ライフサイエンスコーパス: treatment failure

1 at 6 months (or prior, in the event of early treatment failure).

2 how rapid infection of all epithelial cells (treatment failure).

3 al pocket) mainly contributed to determine a treatment failure.

4 n was used to assess factors associated with treatment failure.

5 The presence of fever and wheeze predicted treatment failure.

6 est risk for early toxicity-related death or treatment failure.

7 mors develop acquired resistance, leading to treatment failure.

8 disease were associated with a lower risk of treatment failure.

9 variation in venom composition can result in treatment failure.

10 nt and independent mechanisms of osimertinib treatment failure.

11 ld be reduced while maintaining detection of treatment failure.

12 seen in patients who relapsed or experienced treatment failure.

13 to an initial oncogenic driver, resulting in treatment failure.

14 microbiological relapse, and microbiological treatment failure.

15 and prevent emergence of drug resistance and treatment failure.

16 nto those at risk of disease, recurrence, or treatment failure.

17 5 (38.5%) also harbored NS5B S282C/T RASs at treatment failure.

18 for virus factors associated with sofosbuvir treatment failure.

19 th multidrug-resistant tuberculosis (TB) and treatment failure.

20 t, a positive PET-2 was highly predictive of treatment failure.

21 : 1.8, 95% CI: 1.1-3.0) were associated with treatment failure.

22 w-income countries often delays detection of treatment failure.

23 cal resection remains a significant cause of treatment failure.

24 t for at-risk patients is adapted to prevent treatment failure.

25 ide antimicrobial therapy and possibly avert treatment failure.

26 ons (RASs) have been shown to play a role in treatment failure.

27 alize and/or adjust therapy schemes to avoid treatment failure.

28 ations that correlate with increased risk of treatment failure.

29 sitive PET-2 result was highly predictive of treatment failure.

30 t the presence of Tet(X4) led to tigecycline treatment failure.

31 identify which factors were associated with treatment failure.

32 tment failure, and 8 died without documented treatment failure.

33 oad and euro 1659 per percentage decrease in treatment failure.

34 34 centers admitted for AVB and high risk of treatment failure.

35 es, which contributes to drug resistance and treatment failure.

36 res were glycaemic control, weight gain, and treatment failure.

37 rvival, overall survival, and the pattern of treatment failure.

38 induced bronchodilation is the main cause of treatment failure.

39 with advanced liver disease were at risk of treatment failure.

40 on or deregulated innate immune responses in treatment failure.

41 6 [0.74-1.53]; p = 0.75) was associated with treatment failure.

42 l time between the DAIR procedure and future treatment failure.

43 ortality, persistent bacteremia, relapse, or treatment failure.

44 h may contribute to some instances of fungal treatment failure.

45 n adjunct treatment to reverse antipsychotic treatment failure.

46 failure was 18.5% compared to 10.1% without treatment failure.

47 t gastrointestinal pathogens and the risk of treatment failures.

48 sociated with increasing drug resistance and treatment failures.

49 There were no early treatment failures.

50 chanism of this key mediator of antimalarial treatment failures.

51 ere costs per reduction in log10 viral load, treatment failure (2 consecutive detectable viral loads)

52 nts, and is associated with greater rates of treatment failure (23% vs 12%) and mortality, despite lo

53 n 15.9% (early treatment failure, 7.9%; late treatment failure, 7.9%) of isolates.

54 ASSP failure was recorded in 15.9% (early treatment failure, 7.9%; late treatment failure, 7.9%) o

55 sociated with dihydroartemisinin-piperaquine treatment failure after adjusting for the presence of am

56 atric solid tumor, to identify mechanisms of treatment failure after initial response has become of i

57 patients with HCV genotype 1 infection with treatment failure after sofosbuvir and an NS5A inhibitor

58 tients with hepatitis C (HCV) infection with treatment failure after sofosbuvir plus an NS5A inhibito

59 A very high rate of treatment failure after treatment with dihydroartemisini

60 infections (aIRR 1.47, 95% CI 1.02-2.13) or treatment failure (aIRR 1.80, 95% CI 1.22-2.66) had sign

61 5% confidence interval {CI}, 1.01-1.47]) and treatment failure (aIRR, 1.16 [95% CI, 1.05-1.28]).

62 At treatment failure, all subtype 4r patients harbored two

63 trations, unfavorable outcomes (composite of treatment failure, all-cause mortality, and recurrence),

64 icity among slow NAT2 acetylators and reduce treatment failure among rapid acetylators.

65 In genotype 1 infected patients with treatment failure and 156-RASs, we observed genome-wide

66 of CMV viremia, a higher rate of first-line treatment failure and a longer time to virus clearance.

67 AWC-PCA was associated with reduced treatment failure and a reduced vasopressor requirement

68 rospective cohort, the primary outcomes were treatment failure and adverse events 14 days after diagn

69 earance time (FCT); secondary endpoints were treatment failure and adverse events.

70 Treatment failure and AKI occurred in 18% and 26% of pat

71 stinguish patients with the highest risk for treatment failure and bacteremia-related complications,

72 culture conversion, and the highest rates of treatment failure and death.

73 d neck squamous cell carcinomas (HNSCC), yet treatment failure and disease recurrence are common.

74 Factors associated with treatment failure and enucleation of plaqued eyes were e

75 Local treatment failure and enucleation were relatively infreq

76 imate the cumulative risk of postirradiation treatment failure and enucleation.

77 rt of these patients before ADR will prevent treatment failure and HIV-1 transmission.

78 was performed in all subtype 4r patients at treatment failure and in 6 at baseline, whereas full-len

79 identifying subpopulations at high risk for treatment failure and loss to care is critically importa

80 We aim to describe risk factors for treatment failure and mortality among patients with cUTI

81 osis because it can reduce the high rates of treatment failure and mortality.

82 falciparum parasites to distinguish between treatment failure and new infection occurring during the

83 exposure to critical medications, leading to treatment failure and other medical complications.

84 endocrine differentiation is associated with treatment failure and poor outcome in metastatic castrat

85 medulloblastoma (SHH MB) is associated with treatment failure and poor outcome.

86 herapy has increased long-term survivorship, treatment failure and rapid tumor recurrence remains uni

87 Index admission antibiotic treatment failure and rate of recurrence at 1-year follo

88 In CP-C and CP-B+AB patients, p-TIPS reduced treatment failure and rebleeding (1-year cumulative inci

89 dazole is the first-line treatment; however, treatment failure and recurrence rates remain high.

90 ntratumor heterogeneity the major reason for treatment failure and recurrence.

91 , but these therapies still suffer from high treatment failure and recurrence.

92 eloid leukemias and a significant reason for treatment failure and relapse.

93 were fever clearance time and frequencies of treatment failure and relapse.

94 ukemia, high cortactin levels correlate with treatment failure and relapse.

95 en further, and review different options for treatment failure and resistance.

96 Descriptive analyses were used to report treatment failure and subsequent management and evaluate

97 ts often decreases over time, which leads to treatment failure and symptom recurrence.

98 shed both human immunodeficiency virus (HIV) treatment failure and the acquired resistance to drugs i

99 We studied time to treatment failure and time to viral suppression among 14

100 baseline and outcome characteristics between treatment failures and nonfailures was the distance to t

101 We aimed to differentiate reinfections from treatment failures and to identify transmission linkages

102 This inevitably results in treatment failures and, for some, an unacceptable risk/b

103 dels for time to viral load >1000 copies/mL (treatment failure), and simulated data for 10 000 indivi

104 for time to viral load above 1000 copies/ml (treatment failure), and simulated data for 10,000 indivi

105 nfected with different strains, 1 had a late treatment failure, and 1 was transiently viremic 17 mont

106 Results: 43 patients had hormonal treatment failure, and 8 died without documented treatme

107 who achieved an objective response, time to treatment failure, and overall survival after treatment.

108 icient for daptomycin resistance, antibiotic treatment failure, and persistent infection.

109 variation may contribute to drug tolerance, treatment failure, and relapse in human TB.

110 I); microbiological relapse; microbiological treatment failure; and duration of intravenous antibioti

111 ng stigma; expanding surveillance of AMR and treatment failures; and promoting responsible antimicrob

112 In addition to antimicrobial resistance, treatment failures are increasingly understood to derive

113 archical composite outcome that incorporated treatment failure, asthma control days, and the forced e

114 complex orthopedic infection, as assessed by treatment failure at 1 year.

115 Treatment failure at 30 days occurred in 42 (26%) of 159

116 Secondary outcomes included treatment failure at day 30 (ie, recurrence of acute exa

117 5% CI, 1.47 to 2.80]; moderate SOE) and less treatment failure at the end of the intervention (OR, 0.

118 n for 9 to 56 days were associated with less treatment failure at the end of the intervention (OR, 0.

119 arance times and the increasing frequency of treatment failures, attributed to the increased toleranc

120 idence of an unfavorable outcome, defined as treatment failure (bacteriologic or clinical) or relapse

121 Secondary endpoints were treatment failure (biopsy-proven acute rejection, graft

122 The primary outcome was treatment failure by day 4 for intervention clusters and

123 4 of 1429 (10.8%) in the 5-day group had had treatment failure by day 6 or relapse by day 14 (between

124 The primary outcome was treatment failure by day 6; noninferiority of the 3-day

125 additional patient harbored S282C/T RASs at treatment failure by deep sequencing.

126 The hazard ratio of treatment failures by 28 days between azithromycin and S

127 study is needed to determine if the risk of treatment failure can be decreased by using this assay t

128 ociated with a significantly reduced risk of treatment failure compared with stable dose (OR 0.82, 95

129 The primary treatment failure composite outcome (re-treatment of pro

130 between 68 cases with unfavorable outcomes (treatment failure, death or recurrence) and 136 control

131 Predictors of treatment failure/death were the absence of directly obs

132 o assess independent predictors of RR-TB and treatment failure/death.

133 d with placebo, did not significantly reduce treatment failure (defined as death or persistent respir

134 The time to treatment failure (defined by specific criteria as persi

135 t was the time from randomisation to initial treatment failure, defined as HbA(1c) measurement of at

136 telephone interviews.The primary outcome was treatment failure, defined as need for a secondary inter

137 The primary endpoint was treatment failure, defined as the presence of residual a

138 or each patient and could be responsible for treatment failure despite multi-target approaches.

139 poses one of the key challenges to overcome treatment failure due to resistant cell populations.

140 o 2 drops of prednisolone acetate 1%, and no treatment failure due to safety or intolerability.

141 eting such alterations has frequently led to treatment failures due to underlying genomic complexity

142 The incidence of initial treatment failure during period 1 was 429 (43.6%) patien

143 The primary outcome was treatment failure during the 3-day course of amoxicillin

144 ween the fast clearance of infused bnAbs and treatment failure during the acute period of infection.

145 ever, nearly half of all patients experience treatment failure during the first year.

146 A semiautomated algorithm assessed risk of treatment failure early in treatment in 251 patients und

147 Treatment failure endpoints were primary non-response at

148 ears, of whom 230 (7.2%) had experienced 292 treatment failure events (161 virologic, 128 immunologic

149 Of the 292 treatment failure events, 31 (10.6%) had a subsequent cA

150 9.3%) completed the study, and there were 69 treatment failure events, including 11 deaths in the hyd

151 The basis of fluoroquinolone treatment failure for Mycoplasma genitalium is poorly un

152 Relapse remains the most common cause of treatment failure for patients with acute myeloid leukem

153 Time to treatment failure for patients with CR was time from CR

154 HIV infection (PHIVA) should be a focus for treatment failure given their poorer outcomes compared t

155 Among children with day 6 data available, treatment failure had occurred in 5.9% in the 3-day grou

156 The main secondary outcome was treatment failure (having neither responded nor remitted

157 ed HCV; cured HCV (HCV RNA-negative); or HCV treatment failures (HCV RNA-positive).

158 e of heteroresistance with the potential for treatment failure highlights the limitations of MIC as t

159 s not associated with antibiotic eradication treatment failure; however, nosocomial strain transmissi

160 rvival (OS) (HR = 1.24, p = 0.47) or time to treatment failure (HR = 0.85, p = 0.44).

161 essful treatment in 60 patients (58%), and a treatment failure in 7 patients (7%).

162 hemoresistance, and high expression predicts treatment failure in acute myeloid leukemia (AML).

163 rvoirs, investigation into the mechanism for treatment failure in acutely infected macaques would be

164 ibiotics and systemic corticosteroids reduce treatment failure in adults with mild to severe exacerba

165 Treatment failure in biofilm-associated bacterial infect

166 Treatment failure in eosinophilic esophagitis (EoE) is c

167 0 eligible studies, the pooled prevalence of treatment failure in HIV-infected women was 21.4% (95% c

168 The only significant predictor of treatment failure in HIV-infected women was a positive m

169 is strong evidence for an increased risk of treatment failure in HIV-infected women, in comparison t

170 Risk factors for treatment failure in multivariable analysis were ICU adm

171 define relapses associated with high risk of treatment failure in patients and at the same time empha

172 omenon may be a major contributing factor in treatment failure in patients with atopic dermatitis, ye

173 e a possible mechanism underlying vancomycin treatment failure in patients with CDI, but further work

174 lactam on mortality, bacteremia, relapse, or treatment failure in patients with MRSA bacteremia: a ra

175 faces significant difficulties resulting in treatment failure in several renal disorders.

176 vide important insights into the reasons for treatment failure in some settings.

177 associated with greater risk of relapse and treatment failure in substance use disorder.

178 be shown if the percentage of children with treatment failure in the 3-day group was no more than 1.

179 the fast clearance of infused bnAbs and the treatment failure in the acute period of SHIV infection

180 The median observed time to treatment failure in the monotherapy group was 36.1 (IQR

181 lure were distinct, with all patients having treatment failure in the spine.

182 Despite similar FCT and treatment failure in the two arms, significantly fewer c

183 nSTI-based regimens, factors associated with treatment failure, in particular high viral load and low

184 ive-behavioral therapy (ICBT), where risk of treatment failure is assessed early in treatment and tre

185 Treatment failure is associated with increased risks for

186 Anti-TNF treatment failure is common and is predicted by low drug

187 ts for the management of Crohn's disease but treatment failure is common.

188 Surgical outcomes such as initial treatment failure, late recurrence, neurological improve

189 e in bacterial mortality leading to clinical treatment failure, lengthy hospital stay, intravenous th

190 PN0 unirradiated neck; they also experienced treatment failure locally.

191 n = 8), compared to those from patients with treatment failure (n = 8).

192 samples from CL patients (cures, n = 20, and treatment failure, n = 20), showing putative association

193 The highest rates of treatment failure occur in specific genetic subsets of A

194 s used to treat serious MRSA infections, but treatment failures occur despite MRSA strains being test

195 Treatment failure occurred in 294 patients (38%) and was

196 Treatment failure occurred in 294 patients (38%) and was

197 In a secondary per-protocol analysis, treatment failure occurred in 49 of 339 infants (14.5%)

198 Treatment failure occurred in 74 of 506 participants (14

199 Treatment failure occurred in 78 of 381 infants (20.5%)

200 cer therapy, accumulating reports showed the treatment failure of conventional Pt(II) drugs, which is

201 e apparent intracellular H. pylori (aiHp) on treatment failure of first-line triple therapies.

202 seline minor InSTI resistance mutations, for treatment failure of InSTI-based regimens.

203 ow-up of 53 months, two patients experienced treatment failure of the PN0 unirradiated neck; they als

204 However, treatment failure often ensues due to tumor intrinsic or

205 The primary outcome, treatment failure on day 21, occurred in 32 of 76 patien

206 The primary outcome, treatment failure on day 21, was defined as death or per

207 tarting antibiotics were not associated with treatment failure or 30-day mortality.

208 us 71 (18%) who received placebo experienced treatment failure or disease recurrence, or died (absolu

209 roendocrine biomarker levels did not predict treatment failure or early progression (P >= 0.13).

210 ed secondary analyses included assessment of treatment failure or relapse by day 14.

211 ted with significantly lower odds of initial treatment failure (OR: 0.15, 95% CI 0.09 to 0.24, I(2) 0

212 nts with normal or high BMIs, rates of cure, treatment failure, or death did not vary by glycemic sta

213 howed a difference in the risk of definitive treatment failure (oral group vs. intravenous group) of

214 my were 2.56 times more likely to experience treatment failure (P = 0.002) compared with those who un

215 er two cycles ABVD indicates a high risk for treatment failure, particularly when a Deauville score o

216 There was no significant difference in the treatment failure prevalence for cryotherapy (13.9%, 95%

217 re (13.8%, 95% CI 8.9-18.7; P = .9), but the treatment failure prevalence was significantly higher in

218 Given the substantial risk of treatment failure, primary PDT with vertepofrin is recom

219 eatment response biomarker, while predicting treatment failure prior to treatment initiation.

220 Observed treatment failure rate (8.8%) was significantly lower th

221 No significant difference in treatment failure rate was observed between eculizumab (

222 The primary end point was treatment failure rate, a composite of biopsy-proved gra

223 primary end point was week 9 posttransplant treatment failure rate, a composite of: biopsy-proven ac

224 nevertheless, this afforded no advantage in treatment failure rates nor mortality in these patients.

225 When reassessment included grade I AMR, the treatment failure rates were 11.8% (eculizumab) and 29.4

226 The resulting treatment failure rates were 11.8% and 21.6% for the ecu

227 Treatment failure rates were 3.6% (326) in intervention

228 The 3- and 12-month treatment failure rates, delayed graft function and rena

229 ons and its impact on antibiotic eradication treatment failure rates.

230 at endoscopy (CP-B+AB) are at high risk for treatment failure, rebleeding, and mortality.

231 hypnozoite-derived (relapse), a blood-stage treatment failure (recrudescence), or a newly acquired i

232 ance to either of them increases the risk of treatment failure, relapse, or acquisition of resistance

233 NS5A were observed in 9 and 10 patients with treatment failure, respectively.

234 d (MLL-r) acute lymphoblastic leukemia (ALL) treatment failure resulting from persistence of drug-res

235 l features can be used to effectively define treatment failure risk and to stratify young patients wi

236 cing was performed in two baseline and three treatment failure samples by means of an original shotgu

237 Primary outcome was treatment failure, secondary outcomes included 30 days a

238 sis of cryptococcal meningitis) and those in treatment failure should switch treatment.

239 nce of death and loss to follow-up (LTFU) by treatment failure status.

240 his region and associated with high rates of treatment failure, suggesting a need for rigorous test-o

241 on with low-dose azithromycin could decrease treatment failure (TF) when initiated at hospital admiss

242 The primary outcome was treatment failure (TF), defined as 30-day mortality or p

243 ulted in a significantly higher incidence of treatment failure than CPAP when used in nontertiary spe

244 pted ICBT were not more likely to experience treatment failure than those not at risk (odds ratio=0.5

245 Main outcomes were treatment failure (the proportion of women in which surg

246 n a subset of individuals was the reason for treatment failures, this might be adequately addressed w

247 There is a 20% risk of treatment failure (those who needed further glaucoma sur

248 Antimicrobial treatment failure threatens our ability to control infec

249 initiation and progression and contribute to treatment failure through their intrinsic resistance to

250 on of (18)F-FDG PET/CT with time to hormonal treatment failure (THTF) in men with metastatic castrati

251 ached [NR]) months, while the median time to treatment failure time for those receiving early combina

252 ly associated with outcomes of remission and treatment failure to CBT and antidepressant medication a

253 Time-to-treatment failure (TTF) to EGFR TKI in patients identifi

254 unsuccessful tuberculosis treatment outcome (treatment failure, tuberculosis recurrence, or death) by

255 Treatment failure typically occurred early and was assoc

256 5 mg twice daily plus corticosteroids, until treatment failure, unacceptable toxicity, or death.

257 transplant recipients with CMV-infection and treatment failure upon standard care due to antiviral dr

258 reatment ranged from 41.5% to 77.5%, whereas treatment failure varied from 3% to 15% for different tr

259 incomplete adherence had a small increase in treatment failure versus those with complete adherence (

260 nce interval [CI], 10.0%-15.6%); the risk of treatment failure was 10.3% (95% CI, 8.0%-13.2%).

261 The rate of in-field treatment failure was 17.9% (five of 28) as determined w

262 lative incidence of death and LTFU following treatment failure was 18.5% compared to 10.1% without tr

263 ared with fluorouracil, the hazard ratio for treatment failure was 2.03 (95% CI, 1.36 to 3.04) with i

264 Treatment failure was 20% in the EP group versus 7% in t

265 Most CRs were durable but the probability of treatment failure was 27% at 3 years.

266 the per-protocol analysis, the incidence of treatment failure was 4.9% among placebo recipients (95

267 The number needed to treat to prevent one treatment failure was 44 (95% CI, 31 to 80).

268 w-up of 11 months (IQR 6-18), median time to treatment failure was 6.7 months (95% CI 5.5-8.6), media

269 Local treatment failure was a relatively infrequent event afte

270 Treatment failure was associated independently with plas

271 Local treatment failure was associated weakly with reduced sur

272 Treatment failure was defined according to World Health

273 Treatment failure was defined as (1) any further surgica

274 Treatment failure was defined as 1) any further surgical

275 The risk of treatment failure was greater for regimen A3 (22.5%; 16

276 e with nonsevere pneumonia, the frequency of treatment failure was higher in the placebo group than i

277 Treatment failure was independently associated with LNJS

278 Microbiologic treatment failure was independently associated with recu

279 Time to treatment failure was longer with bevacizumab than with

280 After adjusting for clustering, the risk of treatment failure was lower in intervention clusters (ri

281 The risk for treatment failure was lower when treatment used adalimum

282 Treatment failure was observed in 26.6% (261/981), all c

283 ion in the relative risk for time to initial treatment failure was observed in the early combination

284 g the first 5 years after brachytherapy, and treatment failure was reported for 57 eyes.

285 umulative probability of remaining free from treatment failure was significantly higher among patient

286 Prevalence of S282C/T RASs at treatment failure was significantly higher in patients i

287 Treatment failure was significantly increased in HIV-inf

288 Treatment failure was the most common reason for enuclea

289 evelopment of drug-resistant tuberculosis or treatment failure) was recorded after 6 months of therap

290 r 34 months median follow-up, crude rates of treatment failure were 15.0% with PN and 40.9% with Cont

291 Risk factors for treatment failure were older age, greater tumor thicknes

292 Samples collected at baseline and at time of treatment failure were sequenced for resistance-associat

293 malaria in northeastern Cambodia, where >17% treatment failures were previously reported.

294 l acuity (BCVA) at treatment milestones, and treatment failures were recorded.

295 irst form is likely to persist and result in treatment failure, while the latter two could be stochas

296 ore than 6 months of atrial fibrillation and treatment failure with 1 antiarrhythmic drug or beta-blo

297 s Cambodia in 2008-13, causing high rates of treatment failure with the frontline combination therapy

298 l missing data after 56 days were imputed as treatment failure (with reexpansion in 129 of 138 patien

299 lapse after ASCT remains a frequent cause of treatment failure, with poor subsequent prognosis.

300 The primary end point was definitive treatment failure within 1 year after randomization.