ライフサイエンスコーパス: NSAID

1 NSAID administration beginning within 24 hours after sur

2 NSAID inhibition of COX enzymes, along with luminal aggr

3 NSAID use resulted in noninferior rates of pleurodesis e

4 NSAID use was associated with a lower incidence of PME i

5 NSAID use was not associated with a change in the incide

6 NSAID use was reported by 63% of cases and 62% controls.

7 NSAID users were protected from SAB (OR = 0.78, 95% CI 0

8 NSAIDs allosterically inhibit cytosolic sulfotransferase

9 NSAIDs are not significantly associated with a differenc

10 NSAIDs inhibited signal transducers and activators of tr

11 NSAIDs interact with phospholipids and uncouple mitochon

12 s; 63% men); of these, 34% filled at least 1 NSAID prescription.

13 /benzodiazepines, 69%; anti-psychotics, 43%; NSAIDs, 28%; and metformin, 0.4%.

14 FDC products from ten formulations to 2,739 NSAID FDC products from 124 formulations.

15 s from 14 patients with NSAID-related LTP-A (NSAID-LTP-A), 7 patients with LTP-A, and 13 healthy cont

16 After risk adjustment, NSAIDs were associated with a 24% increased risk for ana

17 ose who experienced isolated urticaria after NSAID intake (P=.024).

18 who experienced reactions over 1 hour after NSAIDs administration (P=.001), and those who experience

19 ytokines, while those involved in NAR to all NSAIDs belonged to arachidonic acid pathway and HLA anti

20 cologic drug synergy from the use of both an NSAID and a corticosteroid is not supported by the liter

21 A prescription for an NSAID was filled by 56.4% of patients.

22 t 11 of the 13 human SULT isoforms harbor an NSAID-binding site.

23 Here, the first structure of an NSAID allosteric site-the MEF-binding site of SULT1A1-is

24 ronic kidney disease or coprescription of an NSAID and an oral anticoagulant without gastroprotection

25 Aspirin and NSAID consumption less than or equal to median entailed

26 .30, 95% CI 0.24-0.38), although aspirin and NSAID users more than median had an increased risk and n

27 tand the determinants of NSAID-dependent and NSAID-independent LTP-induced anaphylaxis (LTP-A).

28 d risk (aOR = 2.65; 95% CI = 2.29-3.06), and NSAIDs use only was associated with a 1.5-fold increased

29 contrast, the overall use of antibiotics and NSAIDs decreased.

30 dictor of studies on NAR to both aspirin and NSAIDs.

31 A combination of topical corticosteroids and NSAIDs significantly reduced the odds of developing CME

32 Walking disability and NSAIDs use have been postulated as potential mechanisms

33 prescribing of antiplatelet medications and NSAIDs and may have improved clinical outcomes.

34 and opioids [n = 29]; or 12F chest tube and NSAIDs [n = 28]).

35 ube and opioids [n = 28]; 24F chest tube and NSAIDs [n = 29]; 12F chest tube and opioids [n = 29]; or

36 < .001) for every 1% increase in the annual NSAID treatment percentage at a given hospital.

37 The association between any NSAID use after diagnosis and OS differed significantly

38 Use of any NSAID after diagnosis was associated with improved OS on

39 As NSAIDs are already in routine use in gynecological treat

40 pproximately the same cardiovascular risk as NSAIDs with less cyclooxygenase-2 inhibitory activity, b

41 nonsevere hypersensitivity reactions to ASA/NSAIDs, an ASA challenge is advisable.

42 We evaluated aspirin and non-aspirin NSAID use and risk of pancreatic adenocarcinoma in 141,9

43 Regular aspirin or non-aspirin NSAID use was not associated with future risk of pancrea

44 Use of aspirin or non-aspirin NSAIDs was not associated with pancreatic cancer risk, e

45 Limited doses of aspirin, NSAIDs, and SSRIs might not increase the risk, although

46 ression is therapeutically important because NSAIDs cause cardiovascular and renal side effects in ot

47 Interaction analyses between NSAID use and SNPs were conducted using logistic regress

48 analysis demonstrated no association between NSAID treatment and the odds of mortality or BPD (odds r

49 etic retinopathy on the relationship between NSAID use and PME was further analyzed.

50 ently reported, and the relationship between NSAID-exacerbated respiratory disease (NERD) and asthma

51 cations to model differing lag times between NSAID exposure and cancer development.

52 Nps complex (2.42 A), it was found that both NSAIDs bind within drug site 2 (DS2) of ESA and both occ

53 genesis and a guide for cancer prevention by NSAID treatment.

54 isms of gastrointestinal damage induction by NSAIDs via COX-mediated and COX-independent processes.

55 GIS variant and SAB risk that is modified by NSAIDs use during pregnancy and directly associated with

56 Colchicine, NSAIDs, and corticosteroids relieve pain in adults with

57 Conclusion: Colchicine, NSAIDs, and corticosteroids relieve pain in adults with

58 The most common NSAID hypersensitivity subgroup was SNIUAA (46.4%) and t

59 combinations, as well as ongoing concomitant NSAID use, was determined.

60 were 4.2 (95% CI, 3.8-4.6) with concomitant NSAID treatment and 2.2 (95% CI, 2.1-2.3) without NSAID

61 intestinal lesions in subjects taking daily NSAIDs.

62 trol period (366-372-day before index date): NSAIDs use during ARI episodes, ARI episodes without NSA

63 ly point out that anaphylaxis with different NSAIDs can be seen in a small group of patients.

64 ients experienced anaphylaxis with different NSAIDs, one patient encountered anaphylaxis with one NSA

65 e last patient had angioedema with different NSAIDs.

66 urticaria, or both have been distinguished: NSAID-exacerbated cutaneous disease, nonsteroidal anti-i

67 opical non-steroidal anti-inflammatory drug (NSAID) added to topical steroid use after uncomplicated

68 through nonsteroidal anti-inflammatory drug (NSAID) administration just after injury similarly hinder

69 nating non-steroidal anti-inflammatory drug (NSAID) alleviates this ischaemia and improves the murine

70 ), and non-steroidal anti-inflammatory drug (NSAID) bleeding prophylaxis.

71 Nonsteroidal anti-inflammatory drug (NSAID) exacerbated cutaneous disease is defined as the e

72 ly used nonsteroidal anti-inflammatory drug (NSAID) for relief of inflammatory pain.

73 NPs) in nonsteroidal anti-inflammatory drug (NSAID) metabolism and related pathways and spontaneous a

74 ects of nonsteroidal anti-inflammatory drug (NSAID) pharmacology with acid-sensing ion channels (ASIC

75 acin, a nonsteroidal anti-inflammatory drug (NSAID) that inhibits cyclooxygenases (COX) -1 and -2.

76 Non-steroidal anti-inflammatory drug (NSAID) treatment suppresses parainflammation in both mur

77 between nonsteroidal anti-inflammatory drug (NSAID) use and AD.

78 in non-nonsteroidal anti-inflammatory drug (NSAID) users (n = 315).During a median follow-up time of

79 ing the nonsteroidal anti-inflammatory drug (NSAID), indomethacin, is reported.

80 Nonsteroidal anti-inflammatory drug (NSAID)-induced urticarial and angioedema reactions are a

81 lure of nonsteroidal anti-inflammatory drug [NSAID] treatment) indicate a poorer prognosis and identi

82 spirin, nonsteroidal antiinflammatory drugs (NSAID), and acetaminophen are commonly used.

83 to ASA/nonsteroidal anti-inflammatory drugs (NSAID) intake.

84 sers of nonsteroidal antiinflammatory drugs (NSAIDs) (Pinteraction = 0.055), the proinflammatory-stab

85 bing of nonsteroidal antiinflammatory drugs (NSAIDs) or selected antiplatelet agents (e.g., NSAID pre

86 ession, nonsteroidal antiinflammatory drugs (NSAIDs), and statins may play a role in chemoprevention.

87 lective nonsteroidal antiinflammatory drugs (NSAIDs), remains uncertain.

88 ly used nonsteroidal antiinflammatory drugs (NSAIDs).

89 ls) and nonsteroidal antiinflammatory drugs (NSAIDs).

90 ), and nonsteroidal anti-inflammatory drugs (NSAIDs) (3.5%).

91 other nonsteroidal anti-inflammatory drugs (NSAIDs) (n = 8), and IR to biologics (n = 3).

92 Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most commonly prescribed drugs wor

93 Non-steroidal anti-inflammatory drugs (NSAIDs) are among the most frequently used classes of me

94 Nonsteroidal anti-inflammatory drugs (NSAIDs) are among the most prevalent drugs inducing hype

95 usion, nonsteroidal anti-inflammatory drugs (NSAIDs) are avoided because they may reduce pleurodesis

96 Nonsteroidal anti-inflammatory drugs (NSAIDs) are efficacious in closing PDA, but the effectiv

97 Non-steroidal anti-inflammatory drugs (NSAIDs) are known gamma-secretase modulators; they influ

98 Nonsteroidal anti-inflammatory drugs (NSAIDs) are the most frequent triggers of drug hypersens

99 quires nonsteroidal anti-inflammatory drugs (NSAIDs) as a triggering cofactor.

100 Are nonsteroidal anti-inflammatory drugs (NSAIDs) associated with better outcomes than cyclooxygen

101 n: Are nonsteroidal anti-inflammatory drugs (NSAIDs) associated with greater pain relief than placebo

102 opical nonsteroidal anti-inflammatory drugs (NSAIDs) associated with reduced pain intensity in acute

103 Nonsteroidal anti-inflammatory drugs (NSAIDs) can damage the gastrointestinal tract, causing w

104 Non-steroidal anti-inflammatory drugs (NSAIDs) damage the gastrointestinal (GI) epithelial cell

105 titive nonsteroidal anti-inflammatory drugs (NSAIDs) have been shown to inhibit COX-2 in a substrate-

106 Nonsteroidal anti-inflammatory drugs (NSAIDs) have many physiologic effects and are being used

107 other nonsteroidal anti-inflammatory drugs (NSAIDs) in relation to survival is unclear.

108 val of nonsteroidal anti-inflammatory drugs (NSAIDs) in synthetic urine can selectively remove pharma

109 Non-steroidal anti-inflammatory drugs (NSAIDs) inhibit cyclooxygenase-1 (COX-1) and COX-2 enzym

110 other nonsteroidal anti-inflammatory drugs (NSAIDs) is associated with lower risk of colorectal canc

111 cts of nonsteroidal anti-inflammatory drugs (NSAIDs) on T-cell activation of the IL-4 pathway in aspi

112 opical nonsteroidal anti-inflammatory drugs (NSAIDs) on the incidence of postoperative macular edema

113 ons to nonsteroidal anti-inflammatory drugs (NSAIDs) proposed by the European Network for Drug Allerg

114 spirin nonsteroidal anti-inflammatory drugs (NSAIDs) reduces the risk of several cancers, but it is n

115 using nonsteroidal anti-inflammatory drugs (NSAIDs) such as the COX-1/2 inhibitor indomethacin and t

116 ity of nonsteroidal anti-inflammatory drugs (NSAIDs) to inhibit cyclooxygenase (Cox)-1 and Cox-2 unde

117 I) and nonsteroidal anti-inflammatory drugs (NSAIDs) use could trigger acute myocardial infarction (A

118 Non-steroidal anti-inflammatory drugs (NSAIDs) use in the year prior to cancer diagnosis was as

119 ety of nonsteroidal anti-inflammatory drugs (NSAIDs) when used for arthritis are difficult to conduct

120 icine, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids reduce pain in patients wit

121 icine, nonsteroidal anti-inflammatory drugs (NSAIDs), and corticosteroids reduce pain in patients wit

122 pirin, nonsteroidal anti-inflammatory drugs (NSAIDs), and selective serotonin reuptake inhibitors (SS

123 use of nonsteroidal anti-inflammatory drugs (NSAIDs), but there have been few human studies of this a

124 of two nonsteroidal anti-inflammatory drugs (NSAIDs), diclofenac (Dic) and naproxen (Nps), were studi

125 roids, nonsteroidal anti-inflammatory drugs (NSAIDs), or colchicine to treat patients with acute gout

126 luding nonsteroidal anti-inflammatory drugs (NSAIDs), which are potent inhibitors of phospholipase A2

127 ective nonsteroidal anti-inflammatory drugs (NSAIDs), which further increase the risk of gastrointest

128 uch as nonsteroidal anti-inflammatory drugs (NSAIDs).

129 ebo or nonsteroidal anti-inflammatory drugs (NSAIDs)?

130 ons, 2 nonsteroidal anti-inflammatory drugs [NSAIDs] or aspirin, 17 hormones, and 7 lipid-lowering ag

131 esia (non-steroidal anti-inflammatory drugs [NSAIDs]), diabetes (metformin), depression/anxiety (anti

132 We evaluated NSAID-hypersensitivity over time in NIUA patients.

133 of healthy control mice or those exhibiting NSAID-induced enteropathy.

134 These data suggest that fenamate NSAIDs could be repurposed as NLRP3 inflammasome inhibit

135 nfants born at 28 weeks or younger following NSAID treatment for PDA initiated 2 to 28 days postnatal

136 For NSAID FDCs, 124 formulations were marketed, of which 34

137 The latest ENDA classification for NSAID hypersensitivity is generally a practical and usef

138 ers of centrally unapproved formulations for NSAID, anti-depressant/benzodiazepine, and anti-psychoti

139 We propose a model for NSAID-induced damage to the gastrointestinal tract that

140 among females and white patients except for NSAIDs, ACE inhibitors, and thiazide diuretics, which we

141 s of approved FDC formulations increased for NSAIDs (26%/28%) and anti-psychotics (0%/38%) and decrea

142 g patients who may particularly benefit from NSAID treatment.

143 stric damage and indeed protects the GI from NSAID-induced damage through a mechanism that requires F

144 d that omega-3 PUFAs can protect the GI from NSAID-induced damages by initiating the gatekeeper actio

145 at high risk for ulcer-related bleeding from NSAIDs should take a PPI if they continue to take NSAIDs

146 AIDs) or selected antiplatelet agents (e.g., NSAID prescription in a patient with chronic kidney dise

147 nd 308 patients who were confirmed as having NSAID hypersensitivity were included in this study.

148 patients, there is strong evidence of higher NSAIDs use 1-3 months compared to 10-12 months prior to

149 However, NSAIDs are associated with higher rates of adverse event

150 uvant applications in EOC and found that (i) NSAID Indomethacin induces robust cell death in primary

151 In conclusion, if NSAIDs use reflects underlying inflammatory symptoms, th

152 preference-based, institutional variation in NSAID treatment frequency to determine the effect of NSA

153 Treatment strategies including NSAIDs, steroids, MMC and corneal transplants have shown

154 For non-metastatic patients, increased NSAIDs use 1-3 months prior to diagnosis was also observ

155 aled that non-steroidal anti-inflammatories (NSAIDs) rank just as high as currently used ovarian canc

156 used drugs such as cyclooxygenase inhibiting NSAIDs, whereas others remain unexploited.

157 efined daily doses (DDDs) of MRP inhibitors (NSAIDs, PDE5-i, salicylates, dipyridamole) were collecte

158 pericarditis in North America and Europe is NSAID therapy.

159 ivity and structural similarities with known NSAIDs, we conducted structure-activity relationship stu

160 imed to evaluate the usability of the latest NSAID hypersensitivity classification of ENDA.

161 n-invasive means of detecting and monitoring NSAID enteropathy (and possibly other gastrointestinal m

162 eeding with NSAID treatment compared with no NSAID treatment (hazard ratio, 2.02 [95% CI, 1.81-2.26])

163 In non-NSAID users, an HR of 1.60 (95% CI: 0.88, 2.93) for high

164 12.3% in the NSAID group and 8.3% in the non-NSAID group (odds ratio, 1.70 [95% CI, 1.11-2.68]; P=.01

165 AID group and 417 patients [4.2%] in the non-NSAID group; P=.16).

166 SAB (OR = 0.78, 95% CI 0.56-1.10), while non-NSAID users were at increased risk (OR = 2.11, 95% CI 1.

167 w-dose aspirin (75 to 150 mg) and nonaspirin NSAIDs was defined according to type, estimated dose, du

168 riptions) of low-dose aspirin and nonaspirin NSAIDs were 1.03 (95% CI, 0.98 to 1.09) and 0.94 (CI, 0.

169 ricted internationally comprised over 12% of NSAID FDC sales and 53% of anti-psychotic FDC sales.

170 The molecular basis of NSAID inhibition of ASICs has remained unknown, hinderin

171 dence that supports the long-term benefit of NSAID therapy to prevent vision loss from CME at 3 month

172 ght to better understand the determinants of NSAID-dependent and NSAID-independent LTP-induced anaphy

173 ren with chronic urticaria, determination of NSAID hypersensitivity in a well-controlled clinical set

174 al bacteria contribute to the development of NSAID-associated enteropathy in human beings.

175 In this cohort of women, longer durations of NSAID and acetaminophen use were associated with slightl

176 f follow-up (1990-2012), longer durations of NSAID use (for >6 years of use compared with <1 year, mu

177 eatment frequency to determine the effect of NSAID treatment for PDA on mortality and BPD.

178 To determine the effectiveness of NSAID treatment for PDA in reducing mortality and modera

179 ous in closing PDA, but the effectiveness of NSAID-mediated PDA closure in improving mortality and pr

180 ts was based on a proved clinical history of NSAID-dependent or NSAID-independent anaphylaxis to LTPs

181 inosinusitis, smoking status, and history of NSAID-induced hypersensitivity reactions were sent to pa

182 The mechanism of NSAID inhibition is explored using molecular dynamics an

183 distal small intestine in a murine model of NSAID enteropathy.

184 Three major clinical phenotypes of NSAID-induced acute skin reactions manifesting with angi

185 The mean prevalence of NSAID-induced dyspnea was 1.9% and was highest in the th

186 ween European countries in the prevalence of NSAID-induced respiratory hypersensitivity reactions, an

187 s analysis was to estimate the prevalence of NSAID-induced respiratory symptoms in population across

188 The proportion of NSAID-treated infants at each infant's hospital within +

189 Proportion of NSAID-treated infants born at each infant's institution

190 stablish the diagnosis of a specific type of NSAID hypersensitivity, whereas in other cases oral prov

191 Although dosing of NSAIDs before surgery may hasten the speed of visual rec

192 , possibly explaining a protective effect of NSAIDs against cancer.

193 ian cancer associated with regular intake of NSAIDs, we assessed whether NSAIDs could have chemoadjuv

194 Also among nonusers of NSAIDs, risks of overall CRC, colon cancer, and proximal

195 proximal colon cancer and among nonusers of NSAIDs.

196 4 or IL-12, with and without the presence of NSAIDs.

197 On the basis of phase 4 RCTs of NSAIDs to date, it appears that a comparatively low dose

198 To determine the role of NSAIDs in colorectal surgery, future evaluations should

199 rdless of antithrombotic treatment, types of NSAIDs, or duration of use.

200 s, and cancer prevention by regular usage of NSAIDs.

201 mong long-term CRC survivors, regular use of NSAIDs after CRC diagnosis was significantly associated

202 bility of walking for 1 kilometer and use of NSAIDs at baseline and death information at follow-up.

203 However, the use of NSAIDs did not alter long-term (>/=3 months) visual outc

204 This toxic action greatly limits the use of NSAIDs in inflammatory bowel disease (IBD) and other chr

205 Use of NSAIDs vs opiates resulted in no significant difference

206 antithrombotic therapy after MI, the use of NSAIDs was associated with increased risk of bleeding an

207 Use of NSAIDs with ongoing antithrombotic treatment after first

208 r events was evident with concomitant use of NSAIDs, regardless of antithrombotic treatment, types of

209 ct effects via walking disability and use of NSAIDs, respectively.

210 one patient encountered anaphylaxis with one NSAID and urticaria with other NSAIDs, and the last pati

211 significant interaction with aspirin and/or NSAID use (P = 4.6 x 10(-9) for interaction).

212 roved clinical history of NSAID-dependent or NSAID-independent anaphylaxis to LTPs, positive skin pri

213 high-dose aspirin and low-dose ibuprofen or NSAID dosing schedules, there were several comparisons,

214 icant interaction with use of aspirin and/or NSAIDs (P = 8.2 x 10(-9) for interaction).

215 information on regular use of aspirin and/or NSAIDs and other risk factors.

216 Regular use of aspirin and/or NSAIDs was associated with lower risk of colorectal canc

217 ironment interactions, use of aspirin and/or NSAIDs was associated with lower risk of colorectal canc

218 ws that prophylaxis with daily colchicine or NSAIDs reduces the risk for acute gout attacks by at lea

219 ality through either a walking disability or NSAIDs use was 1.92 (95% CI: 0.86-4.26) and 1.45 (95% CI

220 rin patients not using antiplatelet drugs or NSAIDs (HR, 0.86; 95% CI, 0.70-1.06).

221 nts concurrently using antiplatelet drugs or NSAIDs, those without PPI co-therapy had 284 upper gastr

222 n patients also taking antiplatelet drugs or NSAIDs.

223 ajority (24; 63.15%) tolerated ASA and other NSAIDs (Group A) while 14 (36.84%) still reacted (Group

224 pectively re-evaluated by DPT with ASA/other NSAIDs at two time points between 2013 and 2015 (V2 and

225 axis with one NSAID and urticaria with other NSAIDs, and the last patient had angioedema with differe

226 the topical PA group, 0.3% in the topical PA+NSAID group (P = 0.13), and 0.8% for the TA group (P = 0

227 or the relationship of macular edema with PA+NSAID was 0.45 (95% CI, 0.21-0.95) and that for TA injec

228 e during ARI episodes, especially parenteral NSAIDs, was associated with a further increased risk of

229 Moreover, parenteral NSAIDs were associated with much higher risk in ARI pati

230 Periconceptional NSAIDs reported through the sixth week of pregnancy were

231 Bottom Line: Compared with placebo, NSAIDs are associated with a small but significant impro

232 Postoperative NSAIDs were associated with a significantly increased ri

233 In some countries, physicians prescribe NSAIDs for patients with ARI for symptom relief.

234 escribed and 1.7% among those not prescribed NSAIDs.

235 xercise appropriate caution when prescribing NSAIDs for patients who have recently experienced MI.

236 Adding a prophylactic NSAID to PA treatment was associated with a reduced risk

237 ] years; 60.7% women), 3158 (24.1%) received NSAIDs.

238 An infant's chances of receiving NSAID treatment increased by 0.84% (95% CI, 0.8-0.9; P <

239 Rectal NSAIDs have been shown in prospective studies to decreas

240 on-exchange would be ineffective at removing NSAIDs and other negatively charged compounds in urine.

241 Patients who required NSAIDs for osteoarthritis or rheumatoid arthritis and we

242 s the obstacles for the development of safer NSAIDs.

243 nium-nonsteroidal anti-inflammatory drug (Se-NSAID) hybrid molecules are reported.

244 uced urticaria/angioedema (NIUA), and single NSAID-induced urticaria and angioedema.

245 For example, in patients with single NSAID-induced reactions, chemically nonrelated COX-1 inh

246 re crucial for the entrance and exit of some NSAIDs from the COX active site.

247 fenamic acid (MEF)-a potent, highly specific NSAID inhibitor of 1A1.

248 pLTF was restored after IH-1 by systemic NSAID administration (ketoprofen; 55 +/- 9%; p < 0.001)

249 s should take a PPI if they continue to take NSAIDs.

250 ts will provide with a rationale for testing NSAIDs as potential chemoadjuvants in EOC patient trials

251 but recent small studies have suggested that NSAIDs may impair anastomotic healing in the gastrointes

252 m; 95% CI, -5.0 to 2.0 mm; P = .40), but the NSAID group required more rescue analgesia (26.3% vs 38.

253 These results thus define the NSAID/ASIC interaction and pave the way for small-molecu

254 Finally, the NSAID-binding site structure offers a template for devel

255 median age, 26 y; 42% female) were given the NSAID diclofenac (75 mg twice daily) plus omeprazole (20

256 for all patients (151 patients [4.8%] in the NSAID group and 417 patients [4.2%] in the non-NSAID gro

257 ry, for which the leak rate was 12.3% in the NSAID group and 8.3% in the non-NSAID group (odds ratio,

258 Using the NSAID-binding site structure of SULT1A1 as a comparative

259 scores in the opiate group (n = 150) vs the NSAID group (n = 144) were not significantly different (

260 wever, there is cross-reactivity between the NSAIDs in patients with NSAID-exacerbated cutaneous dise

261 sary to further investigate the use of these NSAIDs in cockatiels.

262 Correlation of PCME to NSAID use and the presence of pre-operative risk factors

263 are intolerant, or have contraindications to NSAIDs and colchicine.

264 Decreased PGE2 signaling due to NSAIDs or increased PGE2 due to exogenous delivery dicta

265 Within the group of patients with HDRs to NSAIDs, APs can induce immediate SRs.

266 in hypersensitivity drug reactions (HDRs) to NSAIDs, no patient series studies have been performed re

267 h a history of hypersensitivity reactions to NSAIDs among the 1250 outpatients referred for suspected

268 ts (1.6%), the hypersensitivity reactions to NSAIDs did not meet the ENDA classification: Three patie

269 , the prevalence of respiratory reactions to NSAIDs was higher in participants with chronic rhinosinu

270 NIUA patients may develop tolerance to NSAIDs over time, a process that seems to be influenced

271 Topical NSAIDs significantly reduced the odds of developing CME,

272 Topical NSAIDs were associated with a modest reduction of PME in

273 as sprains, strains, and contusions, topical NSAIDs are associated with greater pain relief, but are

274 A combination of topical NSAIDs and corticosteroids reduced the odds of developin

275 had a perioperative prescription of topical NSAIDs filled in addition to topical steroids were compa

276 evidence); and antihypertensives (4 trials), NSAIDs (1 trial), and statins (1 trial) did not alter de

277 ides a molecular framework for understanding NSAID binding and isoform specificity.

278 Unlike NSAIDs, ARN2508 causes no gastric damage and indeed prot

279 I episodes, ARI episodes without NSAIDs use, NSAIDs use only, or no exposure.

280 inhibitors) derivatized with clinically used NSAIDs (indomethacin, sulindac, ketoprofen, ibuprofen, d

281 several clinically approved and widely used NSAIDs of the fenamate class are effective and selective

282 e randomized to receive opiates (n = 103) vs NSAIDs (n = 103), and those not undergoing thoracoscopy

283 egular intake of NSAIDs, we assessed whether NSAIDs could have chemoadjuvant applications in EOC and

284 ver, there is no research evaluating whether NSAIDs use during ARI episodes may increase the risk of

285 As improves GI safety when administered with NSAID.

286 s of that infant's birth was associated with NSAID treatment and not associated with gestation, race/

287 alysis found increased risk of bleeding with NSAID treatment compared with no NSAID treatment (hazard

288 no evidence that the benefits observed with NSAID therapy could not be obtained similarly with equiv

289 ctical clinical approach to the patient with NSAID-induced urticaria and angioedema.

290 activity between the NSAIDs in patients with NSAID-exacerbated cutaneous disease and NIUA, and thus o

291 Conversely, patients with NSAID-LTP-A were characterized by reduced expression of

292 nalysis of blood cells from 14 patients with NSAID-related LTP-A (NSAID-LTP-A), 7 patients with LTP-A

293 (95% CI 1.12-1.67)) compared to people with NSAID-tolerant asthma.

294 lation in patients with LTP-A and those with NSAID-LTP-A of the IFN-gamma pathway, IgG receptors, and

295 ree from the adverse effects associated with NSAIDs.

296 quent triggers of drug hypersensitivity with NSAIDs-induced urticaria/angioedema (NIUA) the most comm

297 zation will allow for chronic treatment with NSAIDs in some patients with NIUA.

298 treatment and 2.2 (95% CI, 2.1-2.3) without NSAID treatment, whereas the rates of cardiovascular eve

299 ence interval [CI] = 2.80-4.16), ARI without NSAIDs use was associated with a 2.7-fold increased risk

300 se during ARI episodes, ARI episodes without NSAIDs use, NSAIDs use only, or no exposure.

301 Several crystal structures with or without NSAIDs indicated that placement of a bulky residue at po