ライフサイエンスコーパス: allopurinol

1 purinol; P=0.23 for 120 mg of febuxostat vs. allopurinol).

2 purinol; P=0.16 for 120 mg of febuxostat vs. allopurinol).

3 (DeltaG( approximately ATP)) increased with allopurinol.

4 oxidative stress was completely abolished by allopurinol.

5 sburicase plus allopurinol, and 27 hours for allopurinol.

6 ontrol of plasma uric acid more rapidly than allopurinol.

7 ase, 92 rasburicase plus allopurinol, and 91 allopurinol.

8 gle agent and in sequential combination with allopurinol.

9 h rasburicase plus allopurinol, and 66% with allopurinol.

10 were more frequent with febuxostat than with allopurinol.

11 FN-alpha transcription was inhibited only by allopurinol.

12 elate to delayed or insufficient dosing with allopurinol.

13 tly by the xanthine oxidoreductase inhibitor allopurinol.

14 not the xanthine/xanthine oxidase inhibitor, allopurinol.

15 not by the xanthine oxidoreductase inhibitor allopurinol.

16 ruct a dose-response curve for the effect of allopurinol.

17 tenuated by inhibiting xanthine oxidase with allopurinol.

18 n a manner reversible by XOR inhibition with allopurinol.

19 thyl ester or the xanthine oxidase inhibitor allopurinol.

20 smokers and controls and were not altered by allopurinol.

21 stance vessels is rapidly reversed with oral allopurinol.

22 rette smokers by administering the inhibitor allopurinol.

23 owering agents and provide an alternative to allopurinol.

24 ge, were actually reduced in the presence of allopurinol.

25 d with the xanthine oxidoreductase inhibitor allopurinol.

26 ylephrine (PE) following maternal vehicle or allopurinol.

27 t compared with those treated with 100 mg of allopurinol (0 [0%] of 10).

28 +1.3 +/- 7.22 mls; p = 0.047), improved FMD (allopurinol +0.82 +/- 1.8% vs. placebo -0.69 +/- 2.8%; p

29 Rash occurred more frequently with allopurinol (10% versus 2%, P=0.01), but there was no di

30 romol/L) and attenuated by the XOR inhibitor allopurinol (100 micromol/L) in acidic and hypoxic condi

31 gmentation index improved significantly with allopurinol (2.6 +/- 7.0%, p < 0.001) but not with place

32 +/- 4.48 g; p = 0.007) and LVM index (LVMI) (allopurinol -2.2 +/- 2.78 g/m(2) vs. placebo -0.53 +/- 2

33 +/- 2.8%; p = 0.017) and augmentation index (allopurinol -2.8 +/- 5.1% vs. placebo +0.9 +/- 7%; p = 0

34 purinol also reduced LV end-systolic volume (allopurinol -2.81 +/- 7.8 mls vs. placebo +1.3 +/- 7.22

35 Allopurinol, 200 mg twice daily for 4 weeks, and placebo

36 ed efficiency was reversed by XO inhibition (allopurinol, 200 mg) or by ascorbate without affecting c

37 serum urate levels <6.0 mg/dl compared with allopurinol (22%) and placebo (0%).

38 response to acetylcholine compared with both allopurinol 300 mg/d and placebo (% change in forearm bl

39 se 0.20 mg/kg/d days 1 to 3 followed by oral allopurinol 300 mg/d days 3 to 5), or allopurinol (300 m

40 emic CHF patients were randomly allocated to allopurinol 300 mg/d or placebo for 1 week.

41 cardiomyopathy in a double-blind fashion to allopurinol (300 mg intravenously) or placebo infusion,

42 ceive either febuxostat (80 mg or 120 mg) or allopurinol (300 mg) once daily for 52 weeks; 760 receiv

43 y oral allopurinol 300 mg/d days 3 to 5), or allopurinol (300 mg/d orally days 1 to 5).

44 by 160 mg weekly) or placebo, and started on allopurinol (300 mg/day, titrated to serum urate <6 mg/d

45 ained serum urate levels <6.0 mg/dl than did allopurinol (300 or 100 mg) or placebo in subjects with

46 daily febuxostat (80 mg, 120 mg, or 240 mg), allopurinol (300 or 100 mg, based on renal function), or

47 cebo, allopurinol significantly reduced LVM (allopurinol -5.2 +/- 5.8 g vs. placebo -1.3 +/- 4.48 g;

48 Allopurinol 600 mg/d significantly increased forearm blo

49 enerated randomisation to assign patients to allopurinol (600 mg per day) or placebo for 6 weeks befo

50 conducted in 80 patients with CAD, comparing allopurinol (600 mg/day) with placebo.

51 Coinfusion of allopurinol (600 microg/min) improved endothelium-depend

52 -III chronic heart failure, comparing 300 mg allopurinol, 600 mg allopurinol, and placebo for the fir

53 Allopurinol, 600 mg/day, or placebo was given over the s

54 This increase was inhibited by allopurinol (a xanthine oxidase inhibitor), Me2SO (a hyd

55 reatment with an xanthine oxidase inhibitor (allopurinol), a Na(+)/H(+) exchange blocker (amiloride),

56 Acute administration of allopurinol, a competitive inhibitor of XO, reduced plas

57 port the first OHCU decarboxylase inhibitor, allopurinol, a structural isomer of hypoxanthine.

58 sed females to blood meals supplemented with allopurinol, a well-characterized XDH inhibitor.

59 Allopurinol, a xanthine oxidase inhibitor, attenuated en

60 Allopurinol, a xanthine oxidase inhibitor, blocks purine

61 Allopurinol, a xanthine oxidase inhibitor, can reverse t

62 Allopurinol, a xanthine oxidase inhibitor, has been show

63 Allopurinol, a xanthine oxidase inhibitor, prolongs the

64 38 phosphorylation in PMECs was inhibited by allopurinol, a xanthine oxidase inhibitor.

65 Allopurinol, a xanthine oxidoreductase (XOR) inhibitor,

66 travenous administration of the XO inhibitor allopurinol acutely improves the relative and absolute c

67 The present study determines the effect of allopurinol administration prior to hypoxia on brain lev

68 00-120 ms) before and after the XO inhibitor allopurinol (ALLO, 50 micromol/L).

69 ricase followed by oral allopurinol and with allopurinol alone in controlling plasma uric acid.

70 and efficiency, respectively, observed with allopurinol alone.

71 Allopurinol (ALP) hypersensitivity is a major cause of s

72 Apocynin and allopurinol also decreased V(2)O(5)-induced IFN-beta mRN

73 We sought to ascertain whether allopurinol also improves endothelial dysfunction in opt

74 potassium supplementation and treatment with allopurinol also increase urinary nitric oxide excretion

75 Allopurinol also reduced LV end-systolic volume (allopur

76 We conclude that maternal treatment with allopurinol alters in vivo maternal, umbilical and fetal

77 Allopurinol ameliorates endothelial dysfunction and arte

78 onses to acetylcholine also were improved by allopurinol (an inhibitor of xanthine oxidase) in vessel

79 Allopurinol, an inhibitor of xanthine oxidoreductase (XO

80 atment period, 31 patients were allocated to allopurinol and 28 were analysed, and 34 were allocated

81 Patients received allopurinol and aspirin for prophylaxis.

82 me activation in cells by treating mice with allopurinol and discovered that allopurinol treatment co

83 Studies of allopurinol and febuxostat lowering of serum urate have

84 Nevertheless, both allopurinol and febuxostat treatment has sustained the h

85 safety of the approved urate-lowering drugs, allopurinol and febuxostat.

86 tors and the xanthine oxidase (XO) inhibitor allopurinol and in NOS-3 knockout (KO) mice.

87 ep dose-response relationship exists between allopurinol and its effect on endothelial function.

88 Importantly, the XOR inhibitors allopurinol and oxypurinol attenuate dysfunction caused

89 point estimate (absolute difference between allopurinol and placebo) was 43 s (95% CI 31-58).

90 wn that the use of uric acid-lowering agents allopurinol and probenecid can lower blood pressure in a

91 ently available urate-lowering drugs include allopurinol and probenecid.

92 Specific inhibition of XOD by allopurinol and sodium tungstate led to an increase in i

93 case alone with rasburicase followed by oral allopurinol and with allopurinol alone in controlling pl

94 or rasburicase, 4 hours for rasburicase plus allopurinol, and 27 hours for allopurinol.

95 with rasburicase, 78% with rasburicase plus allopurinol, and 66% with allopurinol.

96 ts received rasburicase, 92 rasburicase plus allopurinol, and 91 allopurinol.

97 ailure, comparing 300 mg allopurinol, 600 mg allopurinol, and placebo for the first study and 1000 mg

98 GdCl(3), the xanthine oxidase (XO) inhibitor allopurinol, and the Fe(III) chelator Desferal resulted

99 ated the uptake of the anti-leishmanial drug allopurinol, and the nt3((-/-)) mutants were resistant t

100 mass index, use of diuretics, beta-blockers, allopurinol, and uricosuric agents, self-reported hypert

101 nt difference in clinical status between the allopurinol- and placebo-treated patients (worsened 45%

102 Allopurinol (AP) is administered in UA lowering therapy.

103 ions to be used alone or in combination with allopurinol are undergoing rigorous evaluation to use fo

104 ors and for the coadministration of 6-TG and allopurinol as an immunomodulation strategy in inflammat

105 and the practical application of the use of allopurinol as monotherapy for this condition.

106 In participants without diabetes mellitus, allopurinol associated with a trend toward improved flow

107 We randomly assigned 67 subjects to allopurinol at 300 mg/d or placebo for 9 months; 53 pati

108 of 80 mg or 120 mg, was more effective than allopurinol at the commonly used fixed daily dose of 300

109 Allopurinol attenuated both the increase in A1AR express

110 len) but not inhibition of xanthine oxidase (allopurinol), attenuated the effects of stretch on both

111 reatment with the xanthine oxidase inhibitor allopurinol being considered in human complicated pregna

112 Amiloride, and to a lesser extent allopurinol but not vitamin E, significantly decreased l

113 the *NO end products were not suppressed by allopurinol but were by aminoguanidine.

114 treated with the xanthine oxidase inhibitor allopurinol, but the duration of patent parasitemia was

115 This study demonstrates that allopurinol can regress left ventricular mass and improv

116 Allopurinol caused a significant decrease in MVO(2) (pea

117 study sought to ascertain whether high-dose allopurinol causes regression of left ventricular mass (

118 We therefore investigated whether allopurinol causes regression of LVH in patients with T2

119 Allopurinol causes regression of LVM in patients with T2

120 onset mutation or between normal or abnormal allopurinol challenge and neuropsychological outcome.

121 gth evidence showed that neither citrate nor allopurinol combined with thiazide was superior to thiaz

122 choline coinfusion data showed that 600 mg/d allopurinol completely abolished the oxidative stress th

123 egies to treat patients who are sensitive to allopurinol continue to evolve.

124 The mechanism of the anti-ischemic effect of allopurinol could be related to its reducing xanthine ox

125 e by inhibiting xanthine oxidoreductase with allopurinol could improve the proinflammatory endocrine

126 -III chronic heart failure, comparing 300 mg allopurinol daily (1 month) versus placebo.

127 buxostat daily, 0.80 success rate; 300 mg of allopurinol daily, 0.39 success rate) and dose escalatio

128 ostat daily, 0.82 success rate; </=800 mg of allopurinol daily, 0.78 success rate).

129 Although blocking uric acid formation by allopurinol did not affect outcomes, administration of u

130 idence-based QIs for gout management: QI 1 = allopurinol dose <300 mg in gout patients with renal ins

131 rtant to evaluate and document the safety of allopurinol during pregnancy, as it is finding new roles

132 In conclusion, allopurinol effectively and safely lowered serum uric ac

133 cid levels, xanthine oxidase inhibition with allopurinol failed to improve clinical status, exercise

134 Dose-escalation allopurinol-febuxostat sequential therapy is cost-effect

135 effectiveness ratios of dose escalation with allopurinol-febuxostat sequential therapy remained lower

136 Dose-escalation allopurinol-febuxostat sequential therapy was more costl

137 nt; allopurinol- or febuxostat-only therapy; allopurinol-febuxostat sequential therapy; and febuxosta

138 double-blinded manner to receive placebo or allopurinol for 12 weeks.

139 thine oxidase, is a potential alternative to allopurinol for patients with hyperuricemia and gout.

140 um stones, addition of thiazide, citrate, or allopurinol further reduced risk.

141 ase group and 329 +/- 129 mg/dL.hour for the allopurinol group (P <.0001).

142 n the high-dose febuxostat group than in the allopurinol group (P=0.003) or the low-dose febuxostat g

143 ol was restored to near-normal levels in the allopurinol group but was attenuated in untreated mice.

144 percent) and none of the 253 patients in the allopurinol group died; all deaths were from causes that

145 tween the combined febuxostat groups and the allopurinol group).

146 comparison of each febuxostat group with the allopurinol group).

147 The placebo and the allopurinol groups had baseline serum uric acid levels (

148 Allopurinol had no additive effect beyond that of ascorb

149 reatment with the xanthine oxidase inhibitor allopurinol had no effect.

150 has been implicated in LVH development, and allopurinol has been previously shown to reduce vascular

151 The use of allopurinol has been shown to be associated with reduced

152 Allopurinol has been shown to improve endothelial functi

153 Allopurinol has no discernable effects on LV contractile

154 1 allele substantially increases the risk of allopurinol hypersensitivity, it is not an absolute requ

155 Maternal allopurinol impaired fetal alpha1-adrenergic pressor and

156 ive stress and therefore we examined whether allopurinol improved endothelial dysfunction in chronic

157 Compared with placebo, allopurinol improved peak blood flow (venous occlusion p

158 ation of the xanthine oxidase (XO) inhibitor allopurinol improves cardiac high-energy phosphate conce

159 whether lowering serum uric acid levels with allopurinol improves endothelial dysfunction in 80 parti

160 We have shown that allopurinol improves endothelial dysfunction in chronic

161 peruricemic CHF patients, XO inhibition with allopurinol improves peripheral vasodilator capacity and

162 utic potential of xanthine oxidase inhibitor allopurinol in angina; ISRCTN15253766).

163 S might underpin the anti-ischemic effect of allopurinol in CAD.

164 The evidence suggests that the use of allopurinol in clinical practice should be approached wi

165 acid levels were significantly reduced with allopurinol in comparison with placebo (treatment differ

166 (Intravenous Allopurinol in Heart Failure; NCT00181155).

167 (Allopurinol in Patients with Diabetes and LVH; UKCRN 876

168 We report three cases of safe use of allopurinol in pregnancy for women with inflammatory bow

169 The safety of allopurinol in pregnancy is not known however.

170 bitor, represents a potential alternative to allopurinol in refractory gout patients.

171 Allopurinol increased median total exercise time to 393

172 Allopurinol increased the median time to ST depression t

173 Allopurinol increased the time to chest pain from a base

174 mimicked the beneficial energetic effects of allopurinol, increasing both contractility and efficienc

175 in was also suppressed by aminoguanidine and allopurinol independently.

176 oxidase by apocynin and xanthine oxidase by allopurinol individually reduced STAT-1 phosphorylation.

177 Maternal treatment with allopurinol induced maternal hypotension, tachycardia an

178 ss increases left ventricular afterload, any allopurinol-induced improvement in arterial compliance m

179 Allopurinol infusion increased mean cardiac PCr/ATP and

180 Allopurinol inhibited the increase in fetal plasma uric

181 Allopurinol inhibits purine degradation under severe hyp

182 da, and Mexico in patients with severe gout, allopurinol intolerance or refractoriness, and serum uri

183 ic gout, elevated serum uric acid level, and allopurinol intolerance or refractoriness, the use of pe

184 Allopurinol is a frequently prescribed drug.

185 in the context of obstetric trials in which allopurinol is being administered to pregnant women when

186 otential for pregnant women to be exposed to allopurinol is increasing.

187 ards more toxic and less desirable pathways, allopurinol is proving to be an effective add on therapy

188 Introducing the xanthine oxidase inhibitor allopurinol led to rapid normalization of alanine aminot

189 Maternal allopurinol led to significant increases in fetal heart

190 of improvement in endothelial function with allopurinol lies in its ability to reduce vascular oxida

191 Compared with placebo, allopurinol lowered serum uric acid significantly but di

192 Overall, allopurinol lowered urate levels but did not exacerbate

193 This raises the distinct possibility that allopurinol might reduce cardiovascular events and even

194 This raises the possibility that allopurinol might reduce future cardiovascular events an

195 tion) increase the likelihood that high-dose allopurinol might reduce future cardiovascular mortality

196 infused I.V. with either vehicle (n =11) or allopurinol (n =10).

197 re studied the effects of XO inhibition with allopurinol on endothelial function and peripheral blood

198 e in vivo effects of maternal treatment with allopurinol on fetal cardiovascular function in ovine pr

199 The effects of maternal allopurinol on maternal and fetal cardiovascular functio

200 achieved by a single oral dose of 600 mg of allopurinol on the day of the study.

201 tudy was to evaluate the effect of high-dose allopurinol on vascular oxidative stress (OS) and endoth

202 In both dosing scenarios, allopurinol-only therapy was cost-saving.

203 e content, which was unaffected after either allopurinol or chronic pesticide exposure alone, was sig

204 Patients for whom allopurinol or febuxostat is a suitable initial urate-lo

205 idence suggests that urate-lowering therapy (allopurinol or febuxostat) reduces long-term risk for ac

206 Disruption of XDH by allopurinol or XDH1 by RNA interference significantly af

207 ity by pharmacologic (N-acetyl-L-cysteine or allopurinol) or molecular (by small interfering RNA) app

208 thine oxidoreductase (XOR) inhibition (i.e., allopurinol) or nitric oxide donors (i.e., S-nitrosoglut

209 , n = 5) or high dose (150 mg kg(-1), n = 9) allopurinol, or high dose allopurinol with fetal NO bloc

210 h or without the xanthine oxidase inhibitor, allopurinol, or the uricosuric agent, benziodarone.

211 ent strategies were evaluated: no treatment; allopurinol- or febuxostat-only therapy; allopurinol-feb

212 ial design, we administered the XO inhibitor allopurinol orally to mice that had undergone massive my

213 gnificantly greater for rasburicase than for allopurinol (P = .001) in the overall study population,

214 ebuxostat, and 21 percent of those receiving allopurinol (P<0.001 for the comparison of each febuxost

215 compared with 50 percent in those receiving allopurinol (P=0.08 for 80 mg of febuxostat vs. allopuri

216 ebuxostat, and 64 percent of those receiving allopurinol (P=0.99 for 80 mg of febuxostat vs. allopuri

217 opurinol (P=0.08 for 80 mg of febuxostat vs. allopurinol; P=0.16 for 120 mg of febuxostat vs. allopur

218 opurinol (P=0.99 for 80 mg of febuxostat vs. allopurinol; P=0.23 for 120 mg of febuxostat vs. allopur

219 Aged offspring of hypoxic allopurinol pregnancy compared with aged offspring of un

220 inol use in pregnant patients and suggest an allopurinol pregnancy registry to document drug exposure

221 acid check within 6 months of starting a new allopurinol prescription, and QI 3 = complete blood coun

222 types following radiation exposure and that allopurinol prevented radiation-induced inflammasome act

223 After CHF, allopurinol produced significant (P:<0.05) increases in

224 xicity in the PQ+MB model of PD, and/or that allopurinol produces an antioxidant benefit offsetting i

225 in optimally treated CAD patients, high-dose allopurinol profoundly reduces vascular tissue OS and im

226 We ascertained whether high-dose allopurinol prolongs exercise capability in patients wit

227 Allopurinol protected against 6-TG toxicity by acting as

228 /d intravenously days 1-5), rasburicase plus allopurinol (rasburicase 0.20 mg/kg/d days 1 to 3 follow

229 ed OS, and our second aim was to see whether allopurinol really does reduce vascular tissue OS in CAD

230 (Does a Drug Allopurinol Reduce Heart Muscle Mass and Improve Blood V

231 mothers with the xanthine oxidase inhibitor allopurinol reduced placental uric acid levels, prevente

232 Although oral allopurinol reduced serum and striatal urate levels 4-fo

233 s call for further trials to examine whether allopurinol reduces cardiovascular events in patients wi

234 insulin resistance and hypertension, whereas allopurinol reduces serum levels of uric acid and amelio

235 This study sought to ascertain if high-dose allopurinol regresses left ventricular mass (LVM) in pat

236 High-dose allopurinol regresses LVH, reduces LV end-systolic volum

237 Allopurinol remains a dominant urate-lowering agent, how

238 Maternal allopurinol rescued maximal arterial relaxation to acety

239 nt new drug treatment with antiepileptics or allopurinol, respectively.

240 newly diagnosed hypertension, treatment with allopurinol resulted in reduction of BP.

241 rmine whether lowering levels of urate using allopurinol results in exacerbated neurotoxicity in a du

242 xpression; in contrast, inhibition of Xdh by allopurinol results in xdhB repression.

243 Allopurinol reversed endothelial dysfunction in smokers

244 citrates (RR, 0.25 [CI, 0.14 to 0.44]), and allopurinol (RR, 0.59 [CI, 0.42 to 0.84]) each further r

245 lacebo or control, although the benefit from allopurinol seemed limited to patients with baseline hyp

246 Allopurinol seems to be a useful, inexpensive, well tole

247 ebuxostat sequential therapy; and febuxostat-allopurinol sequential therapy.

248 One randomized trial of allopurinol showed short-term benefits but was too small

249 Compared with placebo, allopurinol significantly improved endothelium-dependent

250 Allopurinol significantly increased the forearm blood fl

251 Allopurinol significantly reduced absolute LVM (-2.65 +/

252 Allopurinol significantly reduced LVH (P=0.036), improve

253 Compared to placebo, allopurinol significantly reduced LVM (allopurinol -5.2

254 Allopurinol significantly reduced uric acid levels and b

255 Allopurinol single therapy is cost-saving compared with

256 joints that was resistant to treatment with allopurinol, steroids, and antiinflammatory drugs.

257 (3-aminomethyl)benzylacetamidine (1400W), or allopurinol, suggesting a role for both inducible nitric

258 estoration of vasorelaxation with PEG-SOD or allopurinol suggests that the mechanism(s) by which IL-1

259 ity was elevated in untreated mice after MI; allopurinol suppressed the XO activity to levels compara

260 rum uric acid levels >/=9.5 mg/dL to receive allopurinol (target dose, 600 mg daily) or placebo in a

261 kidney disease imparts a dose limitation on allopurinol that further impairs the effectiveness of ur

262 Therefore, allopurinol therapy may become useful to reduce CV event

263 stly but more effective than dose-escalation allopurinol therapy, with an incremental cost-effectiven

264 onsistent with reduced oxidative stress with allopurinol therapy.

265 ired in smokers (P=0.003), and improved with allopurinol, though not significantly (P=0.06).

266 lubility of uric acid, and administration of allopurinol to block production of uric acid.

267 herapy with a thiazide diuretic, citrate, or allopurinol to prevent recurrent nephrolithiasis in pati

268 dative stress was profound because high-dose allopurinol totally abolished the oxidative stress that

269 c marker associated with the risk for severe allopurinol toxicity has been reported.

270 denosine during hypoxia which is seen in the allopurinol-treated animals may potentiate adenosine's i

271 s were compared to 5 untreated hypoxic and 6 allopurinol-treated hypoxic animals.

272 vs. 162.8 +/- 38.3 nmol/gm), P = 0.05 in the allopurinol-treated hypoxic group.

273 Survival doubled in the allopurinol-treated mice, whereas cardiac contractile fu

274 ifications to proteins were prevented in the allopurinol-treated mice.

275 ys) were studied: 5 untreated normoxic and 6 allopurinol-treated normoxic controls were compared to 5

276 londialdehyde was significantly reduced with allopurinol treatment (346+/-128 nmol/L versus 461+/-101

277 e radical generation, decreased by 20% after allopurinol treatment (P<0.001).

278 and improvement of flow-dependent flow after allopurinol treatment (r=0.63, P<0.05).

279 m blood flow changes between the placebo and allopurinol treatment arms with regard to sodium nitropr

280 ng mice with allopurinol and discovered that allopurinol treatment completely blocked caspase-1 activ

281 entical to that seen in normal control mice, allopurinol treatment of these double-KO mice also enhan

282 Following allopurinol treatment, fetal hypoxia was induced by redu

283 n in TH-positive neurons was not affected by allopurinol treatment.

284 dd significantly to the very limited data on allopurinol use in pregnancy.

285 We encourage reporting of all cases of allopurinol use in pregnant patients and suggest an allo

286 When cherry intake was combined with allopurinol use, the risk of gout attacks was 75% lower

287 ients with IHD and LVH, comparing 600 mg/day allopurinol versus placebo therapy for 9 months.

288 low [mean+/-SEM]: 181+/-19% versus 120+/-22% allopurinol versus placebo; P=0.003).

289 t (346+/-128 nmol/L versus 461+/-101 nmol/L, allopurinol versus placebo; P=0.03), consistent with red

290 casual and ambulatory criteria while taking allopurinol vs 1 participant while taking placebo (P < .

291 and mean 24-hour ambulatory diastolic BP for allopurinol was -4.6 mm Hg (-2.4 to -6.8 mm Hg) vs -0.3

292 ebo, and the mean change in diastolic BP for allopurinol was -5.1 mm Hg (95% CI, -2.5 to -7.8 mm Hg)

293 e in mean 24-hour ambulatory systolic BP for allopurinol was -6.3 mm Hg (95% CI, -3.8 to -8.9 mm Hg)

294 asual BP, the mean change in systolic BP for allopurinol was -6.9 mm Hg (95% confidence interval [CI]

295 Allopurinol was used throughout pregnancy in all patient

296 These effects of maternal allopurinol were restored to control levels during fetal

297 inflammasome activation by sHz is reduced by allopurinol, which is an inhibitor of uric acid synthesi

298 mg kg(-1), n = 9) allopurinol, or high dose allopurinol with fetal NO blockade (n = 6).

299 Addition of potassium supplements and allopurinol with thiazides might be helpful in the manag

300 e dinucleotide phosphate oxidase inhibitor), allopurinol (xanthine oxidase inhibitor), and ACE8/8 cro