ライフサイエンスコーパス: gout

1 ribute substantially to the rising burden of gout.

2 chicine when using colchicine to treat acute gout.

3 nt information of the genetic association of gout.

4 is necessary in patients with possible acute gout.

5 ssociated loci also confer susceptibility to gout.

6 nt inducers of the inflammatory processes in gout.

7 SU crystals in joint aspirate for diagnosing gout.

8 clinical recommendations on the diagnosis of gout.

9 tion includes adults with acute or recurrent gout.

10 ults with joint inflammation suspected to be gout.

11 ssociation between type 2 diabetes (T2D) and gout.

12 p clinicians make a provisional diagnosis of gout.

13 osis, type 2 diabetes, Alzheimer disease, or gout.

14 tion includes adults with acute or recurrent gout.

15 SU crystals in joint aspirate for diagnosing gout.

16 esic effectiveness among patients with acute gout.

17 costeroids relieve pain in adults with acute gout.

18 ions that may be confused with or occur with gout.

19 The primary outcome was a new diagnosis of gout.

20 osteroids reduce pain in patients with acute gout.

21 ive first-line option for treatment of acute gout.

22 itors and glucocorticoids for treating acute gout.

23 ammatory arthritis, such as hypertension and gout.

24 lerosis, type 2 diabetes (T2D), obesity, and gout.

25 d who suffer from its principal consequence, gout.

26 g liver/kidney damage or chronically causing gout.

27 iagnosis, and treatment of hyperuricemia and gout.

28 e therapeutic approach for hyperuricemia and gout.

29 laboratory data), and low baseline risk for gout.

30 Q141K), was shown to cause hyperuricemia and gout.

31 role in treating hypertensive patients with gout.

32 us, present challenges for the management of gout.

33 lar function is an important risk factor for gout.

34 Our study included 633 individuals with gout.

35 pe 2 diabetes mellitus and is known to cause gout.

36 r the dramatic increase in the prevalence of gout.

37 with moderate or severe renal impairment and gout.

38 N: Hyperuricemia is a strong risk factor for gout.

39 r disease flare have been used in studies of gout.

40 s in patients previously diagnosed as having gout.

41 omorbidities are likely to decreased risk of gout.

42 soft tissues in patients suspected of having gout.

43 were men, and 54 of them (26%) had flares of gout.

44 red in 3 individuals with a prior history of gout.

45 al component of the innate immune system, in gout.

46 reabsorption culminated in hyperuricemia and gout.

47 wering therapies used to treat patients with gout.

48 or MSU crystal deposition and development of gout.

49 ults with joint inflammation suspected to be gout.

50 osteroids reduce pain in patients with acute gout.

51 p clinicians make a provisional diagnosis of gout.

52 linical recommendations on the management of gout.

53 , or colchicine to treat patients with acute gout.

54 costeroids relieve pain in adults with acute gout.

55 ibitors or placebo in the treatment of acute gout?

56 .9%] vs. 53 [7.1%]), as was the incidence of gout (18 patients [1.2%] vs. 2 [0.3%]).

57 e analysis I, the RR of diabetes to incident gout (682 cases) was 0.77 (95% CI 0.60-0.97).

58 ith differences of 1.2% in the prevalence of gout (95% confidence interval [95% CI] 0.6, 1.9), 0.15 m

59 a-analysis of GWAS of serum urate levels and gout among 5820 AA and a large candidate gene study amon

60 sporter-2 inhibitors may reduce the risk for gout among adults with type 2 diabetes mellitus, althoug

61 The prevalence of gout among US adults in 2007-2008 was 3.9% (8.3 million

62 For T2D to gout (analysis I), prevalent gout were further excluded

63 ed odds ratio of 1.74 (CI, 1.47 to 2.05) for gout and 1.25 (CI, 1.12 to 1.40) for hyperuricemia.

64 No participant developed gout and 3 receiving inosine developed symptomatic uroli

65 s associated with a 3.6-fold higher risk for gout and a 1.9-fold higher risk for hyperuricemia compar

66 ditionally considered the staple therapy for gout and a second-line treatment for pericarditis, as we

67 Increased serum uric acid (SUA) levels cause gout and are associated with multiple diseases, includin

68 High serum urate is a prerequisite for gout and associated with metabolic disease.

69 isms contribute to common conditions such as gout and cardiovascular disease.

70 factor for several human diseases including gout and cardiovascular disease.

71 Elevated serum urate levels cause gout and correlate with cardiometabolic diseases via poo

72 between self-reported physician diagnosis of gout and degrees of renal impairment were the primary fo

73 Several dietary risk factors for incident gout and gout flares are modifiable.

74 were associated with higher risk of incident gout and higher rate of gout flares.

75 used in the management of acute and chronic gout and how to 'treat to target' to cure the disease.

76 Other signs include early onset diabetes, gout and hyperparathyroidism, elevated liver enzymes, an

77 ys have confirmed the strong relationship of gout and hyperuricaemia with hypertension and diuretic t

78 s have strongly supported the association of gout and hyperuricaemia with hypertension.

79 present study was to estimate prevalence of gout and hyperuricemia among people with impaired GFR in

80 athophysiological nature of the common ABCG2 gout and hyperuricemia associated variant Q141K (rs22311

81 The incidence of gout and hyperuricemia has increased recently, which is

82 vels, and hyperlipidemia, the odds ratios of gout and hyperuricemia were 5.9 (2.2, 15.7) and 9.58 (4.

83 are associated with increased prevalence of gout and hyperuricemia.

84 ES 2007-2008, we estimated the prevalence of gout and hyperuricemia.

85 ther hand, the abnormal level of UA leads to gout and hyperuricemia.

86 ach associated with a lower risk of incident gout and in some cases a lower rate of gout flares.

87 nts more effectively, raising the profile of gout and its best management and introducing the princip

88 e, analytes associated with diseases such as gout and metabolic disorders.

89 including atherosclerosis, type 2 diabetes, gout and obesity.

90 ation that is indicated for the treatment of gout and pericarditis.

91 narily-engineered enzyme capable of treating gout and preventing tumor lysis syndrome in human patien

92 c acid are associated with increased risk of gout and renal and cardiovascular diseases.

93 es were self-reported physician diagnosis of gout and serum urate level.

94 ould be beneficial for both the treatment of gout and the prevention of cardiovascular comorbidities.

95 ainstay of management in diseases other than gout and tumor lysis syndrome.

96 Elevated urate can cause gout and urolithiasis and is associated with cardiovascu

97 ch associated with a higher risk of incident gout and/or gout flares.

98 the pathogenesis of diseases like silicosis, gout, and atherosclerosis.

99 onnections with proteinuria, hyperlipidemia, gout, and hypertension.

100 , renal insufficiency, hypercholesterolemia, gout, and obesity were equally low in both groups.

101 An appreciation that hyperuricaemia and gout are associated with hypertension and chronic kidney

102 nsufficiency, the diagnosis and treatment of gout are discussed.

103 rovide new insights into the pathogenesis of gout arthritis.

104 one is not sufficient for the development of gout arthritis.

105 CI 1.36, 3.91]) was associated with incident gout as compared with not using any diuretic, not using

106 Some of the previously reported gout associated loci (except ALDH16A1), including ABCG2,

107 Most of the gout associated loci identified in previous GWAS were co

108 growing number (>/=8) of the risk alleles on gout associated loci.

109 disequilibrium (LD) with GWAS identified SU/gout associated variants were analyzed in a Han Chinese

110 Other crystallopathies, such as gout, atherosclerosis, and asbestosis, trigger inflammat

111 er, Testicular Cancer, Gallstones, Glaucoma, Gout, Atrial Fibrillation, High Cholesterol, Asthma, Bas

112 he prior 48 hours and the risk of subsequent gout attack (P = 0.01 for linear trend).

113 ciated with approximately 40% higher risk of gout attack compared with moderate temperatures.

114 ering therapy in most patients after a first gout attack or in patients with infrequent attacks.

115 Gout attack risk may be affected by weather (e.g., becau

116 ty were associated with an increased risk of gout attack, despite the likelihood that individuals are

117 tween mean relative humidity and the risk of gout attacks (P = 0.03 for quadratic trend).

118 febuxostat) reduces long-term risk for acute gout attacks after 1 year or more.

119 chicine or NSAIDs reduces the risk for acute gout attacks by at least half in patients starting urate

120 ture and humidity with the risk of recurrent gout attacks by conducting an internet-based case-crosso

121 riod was associated with a 35% lower risk of gout attacks compared with no intake (multivariate OR 0.

122 We estimated the risk of recurrent gout attacks related to cherry intake using conditional

123 ity over the prior 48 hours with the risk of gout attacks using a time-stratified approach and condit

124 s combined with allopurinol use, the risk of gout attacks was 75% lower than during periods without e

125 To review evidence about treatment of acute gout attacks, management of hyperuricemia to prevent att

126 To review evidence about treatment of acute gout attacks, management of hyperuricemia to prevent att

127 tant prophylaxis, in patients with recurrent gout attacks.

128 set of putative risk factors with recurrent gout attacks.

129 ry intake is associated with a lower risk of gout attacks.

130 erum urate levels and reduces risk for acute gout attacks.

131 Fortunately, new insights into gout biology are permitting the development of novel, po

132 Lead toxicity can lead to gouty arthritis (gout), but whether the low lead exposure in the contempo

133 ntified dozens of susceptibility loci for SU/gout, but few have been conducted for Chinese descent.

134 ar analgesic effectiveness for management of gout, but the trials had small sample sizes and other me

135 ios and 95% confidence intervals of incident gout by race among 11,963 men and women using adjusted C

136 ions of crystalline arthropathies, including gout, calcium pyrophosphate deposition, and hydroxyapati

137 We demonstrate that gout can be caused by a mutation in LDHD within the puta

138 Thus, hyperuricemia and gout can result from the accumulation of metabolites who

139 associated with multiple diseases, including gout, cardiovascular disease, and renal disease.

140 k for clinicians in order to provide optimal gout care.

141 investigated our genetic instrument in 3,151 gout cases and 68,350 controls.

142 ence and incidence, suboptimal management of gout continues in many countries.

143 targeting IL-1 in prevalent diseases such as gout, diabetes mellitus, and coronary artery disease.

144 orters implicated in metabolic diseases like gout, diabetes, and chronic kidney disease.

145 oint inflammation and no previous definitive gout diagnosis who had MSU analysis of joint aspirate.

146 oint inflammation and no previous definitive gout diagnosis who had MSU analysis of joint aspirate.

147 CT and ultrasonography also show promise for gout diagnosis, accessibility to these methods may be li

148 a systematic review of published studies on gout diagnosis, identified using several databases, from

149 a systematic review of published studies on gout diagnosis, identified using several databases, from

150 antly improve the efficiency and accuracy of gout diagnosis, reduce costs, and can be deployed even a

151 (FOV) limits the efficiency and accuracy of gout diagnosis.

152 ack men were at increased risk of developing gout during middle and older ages compared with whites,

153 tion, and treatment, millions of people with gout experience repeated attacks of acute arthritis and

154 as a humoral pattern recognition molecule in gout facilitating MSU crystal phagocytosis and contribut

155 e was to develop empirical definitions for a gout flare from patient-reported features.

156 active IL-1beta release in initiation of the gout flare has led to the development of anti-IL-1beta b

157 s used in prophylaxis and treatment of acute gout flare, alleviates the painful inflammatory response

158 hicine, are widely used for the treatment of gout flare; recognition of the importance of NLRP3 infla

159 hich aims to dissolve MSU crystals, suppress gout flares and resolve tophi.

160 l dietary risk factors for incident gout and gout flares are modifiable.

161 -dose anti-inflammatory therapies can reduce gout flares during initiation of urate-lowering therapy.

162 acept significantly reduces the frequency of gout flares during the initial period of treatment with

163 The mean number of gout flares per patient through week 12 (primary efficac

164 her risk of incident gout and higher rate of gout flares.

165 d with a higher risk of incident gout and/or gout flares.

166 ident gout and in some cases a lower rate of gout flares.

167 ment of anti-IL-1beta biological therapy for gout flares.

168 This issue provides a clinical overview of gout, focusing on prevention and screening, diagnosis, a

169 rticipants had an increased risk of incident gout (for women, adjusted hazard ratio (HR) = 1.69, 95%

170 ion of the association of race with incident gout (for women, adjusted HR = 1.62, 95% CI: 1.24, 2.22;

171 ated collagen-induced arthritis, and blocked gout formation in mouse models.

172 metabolic disorders) and 9 disease outcomes (gout, gouty arthropathy, pyogenic arthritis, essential h

173 benecid, a classic pharmacological agent for gout, has also been used historically in combination the

174 Colchicine, a drug long used for gout, has been recently approved (for the first time eve

175 Colchicine, a commonly used treatment for gout, has recently emerged as a novel therapeutic option

176 f comorbidity clustering in individuals with gout have been described.

177 l (1.4%) increase in the 8-year incidence of gout, have also been reported in comparisons to healthy

178 hyperuricemia and related diseases, such as gout, hypertension, and diabetes.

179 successfully replicated the association with gout, hypertension, heart diseases, and blood lipid leve

180 ction of uric acid (UA) in blood may lead to gout, hyperuricaemia and kidney disorder; thus, a fast,

181 d discontinuation of medications for chronic gout in adults.

182 d discontinuation of medications for chronic gout in adults.

183 usly unknown) that improve the prediction of gout in an independent cohort of 334,880 individuals.

184 e associated with serum uric acid levels and gout in Asians, Europeans, and European and African Amer

185 set (n = 56) showed nominal association with gout in our sample (p < 0.05).

186 ar filtration rate (GFR), hyperuricemia, and gout in the general population are not well understood.

187 buxostat versus allopurinol in patients with gout in the UK, Denmark, and Sweden.

188 ere was an estimated 7.5 million people with gout in the US.

189 We examined racial differences in gout incidence among black and white participants in a l

190 The gout incidence rate was lower among patients prescribed

191 lative effect of multiple "risk" variants on gout incidence.

192 Comorbid conditions that often accompany gout, including chronic kidney disease and diabetes mell

193 Long-term outcome data for patients with gout, including medication adherence, are limited.

194 risk score analyses showed that the risk of gout increased for individuals with the growing number (

195 The prevalence of hyperuricemia and gout increases with decreasing glomerular function indep

196 Gout is a chronic arthritis caused by the deposition of

197 Gout is a chronic disease caused by monosodium urate (MS

198 Gout is a chronic disease resulting from elevated serum

199 Gout is a common type of inflammatory arthritis in patie

200 Background: Gout is a common type of inflammatory arthritis in patie

201 Gout is a form of crystal arthropathy where monosodium u

202 Gout is a painful arthritic inflammatory disease caused

203 PURPOSE OF REVIEW: Gout is a true crystal deposition disease, extremely pai

204 Gout is an ancient disease.

205 Gout is caused by deposition of monosodium urate crystal

206 Gout is caused by elevated serum urate levels, which can

207 The incidence of gout is increasing, most likely reflecting increasing ra

208 Gout is more prevalent in men than in women, with increa

209 emporary general population confers risk for gout is not known.

210 Gout is one of the most common types of inflammatory art

211 ed with a lower risk of incident gout, while gout is positively related to diabetes among normal weig

212 Gout is the most common inflammatory arthritis and occur

213 Gout is the most common inflammatory arthritis in the Un

214 Gout is the most common type of inflammatory arthritis.

215 tibiofemural articulation, a murine model of gout, is highly reduced by intravenous injection of CXCL

216 Although we have many treatments to cure gout, it is a disease that is consistently undertreated/

217 -inflammatory effects of colchicine in acute gout-like inflammation can be accounted for by inhibitio

218 ing i.p. and intra-articular mouse models of gout-like inflammation, we found that GEF-H1/GEF-H1/AHRG

219 d specificities of 83% to 92% for diagnosing gout (low SOE).

220 medications have been implemented to improve gout management.

221 outcomes and now represent best practice for gout management.

222 r a uricosuric drug used clinically to treat gout, markedly reduced ER retention of the mutants and i

223 good specificity (up to 96%) for diagnosing gout (moderate SOE).

224 good specificity (up to 96%) for diagnosing gout (moderate SOE).

225 We also evaluate its utility for gout monitoring in patients and healthy controls through

226 ion data (N = 110,347 for SU, N = 69,374 for gout, N = 133,413 for eGFR, N = 117,165 for CKD), electr

227 the improved physiological understanding of gout, new innovative treatments such as anti-IL inhibito

228 ase and chronic kidney disease in those with gout, novel associations of gout with other comorbiditie

229 Gout occurred in 3 individuals with a prior history of g

230 score was associated with increased risk of gout (odds ratio: 5.84; 95% confidence interval: 4.56 to

231 Among patients with epilepsy and gout, odds ratios for SJS/TEN were significantly increas

232 rsons were excluded if they had a history of gout or had received gout-specific treatment previously.

233 atients with diagnosed diabetic nephropathy, gout or hyperuricemia, and can reach 25 microM in certai

234 little clinical importance in the absence of gout or kidney stones.

235 eruricaemia in the absence of a diagnosis of gout or urate nephrolithiasis, an emerging body of evide

236 d that SU has a causal effect on the risk of gout (OR estimates ranging from 3.41 to 6.04 per 1-mg/dl

237 80)) and a 1.75-fold increase in the odds of gout (P = 1.09 x 10(-12)).

238 ans, and American Indians, respectively) and gout (P = 2.83 x 10(-10), P = 0.01, and P = 0.01 in Euro

239 alidated by imaging MSU crystals made from a gout patient's tophus and steroid crystals used as negat

240 ere analyzed in a Han Chinese cohort of 1255 gout patients and 1848 controls.

241 tistage GWAS in Han Chinese using 4,275 male gout patients and 6,272 normal male controls (1,255 case

242 Acute gout patients showed elevated concentration of PTX3 in p

243 inflammatory responses within the joints of gout patients upon encountering monosodium urate (MSU) c

244 n and help improve the treatment and care of gout patients.

245 guidelines for hyperuricemic individuals and gout patients.

246 synovial fluid from rheumatoid arthritis and gout patients.

247 re found abundantly in the synovial fluid of gout patients.

248 ceutical ingredient widely used for treating gout, pericarditis, and familial Mediterranean fever wit

249 serum urate levels observed in patients with gout predispose them to the formation of monosodium urat

250 Gout prevalence is increasing, yet management remains su

251 that MSU crystals, the etiological agent of gout, rapidly activate GSDMD in murine macrophages.

252 cally, only a third to half of patients with gout receive urate-lowering therapy, which is a definiti

253 inflammatory signals in cells responding to gout-related stimuli, but also in other common metabolic

254 Diagnosis of gout relies on identification of MSU crystals under a co

255 by pathological IL-1beta activation, such as gout, remain unclear.

256 iuretic agents was associated with decreased gout risk (adjusted HR 0.64 [95% CI 0.49, 0.86]) compare

257 Many gout risk factors exist, including obesity, dietary fact

258 investigate whether these loci contribute to gout risk in Han Chinese.

259 tory diseases, such as rheumatoid arthritis, gout, sepsis, stroke, and transplant rejection.

260 pathogenesis of numerous diseases, including gout, silicosis, asbestosis, and atherosclerosis.

261 f they had a history of gout or had received gout-specific treatment previously.

262 tigated both for the management of the acute gout symptoms, targeting interleukin-1beta, as well as u

263 We quantitated NET levels in gout synovial fluid supernatants and detected enzymatica

264 c acid in sweat were higher in patients with gout than in healthy individuals, and a similar trend wa

265 ribed an SGLT2 inhibitor had a lower rate of gout than those prescribed a GLP1 agonist.

266 Alternative strategies exist for diagnosing gout that do not rely solely on the documentation of mon

267 Alternative strategies exist for diagnosing gout that do not rely solely on the documentation of mon

268 70), which is currently under evaluation for gout therapy.

269 Among 632 subjects with gout, there was a significant dose-response relationship

270 The gout to diabetes association was modified by BMI (Pinter

271 In the analysis II, the RR of gout to incident diabetes (2223 cases) was 1.36 (1.12-1.

272 For gout to T2D (analysis II), prevalent diabetes were exclu

273 stream inflammation and is a novel target in gout treatment.

274 Limitation: Few studies of acute gout treatments, no placebo-controlled trials of managem

275 ion of many noncommunicable diseases such as gout, type II diabetes, and Alzheimer's disease.

276 Gout typically presents as an acute, self-limiting infla

277 For those with moderate to severe gout, urate-lowering treatment can eliminate acute attac

278 In a mouse peritonitis model of gout, using monosodium urate crystals to activate NLRP3,

279 t reports of the prevalence and incidence of gout vary widely according to the population studied and

280 ished (0.97 AUC) the uric-acid signatures of gout vs. acute leukemia despite not being optimized for

281 The age standardized prevalence of gout was 2.9% among those with normal GFR compared to 24

282 The prevalence of gout was 6.05% (95% CI, 4.49% to 7.62%) among patients i

283 The incidence rate of gout was 8.4 per 10,000 person-years (15.5/10,000 person

284 The association with gout was also significantly stronger in men than in wome

285 Development of murine gout was evaluated through the levels of cytokines (PTX3

286 oximately 2-3 fold increase in prevalence of gout was observed for each 30 ml/min/1.73 m(2) decrease

287 Diagnosis of gout was usually based on clinical criteria rather than

288 when self-reports of diagnosed diabetes and gout were enquired at follow-ups I and II.

289 For T2D to gout (analysis I), prevalent gout were further excluded (final n = 31,137).

290 Individuals with gout were prospectively recruited and followed up online

291 study, adult patients with hyperuricemia and gout were randomized to receive rilonacept administered

292 rapy is vital in the long-term management of gout, which aims to dissolve MSU crystals, suppress gout

293 nic obstructive pulmonary disease (COPD) and gout, which are central to disease progression and hence

294 ogression from hyperuricemia to inflammatory gout, which will provide new insights into the pathogene

295 is associated with a lower risk of incident gout, while gout is positively related to diabetes among

296 003-2010) among subjects with a diagnosis of gout who had 1 or more attacks during 1 year of follow-u

297 r 4 chronic kidney disease and no history of gout who had a urinary albumin:creatinine ratio of 265 o

298 ture, it is likely that new risk factors for gout will be identified and new ways of preventing and m

299 se in those with gout, novel associations of gout with other comorbidities have been reported, includ

300 Familial childhood gout with progressive renal impairment attributable to m