. The relationship of hyperuricemia and gout with cardio results for chance of added advantages in mediation on hyperuricemia was featured in this audit. Imaging procedures have ended up being helpful for location of urate statement, even before the primary clinical indications, empowering the assessment of the degree of testimony and giving target estimation of precious stone exhaustion amid urate-bringing down treatment. In advancement, the indication defines the pre diagnostic of gout and associated commodities is advised to prevent the inflammation, that image procedures will assess the weight on statement as well reaction to urinary bringing down clinical procedure in chose patients, lastly amongst last key goal on social insurance for clinical evaluation with gout is to totally project urate gem stores. In spite of the fact that the formal determination is defined with arthrocentesis and resulting examination, CT and ultrasound discoveries on addition of evaluation and execution of infection administration. The standard therapy methodology is available for the patients and whose disease is refractory to standard therapy.
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References
Dalbeth N, Merriman TR, Stamp LK. Gout. Lancet. 2016;388(10055):2039–52.
Emmerson BT. The management of gout. N Engl J Med. 1996;334(7):445–51.
Pascual E, Sivera F. Time required for disappearance of urate crystals from synovial fluid after successful hypouricaemic treatment relates to the duration of gout. Ann Rheum Dis. 2007;66(8):1056–8.
Singh JA. Challenges faced by patients in gout treatment: a qualitative study. J Clin Rheumatol. 2014;20(3):172–4.
Kuo CF, Grainge MJ, Zhang W, Doherty M. Global epidemiology of gout: prevalence, incidence and risk factors. Nat Rev Rheumatol. 2015;11(11):649–62.
McCarty DJ, Hollander JL. Identification of urate crystals in gouty synovial fluid. Ann Intern Med. 1961;54:452–60.
Mandal AK, Mount DB. The molecular physiology of uric acid homeostasis. Annu Rev Physiol. 2015;77:323–45.
Kamei K, Konta T, Hirayama A, Suzuki K, Ichikawa K, Fujimoto S. A slight increase within the normal range of serum uric acid and the decline in renal function: associations in a community-based population. Nephrol Dial Transpl. 2014;29(12):2286–92.
Torres RJ, Puig JG. Hypoxanthine-guanine phosophoribosyltransferase (HPRT) deficiency: Lesch-Nyhan syndrome. Orphanet J Rare Dis. 2007;2:48.
Reginato AM, Olsen BR. Genetics and experimental models of crystal-induced arthritis. Lessons learned from mice and men: is it crystal clear? Curr Opin Rheumatol. 2007;19(2):134–45.
Kanbara A, Seyama I. Effect of urine pH on uric acid excretion by manipulating food materials. Nucleosides Nucleotides Nucleic Acids. 2011;30(12):1066–71.
Towiwat P, Li ZG. The association of vitamin C, alcohol, coffee, tea, milk and yogurt with uric acid and gout. Int J Rheum Dis. 2015;18(5):495–501.
Mahmoud HH, Leverger G, Patte C, Harvey E, Lascombes F. Advances in the management of malignancy-associated hyperuricaemia. Br J Cancer. 1998;77(Suppl 4):18–20.
Emmerson B. Hyperlipidaemia in hyperuricaemia and gout. Ann Rheum Dis. 1998;57(9):509–10.
Bedir A, Topbas M, Tanyeri F, Alvur M, Arik N. Leptin might be a regulator of serum uric acid concentrations in humans. Jpn Heart J. 2003;44(4):527–36.
Dessein PH, Shipton EA, Stanwix AE, Joffe BI, Ramokgadi J. Beneficial effects of weight loss associated with moderate calorie/carbohydrate restriction, and increased proportional intake of protein and unsaturated fat on serum urate and lipoprotein levels in gout: a pilot study. Ann Rheum Dis. 2000;59(7):539–43.
Ichida K, Matsuo H, Takada T, Nakayama A, Murakami K, Shimizu T. Decreased extra-renal urate excretion is a common cause of hyperuricemia. Nat Commun. 2012;3:764.
Enomoto A, Endou H. Roles of organic anion transporters (OATs) and a urate transporter (URAT1) in the pathophysiology of human disease. Clin Exp Nephrol. 2005;9(3):195–205.
Bobulescu IA, Moe OW. Renal transport of uric acid: evolving concepts and uncertainties. Adv Chronic Kidney Dis. 2012;19(6):358–71.
Han J, Liu Y, Rao F, Nievergelt CM, O’Connor DT, Wang X. Common genetic variants of the human uromodulin gene regulate transcription and predict plasma uric acid levels. Kidney Int. 2013;83(4):733–40.
Parthasarathy P, Vivekanandan S. A comprehensive review on thin film-based nano-biosensor for uric acid determination: arthritis diagnosis. World Rev Sci Technol Sustain Dev. 2018;14(1):52–71.
Cho SK, Kim S, Chung JY, Jee SH. Discovery of URAT1 SNPs and association between serum uric acid levels and URAT1. BMJ Open. 2015;5(11):e009360.
Tan PK, Ostertag TM, Miner JN. Mechanism of high affinity inhibition of the human urate transporter URAT1. Sci Rep. 2016;6:34995.
Phipps-Green AJ, Merriman ME, Topless R, Altaf S, Montgomery GW, Franklin C. Twenty-eight loci that influence serum urate levels: analysis of association with gout. Ann Rheum Dis. 2016;75(1):124–30.
Parthasarathy P, Vivekanandan S. A numerical modelling of an amperometric-enzymatic based uric acid biosensor for GOUT arthritis diseases. Inform Med Unlocked. 2018. https://doi.org/10.1016/j.imu.2018.03.001.
Kolz M, Johnson T, Sanna S, Teumer A, Vitart V, Perola M. Meta-analysis of 28,141 individuals identifies common variants within five new loci that influence uric acid concentrations. PLoS Genet. 2009;5(6):e1000504.
Liu R, O’Connell M, Johnson K, Pritzker K, Mackman N, Terkeltaub R. Extracellular signal-regulated kinase 1/extracellular signal-regulated kinase 2 mitogen-activated protein kinase signaling and activation of activator protein 1 and nuclear factor kappaB transcription factors play central roles in interleukin-8 expression stimulated by monosodium urate monohydrate and calcium pyrophosphate crystals in monocytic cells. Arthritis Rheum. 2000;43(5):1145–55.
Cronstein BN, Sunkureddi P. Mechanistic aspects of inflammation and clinical management of inflammation in acute gouty arthritis. J Clin Rheumatol. 2013;19(1):19–29.
Parthasarathy P, Vivekanandan S. Investigation on uric acid biosensor model for enzyme layer thickness for the application of arthritis disease diagnosis. Health Inf Sci Syst. 2018;6:1–6.
Busso N, Ea HK. The mechanisms of inflammation in gout and pseudogout (CPP-induced arthritis). Reumatismo. 2012;63(4):230–7.
Ea HK. Mechanisms of gout inflammation. Presse Med. 2011;40(9 Pt 1):836–43.
Dalbeth N, Lauterio TJ, Wolfe HR. Mechanism of action of colchicine in the treatment of gout. Clin Ther. 2014;36(10):1465–79.
Steiger S, Harper JL. Mechanisms of spontaneous resolution of acute gouty inflammation. Curr Rheumatol Rep. 2014;16(1):392.
Nuki G, Simkin PA. A concise history of gout and hyperuricemia and their treatment. Arthr Res Ther. 2006;8(suppl 1):S1.
Zhu Y, Pandya BJ, Choi HK. Prevalence of gout and hyperuricemia in the US general population: the National Health and Nutrition Examination Survey 2007-2008. Arthritis Rheum. 2011;63(10):3136–41.
Parthasarathy P, Vivekanandan S. A typical IoT architecture-based regular monitoring of arthritis disease using time wrapping algorithm. Int J Comput Appl. 2018. https://doi.org/10.1080/1206212X.2018.1457471.
Dirken-Heukensfeldt KJ, Teunissen TA, van de Lisdonk H, Lagro-Janssen AL. Clinical features of women with gout arthritis. A systematic review. Clin Rheumatol. 2010;29(6):575–82.
Reginato AM, Mount DB, Yang I, Choi HK. The genetics of hyperuricaemia and gout. Nat Rev Rheumatol. 2012;8(10):610–21.
Yang Q, Köttgen A, Dehghan A, et al. Multiple genetic loci influence serum urate levels and their relationship with gout and cardiovascular disease risk factors. Circ Cardiovasc Genet. 2010;3(6):523–30.
Mount DB. The kidney in hyperuricemia and gout. Curr Opin Nephrol Hypertens. 2013;22(2):216–23.
Ning TC, Keenan RT. Unusual clinical presentations of gout. Curr Opin Rheumatol. 2010;22(2):181–7.
Campion EW, Glynn RJ, DeLabry LO. Asymptomatic hyperuricemia. Risks and consequences in the Normative Aging Study. Am J Med. 1987;82(3):421–6.
Schumacher HR Jr. The pathogenesis of gout. Clevel Clin J Med. 2008;75(suppl 5):S2–4.
Roddy E, Zhang W, Doherty M. Are joints affected by gout also affected by osteoarthritis? Ann Rheum Dis. 2007;66(10):1374–7.
Choi HK, Atkinson K, Karlson EW, et al. Purine-rich foods, dairy and protein intake, and the risk of gout in men. N Engl J Med. 2004;350(11):1093–103.
Zhang Y, Neogi T, Chen C, et al. Cherry consumption and decreased risk of recurrent gout attacks. Arthritis Rheum. 2012;64(12):4004–11.
Pillinger MH, Goldfarb DS, Keenan RT. Gout and its comorbidities. Bull NYU Hosp Jt Dis. 2010;68(3):199–203.
Agarwal V, Hans N, Messerli F. Effect of allopurinol on blood pressure: a systematic review and meta-analysis. J Clin Hypertens (Greenwich). 2013;15(6):435–42.
Krishnan E, Baker JF, Furst DE, Schumacher HR. Gout and the risk of acute myocardial infarction. Arthritis Rheum. 2006;54(8):2688–96.
Schumacher HR Jr, Chen LX. Newer therapeutic approaches: gout. Rheum Dis Clin N Am. 2006;32(1):235–44.
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Parthasarathy, P., Vivekanandan, S. Urate crystal deposition, prevention and various diagnosis techniques of GOUT arthritis disease: a comprehensive review. Health Inf Sci Syst 6, 19 (2018). https://doi.org/10.1007/s13755-018-0058-9
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DOI: https://doi.org/10.1007/s13755-018-0058-9