ライフサイエンスコーパス: acetaminophen

1 is neither mitigated nor inflated by use of acetaminophen.

2 to prevent and rescue liver injury caused by acetaminophen.

3 luding uric acid, ascorbic acid, glucose and acetaminophen.

4 aminophen; or 30 mg of codeine and 300 mg of acetaminophen.

5 ite of the cannabinoid-mediated analgesia by acetaminophen.

6 cultured in the bioreactor were treated with acetaminophen.

7 s of the drugs indomethacin, felodipine, and acetaminophen.

8 An infusion of acetaminophen 1 g or saline placebo over 15 minutes.

9 ere randomized to receive either intravenous acetaminophen, 1 g (n = 289), or normal saline placebo (

10 erference from 170 muM ascorbic acid, 1.3 mM acetaminophen, 1.4 mM uric acid or 20 mM glucose.

11 Acetaminophen [100 mg/kg intraperitoneal (ip)] and/or si

12 ants were randomized to receive paracetamol (acetaminophen) 1000 mg plus ibuprofen 400 mg (n = 136; P

13 tio 6,12] versus 7 hours [6,10]) and initial acetaminophen (124 mg/L [58,171] versus 146 mg/L [66,204

14 the primary outcome, did not differ between acetaminophen (30 pg/mL; interquartile range, 24-41) and

15 The most common causes of DILI were acetaminophen (35.0 %) and anti-tuberculous drugs (34.7

16 prescription of either 10 or 30 hydrocodone/acetaminophen (5/325 mg) pills after surgery.

17 etaminophen; 5 mg of oxycodone and 325 mg of acetaminophen; 5 mg of hydrocodone and 300 mg of acetami

18 received 400 mg of ibuprofen and 1000 mg of acetaminophen; 5 mg of oxycodone and 325 mg of acetamino

19 fidence interval (CI): 0.91, 1.13), 0.89 for acetaminophen (95% CI: 0.77, 1.03), 1.07 for naproxen (9

20 to track the temporal profile of circulating acetaminophen (a widely used analgesic and antipyretic)

21 Drug-induced liver injury caused by acetaminophen (acetyl-para-aminophenol [APAP]) is the ma

22 e effects of acute 2-bromophenol and chronic acetaminophen administration.

23 emia reperfusion and N-acetyl-p-aminophenol (acetaminophen) administration.

24 pregnant rats to analgesics (indomethacin or acetaminophen) affected GC development and reproductive

25 this work, we find suggestive evidence that acetaminophen affects the basic social process of trust

26 e and cultured or treated with Fas ligand or acetaminophen after different culture times.

27 lso responsible for the analgesic effects of acetaminophen against inflammatory pain.

28 harge, 207 of 216 patients were treated with acetaminophen alone.

29 of proinflammatory prostaglandin formation, acetaminophen also reversed hyperalgesia induced by intr

30 e cannabinoid system contributes not only to acetaminophen analgesia against acute pain but also agai

31 Here, we analyzed acetaminophen analgesia in mice of either sex with infla

32 ps, with a mean of 0.81 per participant with acetaminophen and 0.87 per participant with ibuprofen ov

33 al and a supraspinal action, we administered acetaminophen and AM 404 to hoxB8-CB1(-/-) mice, which l

34 e signal was not affected by the presence of acetaminophen and ascorbic acid in the sample solution.

35 f the antibiotic and hormone treatments plus acetaminophen and caffeine and, 4) an untreated control.

36 est closure and continued for up to 6 hours (acetaminophen and dexmedetomidine: n = 29; placebo and d

37 In this study, we associate maternal acetaminophen and ibuprofen intake during pregnancy and

38 ignificant differences were detected between acetaminophen and ibuprofen with respect to the percenta

39 sotopologues were in turn used to quantitate acetaminophen and its corresponding metabolites in rat p

40 enatal, postnatal, and partner's exposure to acetaminophen and mutually adjusted each association.

41 research, including comparison of IV vs oral acetaminophen and other potentially opioid-sparing analg

42 nd points differed significantly between the acetaminophen and placebo groups.

43 characteristics were similar in those given acetaminophen and placebo.

44 n = 29; placebo and dexmedetomidine: n = 30; acetaminophen and propofol: n = 31; placebo and propofol

45 lin/neomycin can alter the biodisposition of acetaminophen and that these alterations could be due to

46 electrochemical interferants (ascorbic acid, acetaminophen and uric acid), was revealed to be negligi

47 s still unknown, the question whether or not acetaminophen and/or ibuprofen are safe pain medications

48 rugs (nicotine, coumarin, chlorzoxazone, and acetaminophen) and the prodrug (tamoxifen) as P450 subst

49 eptides 1 and 2, gastric inhibitory peptide, acetaminophen, and 3-O-methylglucose.

50 a diameter of less than 2.5 mum [PM(2.5)]), acetaminophen, and smoking.

51 st inflammatory pain, the main indication of acetaminophen, and the precise site of the relevant CB1

52 Acetaminophen (APAP) and ibuprofen (IB) are drugs common

53 ich are elevated plasma ALT values following acetaminophen (APAP) exposure in mice.

54 32.9% were male, and ALF etiologies included acetaminophen (APAP) hepatotoxicity (29%), indeterminate

55 allowing the ultrasensitive determination of acetaminophen (APAP) in the presence of its common inter

56 Acetaminophen (APAP) is a commonly used analgesic respon

57 Acetaminophen (APAP) is a proven lethal oral toxicant in

58 Acetaminophen (APAP) is the active component of many med

59 Accidental or intentional misuse of acetaminophen (APAP) is the leading cause of acute liver

60 Overdose of acetaminophen (APAP) is the leading cause of acute liver

61 Acetaminophen (APAP) is the main cause of acute liver fa

62 Acetaminophen (APAP) is widely used as an antifebrile an

63 tion of the metabolism-dependent hepatotoxin acetaminophen (APAP) or the direct nephrotoxin cisplatin

64 Acetaminophen (APAP) overdose (APAPo) is predominant in

65 Acetaminophen (APAP) overdose is one of the leading caus

66 Acetaminophen (APAP) overdose represents the most freque

67 rophages are critical for liver repair after acetaminophen (APAP) overdose.

68 Acetaminophen (APAP) overdoses are of major clinical con

69 te the cytochrome P-450 isoforms involved in acetaminophen (APAP) toxicity were examined in HepaRG ce

70 s induced in hepatocytes in ALF, and in both acetaminophen (APAP)- and carbon tetrachloride (CCl4)-tr

71 In acetaminophen (APAP)- or carbon tetrachloride-induced ac

72 Acetaminophen (APAP)-induced acute liver failure (ALF) i

73 mined the role of phospholipase D2 (PLD2) on acetaminophen (APAP)-induced acute liver injury using a

74 nts with acute liver failure (ALF) and in an acetaminophen (APAP)-induced ALF mouse model.

75 es evolution of coagulopathy in 10 pigs with acetaminophen (APAP)-induced ALI compared to 3 Controls.

76 cal induction of autophagy protected against acetaminophen (APAP)-induced liver injury in mice by cle

77 ensitivity to the albumin-bound hepatotoxin, acetaminophen (APAP).

78 Acetaminophen (APAP, paracetamol) poisoning is a leading

79 healthy controls and patients suffering from acetaminophen (APAP, paracetamol)-induced acute liver fa

80 is well-known to mediate alcohol- (ALC) and acetaminophen- (APAP) induced toxicity in hepatic and ex

81 dose of an NSAID with an appropriate dose of acetaminophen appears to further enhance analgesic effic

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

83 Opiates and acetaminophen are preferred analgesic agents, and gabape

84 ologue and a stable ((13)C6) isotopologue of acetaminophen as substrates for in vitro biosynthesis of

85 omise as a rapid and simple POC quantitative acetaminophen assay.

86 ation and at 12 hours, and less than 20 mg/L acetaminophen at 12 hours.

87 n, leading some physicians to recommend that acetaminophen be avoided in children with asthma; howeve

88 eated animals was associated with changes in acetaminophen biodisposition.

89 ecrotic human primary hepatocytes exposed to acetaminophen, but not hepatic sinusoidal endothelial ce

90 Although it is known that acetaminophen causes oxidative injury in the liver, it i

91 Removal of acetaminophen, ciprofloxacin, trimethoprim, propranolol,

92 Acetaminophen, cirrhosis and age >/= 60 years were seen

93 r risks of death except in patients with non-acetaminophen, cirrhosis, elderly or concomitant disease

94 achieved quantitative validation targets for acetaminophen clearance and metabolism but failed to ach

95 acetaminophen or with 3 different opioid and acetaminophen combination analgesics.

96 cardiac surgery, postoperative scheduled IV acetaminophen, combined with IV propofol or dexmedetomid

97 al surgery, use of postoperative intravenous acetaminophen, compared with placebo, did not significan

98 on in fecundability among males with urinary acetaminophen concentrations in the highest quartile (>7

99 Acetaminophen concentrations were measured by liquid chr

100 ebrile critically ill adults, treatment with acetaminophen decreased temperature, blood pressure, and

101 iability after exposure to allyl alcohol and acetaminophen demonstrated the in vitro creation of hepa

102 results reveal a critical role of miR-122 in acetaminophen detoxification and implicate its therapeut

103 f the patients who received IV injections of acetaminophen developed hypotension, and up to one third

104 n-propofol groups (46% and 45%) and 7 in the acetaminophen-dexmedetomidine and placebo-propofol group

105 Acetaminophen DILI yielded lower risks of mortality (HR

106 Acetaminophen diminished NPSH in nasal, thoracic extrapu

107 than control mice when injected i.p. with an acetaminophen dose not lethal to the control.

108 verse mouse strains following a single toxic acetaminophen dose.

109 auses of ALF were indeterminate (69.4%), non-acetaminophen drug-induced (26.1%), and viral hepatitis

110 explored the association between exposure to acetaminophen during pregnancy and pubertal development

111 administration of damaging chemicals (CCl4 , acetaminophen, etc.).

112 Here, we demonstrate that acetaminophen, even at low-dose, disrupts the integrity

113 er sex with inflammatory pain and found that acetaminophen exerted a dose-dependent antihyperalgesic

114 ed when we compared POA-exposed infants with acetaminophen-exposed infants (OR = 1.18, 95% CI 1.07-1.

115 analysis of the association between in utero acetaminophen exposure and risks of attention deficit hy

116 se of prior reports suggesting that prenatal acetaminophen exposure may influence neurodevelopment.

117 gher risk of ADHD and ASD following prenatal acetaminophen exposure.

118 ne cumulative (weeks) and trimester-specific acetaminophen exposure.

119 l development had no strong association with acetaminophen exposure.

120 ts were similar whether the mother had taken acetaminophen for their fever or not.

121 ndings do not support the use of intravenous acetaminophen for this purpose.

122 an be used directly to determine the unbound acetaminophen fraction without the need for any addition

123 Mice were given acetaminophen gavage or intravenous injections of fluore

124 Although it had no effect by itself, acetaminophen greatly increased the reflex irritant resp

125 acetaminophen group and the hydrocodone and acetaminophen group (0.9; 99.2% CI, -0.1 to 1.8), which

126 A total of 55 of 345 patients in the acetaminophen group (15.9%) and 57 of 344 patients in th

127 3.9 (95% CI, 3.2 to 4.5) in the codeine and acetaminophen group (P = .053).

128 e group 19 (IQR,17-21), and in the oxycodone/acetaminophen group 20 (IQR,17-22).

129 -5.1) minutes per hour among patients in the acetaminophen group and 1.1 (IQR, 0.1-6.6) minutes per h

130 ostoperative hours were 4.2 (SD, 1.8) in the acetaminophen group and 4.4 (SD, 1.8) in the placebo gro

131 ine to 2 hours was between the oxycodone and acetaminophen group and the hydrocodone and acetaminophe

132 The acetaminophen group had significantly lower adjusted tim

133 relative rate of asthma exacerbations in the acetaminophen group vs. the ibuprofen group, 0.94; 95% c

134 In the acetaminophen group, 49% of participants had at least on

135 (95% CI, 2.9 to 4.2) in the hydrocodone and acetaminophen group; and by 3.9 (95% CI, 3.2 to 4.5) in

136 .4 (95% CI, 3.7 to 5.0) in the oxycodone and acetaminophen group; by 3.5 (95% CI, 2.9 to 4.2) in the

137 .3 (95% CI, 3.6 to 4.9) in the ibuprofen and acetaminophen group; by 4.4 (95% CI, 3.7 to 5.0) in the

138 Patients treated with IV acetaminophen had a significant reduction in delirium (1

139 Patients given acetaminophen had an adjusted time-weighted average temp

140 Hepatocytes from Jnk(Deltahepa) mice given acetaminophen had an increased oxidative stress response

141 Acetaminophen has long been assumed to selectively allev

142 usal explanation of key temporal features of acetaminophen hepatotoxicity in mice.

143 Moreover, Pml(-/-) animals are resistant to acetaminophen hepatotoxicity or fasting-induced steatosi

144 d KC could affect outcomes in the context of acetaminophen hepatotoxicity or hepatic ischemia-reperfu

145 are relevant to the clinical presentation of acetaminophen-hepatotoxicity and may inform future mecha

146 In acetaminophen-hepatotoxicity, the mechanism by which tis

147 As the oral bioavailability of acetaminophen in critically ill children is unknown, we

148 Frequent maternal use of acetaminophen in pregnancy has been linked to attention-

149 The test strips were able to detect acetaminophen in small 40 muL samples with a detection l

150 sible to predict the depth of a paracetamol (acetaminophen) inclusion within a turbid matrix consisti

151 anipulated trust game investor expectations, acetaminophen increased investments regardless of expect

152 At supratherapeutic levels, acetaminophen induced oxidative stress throughout the re

153 phils and their function in 24 patients with acetaminophen-induced acute liver failure and compared w

154 eutrophil Toll-like receptor 9 expression in acetaminophen-induced acute liver failure being mediated

155 idative burst increased in all patients with acetaminophen-induced acute liver failure compared with

156 -like receptor 9 expression was increased in acetaminophen-induced acute liver failure on day 1 compa

157 To examine the influence of acetaminophen-induced acute liver failure plasma and end

158 ion, healthy neutrophils were incubated with acetaminophen-induced acute liver failure plasma with an

159 9 expression increased upon stimulation with acetaminophen-induced acute liver failure plasma, which

160 whether this is protective or detrimental in acetaminophen-induced acute liver failure remains unknow

161 ere is a marked propensity for patients with acetaminophen-induced acute liver failure to develop sep

162 nto the rostral ventromedial medulla blocked acetaminophen-induced antihyperalgesia, while local rost

163 targets and pathways that may be altered in acetaminophen-induced hepatic depolarization.

164 Eighty-three patients (51.9%) experienced acetaminophen-induced hypotension according to our defin

165 Among patients with acetaminophen-induced hypotension, 29 (34.9%) required t

166 n accurate estimation of the consequences of acetaminophen-induced hypotension, and assess the pathop

167 In patients with acetaminophen-induced hypotension, the nadir mean arteri

168 perature) were independently associated with acetaminophen-induced hypotension.

169 We sought to assess the incidence of acetaminophen-induced hypotension.

170 ibitor of MCJ expression protects liver from acetaminophen-induced liver injury at a time when N-acet

171 Carbon monoxide ameliorates acetaminophen-induced liver injury by increasing hepatic

172 Sera from mice with acetaminophen-induced liver injury contained high levels

173 Acetaminophen-induced liver injury in mice is a model fo

174 es from patients and controls, and mice with acetaminophen-induced liver injury using enzyme-linked i

175 ed effects in protecting mice from CCl4- and acetaminophen-induced liver injury.

176 t a human ex-vivo liver model to investigate acetaminophen-induced liver injury.

177 a JNK inhibitor, has been reported to block acetaminophen-induced liver injury.

178 Nrf2 downstream genes, and rescue mice from acetaminophen-induced liver injury.

179 PCI-IS assisted method was applied to study acetaminophen-induced liver toxicity.

180 ed by senescence-inducing irradiation and/or acetaminophen-induced mitochondria dysfunction.

181 The goal of this study was to determine if acetaminophen induces respiratory tract oxidative stress

182 y, chronic heart disease, and indication for acetaminophen infusion) or clinically relevant character

183 as observed 30 minutes (95% CI, 15-71) after acetaminophen infusion.

184 However, an association between prenatal acetaminophen intake and increased infantile IgEs relate

185 , no association was found for ibuprofen and acetaminophen intakes during breastfeeding.

186 ociceptive pain, indicated that analgesia by acetaminophen involves an indirect activation of CB1 rec

187 ventromedial medulla.SIGNIFICANCE STATEMENT Acetaminophen is a widely used analgesic drug with multi

188 New evidence suggests that acetaminophen is ineffective for acute low back pain, an

189 dentical K(ow) as the shake-flask method for acetaminophen, K(ow) = 2.48 +/- 0.02.

190 o consideration, especially after the use of acetaminophen, lopinavir/ritonavir and remdesivir, which

191 e of well-removed OWCs, such as caffeine and acetaminophen, may indicate discharges of poorly treated

192 -derived substructures including paracetamol/acetaminophen mercapturate and dimethylpyrogallol.

193 Local injections of the acetaminophen metabolite AM 404 and of cannabinoid recep

194 indirect activation of CB1 receptors by the acetaminophen metabolite and endocannabinoid reuptake in

195 Relative amounts of acetaminophen metabolite and hGSTP adducts were compared

196 ant administration of an oral C radiolabeled acetaminophen microtracer (3 ng/kg) with IV acetaminophe

197 ntral venous catheter up to 24 hours after C acetaminophen microtracer administration.

198 Acetaminophen (N-acetyl-p-aminophenol, APAP) and (13)C6-

199 Acetaminophen (N-acetyl-para-aminophenol; APAP) overdose

200 medications by active ingredient (ibuprofen, acetaminophen, naproxen, aspirin) and cumulative monthly

201 sic drug classes (cyclooxygenase inhibitors, acetaminophen, nefopam, or metamizol) were required to p

202 Observations: Regional analgesia, acetaminophen, nonsteroidal anti-inflammatory agents, ga

203 the use of non-opioid interventions such as acetaminophen, nonsteroidal anti-inflammatory drugs, cyc

204 shows that non-opioid interventions such as acetaminophen, nonsteroidal anti-inflammatory drugs, cyc

205 In addition, the effects of acetaminophen on airway irritation reflex responses to E

206 Although the impact of early life acetaminophen on asthma risk is still not clear, potenti

207 To determine the effects of IV acetaminophen on core body temperature, blood pressure,

208 Effects of acetaminophen on oxidant and irritant respiratory tract

209 m these findings and determine the effect of acetaminophen on patient-centered outcomes.

210 t populations, in which a short course of an acetaminophen/opioid combination may provide a more favo

211 ognized direct toxicity of super-therapeutic acetaminophen or chemotherapeutic agents in children, li

212 An association between prenatal acetaminophen or ibuprofen intake and an increased risk

213 t asthma and assigned them to receive either acetaminophen or ibuprofen when needed for the alleviati

214 ps receiving postoperative analgesia with IV acetaminophen or placebo every 6 hours for 48 hours and

215 stained JNK activation and liver injury from acetaminophen or tumor necrosis factor/galactosamine.

216 ong single-dose treatment with ibuprofen and acetaminophen or with 3 different opioid and acetaminoph

217 ry tract infections attenuated estimates for acetaminophen (OR, 1.03; 95% CI, 0.88-1.22) and ibuprofe

218 tment with NAPQI, the reactive metabolite of acetaminophen, or the PKCalpha-activator and TJ-disrupto

219 activated via phosphorylation in response to acetaminophen- or carbon tetrachloride (CCl4)-induced li

220 aminophen; 5 mg of hydrocodone and 300 mg of acetaminophen; or 30 mg of codeine and 300 mg of acetami

221 ly identified patients at risk of DILI after acetaminophen overdose (area under ROC curve 0.98 (95% C

222 primary miR-122 expression occurs in mice on acetaminophen overdose because of suppression of its key

223 olled subjects following single or staggered acetaminophen overdose with normal serum alanine transam

224 levels of MCJ in the liver of patients with acetaminophen overdose.

225 tients at very low risk of liver injury from acetaminophen overdose.

226 be at any risk for hepatotoxicity following acetaminophen overdose.

227 Of the 449 acetaminophen overdoses receiving acetylcysteine, 100 we

228 t 18 years (interaction between GSTM1/T1 and acetaminophen P < .05).

229 itative point-of-care (POC) determination of acetaminophen (paracetamol) in plasma and finger-prick w

230 Acetaminophen (paracetamol) is a widely used analgesic a

231 Importance: Acetaminophen (paracetamol) is used by a large proportio

232 The combination of ibuprofen and acetaminophen (paracetamol) may represent a viable nonop

233 cate, with self-reported prescribing of both acetaminophen/paracetamol and opiates in 97% of patients

234 Australian and New Zealand ICUs suggest that acetaminophen/paracetamol is the most common first-line

235 Low-dose, short-term acetaminophen, pharmaceutical grade glucosamine and chon

236 ver sections from patients with DILI (due to acetaminophen, phenprocoumon, nonsteroidal anti-inflamma

237 Regarding opioids, compared with placebo, acetaminophen plus an opioid improved intermediate pain

238 The response to acetaminophen plus ETS was equal to or greater than the

239 nclusions and Relevance: Children exposed to acetaminophen prenatally are at increased risk of multip

240 ents in both the placebo-dexmedetomidine and acetaminophen-propofol groups (46% and 45%) and 7 in the

241 Administration of SP600125 before or with acetaminophen protected Jnk(Deltahepa) and control mice

242 Method performance was evaluated by trapping acetaminophen reactive metabolite N-acetyl-p-benzoquinon

243 In a series of lab experiments (N = 767), acetaminophen reduced the influence of self-generated ex

244 re, we showed that enteral administration of acetaminophen results in less predictable exposure and h

245 Three liver sections incubated with low-dose acetaminophen revealed strong damage, with ICG half-live

246 rystallization method was investigated where acetaminophen single crystals were recrystallized from s

247 ry metabolite profiles revealed decreases in acetaminophen-sulfate metabolite levels in both the amox

248 ication of batches of analgesic paracetamol (acetaminophen) tablets using nitrogen-14 nuclear quadrup

249 IV acetaminophen thus produces modest fever reduction in cr

250 1 subfamily A member 2 (CYP1A2) that convert acetaminophen to highly reactive N-acetyl-p-benzoquinone

251 Administration of acetaminophen to Jnk(Deltahepa) mice produced a greater

252 d to improve physical function, or with oral acetaminophen to reduce pain (Grade: conditional recomme

253 n injections of CCl4 (to induce fibrosis) or acetaminophen (to induce toxic liver injury).

254 Acetaminophen toxicity accounted for 21 (60% of the rema

255 Here we investigate hepatic adaptation to acetaminophen toxicity from a whole proteome perspective

256 Acetaminophen toxicity is a leading cause of acute liver

257 sitized differentiated human HepaRG cells to acetaminophen toxicity that correlated with upregulation

258 [P < 0.001] in patients with ALF not due to acetaminophen toxicity).

259 biopsy specimens of patients with ALF and in acetaminophen-treated mice.

260 of microRNA-122 was significantly higher in acetaminophen-treated than in non-treated livers.

261 acetaminophen microtracer (3 ng/kg) with IV acetaminophen treatment (15 mg/kg every 6 hr).

262 In a national community sample (MIDUS II), acetaminophen usage was negatively associated with neigh

263 terval: 1.06, 1.15; P for trend < 0.001) and acetaminophen use (for >6 years of use compared with <1

264 investigate associations between early life acetaminophen use and adolescent asthma and lung functio

265 d the associations between maternal prenatal acetaminophen use and all the SDQ domains unchanged even

266 ve suggested an association between frequent acetaminophen use and asthma-related complications among

267 Results: Maternal prenatal acetaminophen use at 18 (n = 4415; 53%) and 32 weeks of

268 RR, 1.31; 95% CI, 1.16-1.49), while maternal acetaminophen use at 32 weeks was also associated with h

269 Our NCE analysis suggested that only acetaminophen use at the time of pregnancy was associate

270 evaluated the associations between maternal acetaminophen use during different exposure periods and

271 ith GSTM1 null and GSTT1 present, increasing acetaminophen use for nonrespiratory reasons was associa

272 Research suggests that acetaminophen use in pregnancy is associated with abnorm

273 The lack of an association between acetaminophen use in the pre- and postpregnancy exposure

274 sured behavioral or social factors linked to acetaminophen use insofar as they are not observed for p

275 Exposures: Acetaminophen use was assessed by questionnaire completi

276 Increased acetaminophen use was associated with asthma at 18 years

277 Doubling of days of acetaminophen use was associated with reduced prebroncho

278 Information on regular maternal acetaminophen use was collected prospectively in biennia

279 Acetaminophen use was recorded 18 times up to age 2 year

280 hort of women, longer durations of NSAID and acetaminophen use were associated with slightly higher r

281 ehavioral problems and (1) maternal prenatal acetaminophen use, (2) maternal postnatal acetaminophen

282 al acetaminophen use, (2) maternal postnatal acetaminophen use, and (3) partner's acetaminophen use.

283 susceptible to respiratory consequences from acetaminophen use.

284 djusting for maternal postnatal or partner's acetaminophen use.

285 (n = 6916; 89%) or partner's (n = 3454; 84%) acetaminophen use.

286 d by unmeasured behavioral factors linked to acetaminophen use.

287 are not observed for postnatal or partner's acetaminophen use.

288 stnatal acetaminophen use, and (3) partner's acetaminophen use.

289 There were significant differences favoring acetaminophen vs placebo for 3 prespecified secondary ou

290 Prenatal acetaminophen was associated with increased asthma (OR,

291 New evidence found that acetaminophen was ineffective for acute low back pain, n

292 ith mild persistent asthma, as-needed use of acetaminophen was not shown to be associated with a high

293 Use of acetaminophen was reported 3 times during pregnancy and

294 Acetaminophen was the presumptive cause in 1.7% of patie

295 Rescue medication (1,000 mg acetaminophen) was made available to each patient, and t

296 harmacokinetics (PK), and biodistribution of acetaminophen were assessed in C57Bl/6 mice after treatm

297 Altered PK, and excretion profiles of acetaminophen were observed in antibiotic exposed animal

298 physicians tend to assume that oral doses of acetaminophen will be completely absorbed and therefore

299 Topical NSAIDs, followed by oral NSAIDs and acetaminophen with or without diclofenac, showed the mos

300 est net benefit, followed by oral NSAIDs and acetaminophen with or without diclofenac.