ライフサイエンスコーパス: NSAID

1 NSAID exposure was assessed by duration, dosage, and typ

2 NSAID inhibition of COX enzymes, along with luminal aggr

3 NSAID prescriptions, patient characteristics, and estima

4 NSAID use at baseline, NSAID use during the trial (incid

5 NSAID use during the trial, and the interaction between

6 NSAID use may carry significant risks in certain patient

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

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

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

10 NSAID-exacerbated respiratory disease (NERD) is recogniz

11 NSAIDs are known to modulate macroautophagy, a process i

12 NSAIDs containing benzoate or salicylate groups were ide

13 NSAIDs have analgesic, opioid-sparing, and anti-inflamma

14 NSAIDs interact with phospholipids and uncouple mitochon

15 D = 43 (49%), CD = 17 (19%), IBS = 14 (16%), NSAIDs = 12 (14%) and persistent NSE = 2 (2%).

16 th a total of 29 980 years of follow-up; 671 NSAID prescriptions in 273 (5.4%) patients (2.24 per 100

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 pical nonsteroidal anti-inflammatory agents (NSAIDs) proved to have the greatest net benefit, followe

20 Although NSAID use is discouraged in patients with cardiovascular

21 sible new drug candidates such as SC-560 (an NSAID), and amoxapine (an antidepressant), as well as na

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

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

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

25 Combining an optimal dose of an NSAID with an appropriate dose of acetaminophen appears

26 favorable benefit versus risk ratio than an NSAID regimen.

27 ents who had a gastrointestinal anastomosis, NSAIDs were not associated with anastomotic leak (adjust

28 n bacterial flora in the small intestine and NSAID-induced enteropathy.

29 D-exacerbated respiratory disease (NERD) and NSAID-exacerbated cutaneous disease (NECD).

30 Among eyes with steroid and NSAID combination therapy (n = 55), CRT increased 3.6 +/

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

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

33 se, NSAIDs-exacerbated cutaneous disease and NSAIDs-induced urticaria/angioedema.

34 Combination therapy of steroids and NSAIDs had no added benefit over steroids alone.

35 ent with combination therapy of steroids and NSAIDs showed no added benefit over steroid monotherapy

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

37 Tri a 19 sensitization, anaphylaxis, and any NSAID different from pyrazolones), 95.3% of cases were c

38 to early postoperative NSAIDs was defined as NSAID administration on postoperative days 0 to 3.

39 As NSAIDs are already in routine use in gynecological treat

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

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

42 d to the following variables: use of aspirin/NSAIDs/anti-coagulants/anti-platelets, pathologic diagno

43 Those with baseline NSAID use (n=832 [4.8%]), incident NSAID use (n=2185 [13

44 NSAID use at baseline, NSAID use during the trial (incident NSAID use), and nev

45 ly studies indicating an association between NSAID use and increased risks of heart failure and eleva

46 ure, subsequent studies found a link between NSAID use and an increased risk of thrombotic events.

47 significant interaction was observed between NSAID use and randomized treatment for any outcome.

48 on patterns of DHR, cross-reactivity between NSAID and pharmacological effects of these all drugs.

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

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

51 In the bloodstream, NSAIDs are mostly bound to serum albumin (SA).

52 appeared not significantly to be altered by NSAID use.

53 nding was consistent in subgroup analyses by NSAID dosage and timing.

54 the most frequent clinical entity induced by NSAID hypersensitivity.

55 from intestinal epithelial injury induced by NSAID.

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

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

58 d with steroid monotherapy (28.9% of cases), NSAID monotherapy (62.2%), or a combination of both (8.9

59 In this study, we have characterized NSAID interactions with human DHFR based on kinetic, NMR

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

61 arbamate group is readily attached to common NSAIDs, such as naproxen, to generate YZ-597 as an effic

62 ples were taken from patients with confirmed NSAID-induced urticaria and healthy controls, at baselin

63 i-inflammatory agents, such corticosteroids, NSAIDs and colchicine, are widely used for the treatment

64 egative oral provocation test to the culprit NSAID.

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

66 One 7-day NSAID course was associated with 5% higher odds of incre

67 and respiratory symptoms) or food-dependent NSAID-induced anaphylaxis.

68 NSAIDH occur in patients with food-dependent NSAID-induced hypersensitivity (FDNIH).

69 oup: NSAIDs-exacerbated respiratory disease, NSAIDs-exacerbated cutaneous disease and NSAIDs-induced

70 High-dose NSAID prescriptions were associated with 2.83 (95% confi

71 sing the nonsteroidal antiinflammatory drug (NSAID) Glafenine.

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

73 erative nonsteroidal anti-inflammatory drug (NSAID) administration and postoperative acute kidney inj

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

75 eported nonsteroidal anti-inflammatory drug (NSAID) allergies may predispose to use of stronger pain

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

77 yes and nonsteroidal anti-inflammatory drug (NSAID) drops in 2 eyes.

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

79 es with nonsteroidal anti-inflammatory drug (NSAID) monotherapy (n = 157), CRT increased 5.7 +/- 18.4

80 odified nonsteroidal anti-inflammatory drug (NSAID) naproxen.

81 topical nonsteroidal anti-inflammatory drug (NSAID) or steroid therapy affected the efficacy of selec

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

83 ed from nonsteroidal anti-inflammatory drug (NSAID) sulindac, suppresses the growth of tRXRalpha-medi

84 but not nonsteroidal anti-inflammatory drug (NSAID) treatment with sulindac prevented NASH and subseq

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

86 Nonsteroidal anti-inflammatory drug (NSAID) use is recommended to be avoided in kidney transp

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

88 itarget nonsteroidal anti-inflammatory drug (NSAID)-carbonic anhydrase inhibitor (CAI) agents for the

89 Nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD) asthma is

90 entiate nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (N-ERD).

91 ated in nonsteroidal anti-inflammatory drug (NSAID)-exacerbated respiratory disease (NERD).

92 del of non-steroidal anti-inflammatory drug (NSAID)-induced SI epithelial injury to show that IL-10 i

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

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

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

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

97 using nonsteroidal anti-inflammatory drugs (NSAIDs) alone (hazard ratio, 3.34; P = 0.042), and patie

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

99 Nonsteroidal anti-inflammatory drugs (NSAIDs) are effective, widely used analgesics.

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

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

102 Non-steroidal anti-inflammatory drugs (NSAIDs) cause damage in the small intestine in a bacteri

103 opical nonsteroidal anti-inflammatory drugs (NSAIDs) for the reduction of ocular pain after intravitr

104 th of non-steroidal anti-inflammatory drugs (NSAIDs) has progressively raised the attention toward th

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

106 which nonsteroidal anti-inflammatory drugs (NSAIDs) induce apoptosis in gastric cancer and normal mu

107 ity to nonsteroidal anti-inflammatory drugs (NSAIDs) is of great concern because they are frequently

108 act of nonsteroidal anti-inflammatory drugs (NSAIDs) on survival in a PIK3CA-characterized cohort of

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

110 ced by nonsteroidal anti-inflammatory drugs (NSAIDs) remains an under-recognized clinical disorder.

111 acy of nonsteroidal anti-inflammatory drugs (NSAIDs) such as ibuprofen, naproxen sodium, etodolac, di

112 though nonsteroidal anti-inflammatory drugs (NSAIDs) target primarily cyclooxygenase enzymes, a subse

113 ion to nonsteroidal anti-inflammatory drugs (NSAIDs) to access H(2)S-NSAID hybrids with significantly

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

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

116 opical nonsteroidal anti-inflammatory drugs (NSAIDs) with or without menthol gel as first-line therap

117 use of nonsteroidal anti-inflammatory drugs (NSAIDs) with oral anticoagulants has been associated wit

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

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

120 e take nonsteroidal anti-inflammatory drugs (NSAIDs), often in conjunction with multiple other medica

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

122 Nonsteroidal anti-inflammatory drugs (NSAIDs), the medications most commonly used for treating

123 ce to non-steroidal anti-inflammatory drugs (NSAIDs).

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

125 s to detect eliciting dose thresholds during NSAIDs DPT in order to suggest optimal step doses, using

126 AKI rates were 10.6% in the early NSAID group and 14.9% in the no NSAID group.

127 19.8% (1039/5240) of patients received early NSAIDs.

128 able bowel syndrome (IBS), NSAIDs enteritis (NSAIDs), persistent NSE and no significant disease (NAD)

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

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

131 ltered HNSCC, predicted 5-yr DSS was 72% for NSAID users and 25% for nonusers; predicted 5-yr OS was

132 However, no information is available for NSAID-induced urticarial/angioedema (NIUA), despite it b

133 persensitivity has been studied in depth for NSAID-exacerbated respiratory disease (NERD) and NSAID-e

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

135 Drug provocation test protocols for NSAID are empirical, driven by the knowledge on patterns

136 ysis of variance] and P = 0.002 [t test] for NSAID vs. placebo groups; P = 0.02 for steroid vs. place

137 ion tests (DPTs) are particularly needed for NSAIDs.

138 Prescriptions for NSAIDs were uncommon in this cohort but were associated

139 of equine serum albumin complexed with four NSAIDs (ibuprofen, ketoprofen, etodolac, and nabumetone)

140 g patients who may particularly benefit from NSAID treatment.

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

142 Three phenotypes fill into the first group: NSAIDs-exacerbated respiratory disease, NSAIDs-exacerbat

143 gy is essential for gastrointestinal health, NSAID-induced inhibition of macroautophagy might contrib

144 he risk of AKI, which was impacted by higher NSAID dose and longer NSAID durations.

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

146 isease (CD), Irritable bowel syndrome (IBS), NSAIDs enteritis (NSAIDs), persistent NSE and no signifi

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

148 iologically plausible rationale to implement NSAID therapy in PIK3CA-altered HNSCC.

149 The role of arachidonic acid metabolites in NSAID-induced hypersensitivity has been studied in depth

150 a was more frequent in N-ERD (54.5%) than in NSAID-tolerant asthma (9.5% [P = .009]).

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

152 Incident NSAID use was associated with major and clinically relev

153 baseline NSAID use (n=832 [4.8%]), incident NSAID use (n=2185 [13.2%]), and never users were similar

154 hose with NSAID use at baseline and incident NSAID use were more likely to have a history of bleeding

155 ng NSAID at baseline, we found that incident NSAID use was associated with an increased risk of major

156 seline, NSAID use during the trial (incident NSAID use), and never users were described.

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

158 Non-steroidal anti-inflammatories (NSAIDs), such as meloxicam, are the mainstay for treatin

159 Patients with listed NSAID ADRs also had higher odds of a documented opioid p

160 was impacted by higher NSAID dose and longer NSAID durations.

161 nonsteroidal anti-inflammatory medications (NSAIDs), or their combination.

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

163 We hypothesize that some negative NSAID challenge tests and an overdiagnosis of NSAIDH occ

164 in the early NSAID group and 14.9% in the no NSAID group.

165 4.8% in the NSAIDs group and 6.0% in the no NSAIDs group.

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

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

168 , 95% CI 0.14-0.69) compared with nonregular NSAID users.

169 Fasting and excess of allergen, but not NSAID and exercise, were other relevant cofactors for sy

170 ermeability, resulting in the aggravation of NSAID-induced small intestinal damage.

171 We discuss the consequences of NSAID binding to SA in a broader scientific and medical

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

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

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

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

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

177 rrelates with the clinical manifestations of NSAID enteropathy, however, remains unknown.

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

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

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

181 Short-term postoperative use of NSAID or steroid drops may improve IOP reduction after S

182 The administration of NSAIDs before the procedure, specifically topical nepafe

183 effect size was seen with administration of NSAIDs before versus after IVI, as well as topical nepaf

184 ans; however, the repeated administration of NSAIDs can cause adverse effects, limiting the long-term

185 Administration of NSAIDs in the early postoperative period is safe in sele

186 The latest classification of NSAIDs hypersensitivity by the European Academy of Aller

187 Diagnosis of NSAIDs hypersensitivity is hampered by different factors

188 warrants more investigation of the effect of NSAIDs on the outcomes of patients treated with apixaban

189 nding our understanding about the effects of NSAIDs in the body could lead to the discovery of mechan

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

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

192 proximal colon cancer and among nonusers of NSAIDs.

193 ophagy were dysfunctional in the presence of NSAIDs.

194 ent evidence on the cardiovascular safety of NSAIDs and present an approach for their use in the cont

195 rimarily cyclooxygenase enzymes, a subset of NSAIDs containing carboxylate groups also has been repor

196 opioid achieved benefit greater than that of NSAIDs, and opioids caused the most harms.

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

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

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

200 as opioids) for pain management, the use of NSAIDs is likely to rise.

201 wing propensity score matching, early use of NSAIDs was not significantly associated with AKI (adjust

202 Furthermore, non-prescription use of NSAIDs, even among people with underlying cardiovascular

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

204 es are focused on optimizing the safe use of NSAIDs.

205 ibitors, chemopreventive strategies based on NSAIDs and statins are currently being investigated for

206 circumferential trabeculotomy and using only NSAIDs may be more likely to result in surgical success

207 was measured in eyes treated with steroid or NSAID drops after SLT.

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

209 cal NSAIDs as first-line treatments and oral NSAIDs and intra-articular injections for persistent pai

210 Topical NSAIDs, followed by oral NSAIDs and acetaminophen with or without diclofenac, sho

211 e the greatest net benefit, followed by oral NSAIDs and acetaminophen with or without diclofenac.

212 low back, musculoskeletal injuries with oral NSAIDs to reduce or relieve symptoms, including pain, an

213 Other NSAIDs did not induce IEC delamination; however, Glafeni

214 apsulotomy rates with steroid treatment over NSAIDs (HR 0.70, 95% CI 0.52-0.88, P = .001).

215 mproved pain relief compared with the parent NSAIDs.

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

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

218 Periconceptional NSAIDs reported through the sixth week of pregnancy were

219 Exposure to early postoperative NSAIDs was defined as NSAID administration on postoperat

220 ation than those that received postoperative NSAIDs alone, which may suggest corticosteroid-mediated

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

222 escribed and 1.7% among those not prescribed NSAIDs.

223 At 6 hours after the procedure, NSAIDs provide a clinically meaningful reduction in pain

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

225 didates for discriminating animals receiving NSAIDs from healthy controls.

226 h PIK3CA mutations or amplification, regular NSAID use (>=6 mo) conferred markedly prolonged disease-

227 users; predicted 5-yr OS was 78% for regular NSAID users and 45% for nonregular users.

228 ronic back pain, 3,620 (7.7%) had a reported NSAID ADR.

229 Adults with chronic back pain and reported NSAID ADRs are at a higher risk of developing OUD and re

230 investigate the clinical impact of reported NSAID allergy on OUD in patients with chronic back pain.

231 sion to estimate the impact of self-reported NSAID adverse drug reactions (ADRs) on risk of OUD, adju

232 tential delabeling of patients with reported NSAID allergies and chronic pain.

233 en, to generate YZ-597 as an efficient H(2)S-NSAID hybrid, which we demonstrate releases H(2)S in cel

234 -inflammatory drugs (NSAIDs) to access H(2)S-NSAID hybrids with significantly reduced toxicity, but t

235 s the obstacles for the development of safer NSAIDs.

236 cs that are at least as effective but safer, NSAIDs are frequently prescribed.

237 associated with the usage of COX-2 selective NSAIDs.

238 ts but concern also relates to non-selective NSAIDs, especially those with strong COX2 inhibition suc

239 selective but also extended to non-selective NSAIDs, such as Diclofenac and Ketoprofen.

240 ral confounding factors, including male sex, NSAID coadministration, advanced age, and prior diagnose

241 urticaria/angioedema/anaphylaxis and single-NSAID-induced delayed reactions.

242 atients, using patients with NECD and single-NSAID-induced urticaria/angioedema or anaphylaxis (SNIUA

243 phenotypes fill into the second one: single-NSAID-induced urticaria/angioedema/anaphylaxis and singl

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

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

246 , 2.3) years and when excluding those taking NSAID at baseline, we found that incident NSAID use was

247 in patients with atrial fibrillation taking NSAIDs and apixaban or warfarin.

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

249 We show that NSAID treatment of IECs inhibits macroautophagy in vitro

250 The NSAID, steroid, and placebo groups were similar in basel

251 Both the NSAID and steroid groups showed a statistically signific

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

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

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

255 vage in rat or human plasma depending on the NSAID portion.

256 astric injury model, here we report that the NSAID indomethacin activates the protein kinase Czeta (P

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

258 The NSAIDs target a region of the folate binding site that i

259 who received an anastomosis was 4.8% in the NSAIDs group and 6.0% in the no NSAIDs group.

260 a 1- or 2-d course of opioids added to their NSAID regimen.

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

262 an inadequate response or were intolerant to NSAID therapy.

263 cutaneous symptoms or anaphylaxis related to NSAID, (3) positive skin prick test to foods and/or spec

264 s about the disadvantages of alternatives to NSAIDs (such as opioids) for pain management, the use of

265 y lower Nd:YAG capsulotomy rates compared to NSAIDs (hazard ratio [HR] 0.76, 95% confidence interval

266 In addition to being on average inferior to NSAIDs as analgesics in postsurgical dental pain, opioid

267 mechanism(s) associated with intolerance to NSAIDs.

268 spicion of drug hypersensitivity reaction to NSAIDs.

269 PIK3CA mutation predicted sensitivity to NSAIDs in preclinical models in association with increas

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

271 mber of patients in the ARISTOTLE trial took NSAIDs.

272 he RCTs that treated patients with a topical NSAID and assessed postprocedural pain were included.

273 scale was significantly lower after topical NSAID administration relative to control at 1 hour or le

274 eroid therapy that resolved when the topical NSAID was stopped and difluprednate was tapered down to

275 evation of intraocular pressure with topical NSAID and steroid therapy that resolved when the topical

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

277 Topical NSAIDs, followed by oral NSAIDs and acetaminophen with o

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

279 and weight loss as core treatments, topical NSAIDs as first-line treatments and oral NSAIDs and intr

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

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

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

283 Whether NSAIDs stimulate or repress macroautophagy and how this

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

285 ives of this study were to determine whether NSAIDs impaired macroautophagy and how this affects macr

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

287 en is reported, the mechanisms through which NSAIDs cause adverse cardiovascular events are not entir

288 1 to 2010 that assessed for risk of AKI with NSAID prescriptions.

289 s the risk of acute kidney injury (AKI) with NSAID use.

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

291 ensity score-matched analysis, patients with NSAID ADRs had higher odds (odds ratio, 1.34; 95% CI, 1.

292 patients with N-ERD (n = 22), patients with NSAID-tolerant asthma (n = 21), and control subjects (n

293 Those with NSAID use at baseline and incident NSAID use were more l

294 Older age was associated with NSAIDs enteritis, while more subjects without significan

295 oint pain and improve function compared with NSAIDs for a duration of up to 8 weeks.

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

297 ule opacification compared to treatment with NSAIDs alone.

298 eveloping OUD as compared with those without NSAID ADRs.

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.