ライフサイエンスコーパス: gout

1 ults with joint inflammation suspected to be gout.

2 itors and glucocorticoids for treating acute gout.

3 ammatory arthritis, such as hypertension and gout.

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

5 linical recommendations on the management of gout.

6 d who suffer from its principal consequence, gout.

7 g liver/kidney damage or chronically causing gout.

8 iagnosis, and treatment of hyperuricemia and gout.

9 e therapeutic approach for hyperuricemia and gout.

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

11 role in treating hypertensive patients with gout.

12 us, present challenges for the management of gout.

13 lar function is an important risk factor for gout.

14 Our study included 633 individuals with gout.

15 r the dramatic increase in the prevalence of gout.

16 with moderate or severe renal impairment and gout.

17 , or colchicine to treat patients with acute gout.

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

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

20 s in patients previously diagnosed as having gout.

21 omorbidities are likely to decreased risk of gout.

22 soft tissues in patients suspected of having gout.

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

24 costeroids relieve pain in adults with acute gout.

25 levated serum urate is a key risk factor for gout.

26 tic review of risk factors and prevention of gout.

27 health professional- or physician-diagnosed gout.

28 e documented 896 confirmed incident cases of gout.

29 ing of the pathogenesis of hyperuricemia and gout.

30 of the American College of Rheumatology for gout.

31 likely translate into those with the risk of gout.

32 eruricemia or the clinical manifestations of gout.

33 chicine when using colchicine to treat acute gout.

34 f uric acid levels and likely of the risk of gout.

35 ew drugs and the already available drugs for gout.

36 between higher coffee intake and the risk of gout.

37 e documented 778 confirmed incident cases of gout.

38 nt information of the genetic association of gout.

39 College of Rheumatology survey criteria for gout.

40 roposed to improve the care of patients with gout.

41 s to a rational approach to the treatment of gout.

42 osteroids reduce pain in patients with acute gout.

43 is necessary in patients with possible acute gout.

44 ssociated loci also confer susceptibility to gout.

45 nt inducers of the inflammatory processes in gout.

46 SU crystals in joint aspirate for diagnosing gout.

47 clinical recommendations on the diagnosis of gout.

48 tion includes adults with acute or recurrent gout.

49 ults with joint inflammation suspected to be gout.

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

51 p clinicians make a provisional diagnosis of gout.

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

53 tion includes adults with acute or recurrent gout.

54 SU crystals in joint aspirate for diagnosing gout.

55 esic effectiveness among patients with acute gout.

56 p clinicians make a provisional diagnosis of gout.

57 costeroids relieve pain in adults with acute gout.

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

59 osteroids reduce pain in patients with acute gout.

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

61 ibitors or placebo in the treatment of acute gout?

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

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

64 ltivariate relative risks (RRs) for incident gout according to coffee-consumption categories [ie, 0,

65 t gout was defined as self-reported onset of gout after baseline.

66 , Canada, and Mexico in patients with severe gout, allopurinol intolerance or refractoriness, and ser

67 ssociated with an increased risk of incident gout, although the contribution of these beverages to th

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

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

70 pite the recent doubling of the incidence of gout among women and its substantial prevalence particul

71 evaluate purported risk factors for incident gout among women and to compare them with those among me

72 ging female population, the risk factors for gout among women remain unknown.

73 se were associated with the risk of incident gout among women.

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

75 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.

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

77 uctions of 33-66% for the treatment of acute gout and 50-75% for prophylaxis were calculated for conc

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

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

80 To review the association of hyperuricemia, gout and chronic kidney damage and whether hyperuricemia

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

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

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

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

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

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

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

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

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

90 S adults suggest that the prevalence of both gout and hyperuricemia remains substantial and may have

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

92 are associated with increased prevalence of gout and hyperuricemia.

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

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

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

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

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

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

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

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

101 of tissue inflammation in diseases including gout and those that previously have not been considered

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

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

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

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

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

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

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

109 tween coffee intake and the risk of incident gout are limited.

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

111 rovide new insights into the pathogenesis of gout arthritis.

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

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

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

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

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

117 ed data from 78,906 women with no history of gout at baseline who provided information on intake of b

118 ey answered a query about gout, were free of gout at baseline, and had hypertension (defined as takin

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

136 set of putative risk factors with recurrent gout attacks.

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

138 tant prophylaxis, in patients with recurrent gout attacks.

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

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

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

142 erum uric acid levels and, thus, the risk of gout, but prospective data on the relationship are limit

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

144 describe obstacles to optimum management of gout by primary care physicians and to propose education

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

146 confidence intervals [95% CIs]) for incident gout by time-varying diuretic use, both adjusted for con

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

148 t-centered education that quality of care in gout can be enhanced.

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

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

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

152 It is through better gout-centered education that quality of care in gout can

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

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

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

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

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

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

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

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

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

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

163 In the past, gout education has been hampered by infrequency of conti

164 Among patients with chronic gout, elevated serum uric acid level, and allopurinol in

165 using keywords including but not limited to 'gout', 'epidemiology', 'primary prevention', 'secondary

166 l consumption increased the risk of incident gout, especially beer and hard liquor.

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

168 8 international sites to evaluate potential gout flare criteria against the gold standard of an expe

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

170 ine (prolonged over 6 hours) with placebo in gout flare, using regimens producing comparable maximum

171 most strongly associated with presence of a gout flare.

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

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

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

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

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

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

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

179 ened soda, the multivariate relative risk of gout for 1 serving per day was 1.74 (95% confidence inte

180 The incidence rates of gout for women per 1,000 person-years according to serum

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

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

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

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

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

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

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

188 vels of serum uric acid increase the risk of gout in a graded manner among women, but the rate of inc

189 d discontinuation of medications for chronic gout in adults.

190 d discontinuation of medications for chronic gout in adults.

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

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

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

194 ntribution of these beverages to the risk of gout in the population is likely modest given the low in

195 se intake, the multivariate relative risk of gout in the top quintile was 1.62 (95% CI, 1.20-2.19; P

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

197 is associated with a lower risk of incident gout in women.

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

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

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

201 etary factors increased the risk of incident gout, including meat intake, seafood intake, sugar sweet

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

203 regards to the genetics of hyperuricemia and gout, including recent data from genome-wide association

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

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

206 Gout is a chronic disease resulting from elevated serum

207 Gout is a common type of inflammatory arthritis in patie

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

209 Gout is a form of crystal arthropathy where monosodium u

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

211 Gout is an ancient disease.

212 Because refractory gout is associated with high oxidative stress in spite o

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

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

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

216 n preventive strategies for the treatment of gout is needed.

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

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

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

220 tions in patients with otherwise untreatable gout is progressing.

221 Gout is the most common inflammatory arthritis in the Un

222 Gout is the most common type of inflammatory arthritis.

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

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

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

226 medications have been implemented to improve gout management.

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

228 ytes showed less migration in vitro and in a gout model in vivo.

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

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

231 blications address the optimum management of gout, national re-education can occur.

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

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

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

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

236 drinks were not associated with the risk of gout (P = .27 for trend).

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 Data were collected from 210 gout patients at 8 international sites to evaluate poten

243 rotein oxidation, in plasma of 26 refractory gout patients receiving up to five infusions of peglotic

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

245 guidelines for hyperuricemic individuals and gout patients.

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

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

248 out show promise for unmet needs in selected gout populations.

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 Patients with chronic disabling gout refractory to conventional urate-lowering therapy n

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

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

254 oral colchicine therapy and dosing in acute gout remains limited.

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

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

257 oop diuretics were associated with increased gout risk, an association mediated by a change in serum

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

259 e chimera system as a viable animal model of gout, serving to identify the primary function of CXCL16

260 Emerging therapies for gout show promise for unmet needs in selected gout popul

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

262 se data for several other pipeline drugs for gout, such as the selective uricosuric drug RDEA594 and

263 olymorphisms of the gene have been linked to gout susceptibility and to hereditary hypouricemia.

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

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

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 al caffeine from all sources and the risk of gout; the multivariate RR of the highest quintile compar

269 s demonstrate an opportunity to use existing gout therapies more effectively in order to improve both

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

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

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

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

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

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

276 caspase-1 activity, common diseases such as gout, type 2 diabetes, heart failure, recurrent pericard

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

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

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

280 ages in the world and may affect the risk of gout via various mechanisms, but prospective data on the

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

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

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

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

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

286 Incident gout was defined as self-reported onset of gout after ba

287 el, the association between diuretic use and gout was null.

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

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

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

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

292 Individuals with gout were prospectively recruited and followed up online

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

294 this analysis if they answered a query about gout, were free of gout at baseline, and had hypertensio

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

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

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

298 003-2010) among subjects with a diagnosis of gout who had 1 or more attacks during 1 year of follow-u

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

300 Familial childhood gout with progressive renal impairment attributable to m