ライフサイエンスコーパス: acetaminophen

1 o 0.33) for the least efficacious treatment (acetaminophen).

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

3 to prevent and rescue liver injury caused by acetaminophen.

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

5 y of factors, including common drugs such as acetaminophen.

6 h between healthy liver and liver damaged by acetaminophen.

7 108 each to cyclobenzaprine and to oxycodone/acetaminophen.

8 ects, as measured by the pharmacokinetics of acetaminophen.

9 epletion after incubation with high doses of acetaminophen.

10 blems in children after prenatal exposure to acetaminophen.

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

12 ite of the cannabinoid-mediated analgesia by acetaminophen.

13 cultured in the bioreactor were treated with acetaminophen.

14 Patients were randomized 1:1 to enteral acetaminophen 1 g every 6 hours for 3 days (n = 18) or p

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

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

17 and 75 muM glucose in the presence of 10 muM acetaminophen, 100 muM ascorbic acid, and 100 muM uric a

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

19 o; cyclobenzaprine, 5 mg; or oxycodone, 5 mg/acetaminophen, 325 mg.

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

21 ignificant difference in hospital mortality (acetaminophen 5.6% vs placebo 18.2%; p = 0.355) or adver

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

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

24 ansferase or alanine aminotransferase > 400; acetaminophen 9.5% vs placebo 4.3%; p = 0.599).

25 ions by investigating the effect of FABP1 on acetaminophen (AAP)-induced hepatotoxicity.

26 y endpoint was a pharmacokinetic analysis of acetaminophen absorption in subjects receiving tedugluti

27 or-Epineprhine (Nor-Ep), Ascorbic Acid (AA), Acetaminophen (Ac) and Uric Acid (UA).

28 mmon active pharmaceutical ingredient (API), acetaminophen (ACM) which itself is redox active, typica

29 The use of intracranial pressure monitor in acetaminophen acute liver failure did not confer a signi

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

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

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

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

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

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

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

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

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

39 range, 13 to 25) among patients assigned to acetaminophen and 22 days (interquartile range, 12 to 25

40 Jo2 FAS/CD95 activating model and models of acetaminophen and alpha-amanitin poisoning were used.

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

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

43 We examined the associations of acetaminophen and ibuprofen (per unit increase in exposu

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

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

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

47 e synthesized that mimic the pharmaceuticals acetaminophen and mefenamic acid and also possess polyme

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

49 characteristics were similar in those given acetaminophen and placebo.

50 nt with two different hepatotoxic compounds (acetaminophen and thioacetamide) caused DNA release into

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

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

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

54 rats that were administered a 1:1 mixture of acetaminophen (APAP) and (13)C6-APAP resulted in mass sp

55 talk between signaling pathways activated by acetaminophen (APAP) and insulin signaling in hepatocyte

56 32.9% were male, and ALF etiologies included acetaminophen (APAP) hepatotoxicity (29%), indeterminate

57 The diurnal variation in acetaminophen (APAP) hepatotoxicity (chronotoxicity) rep

58 Acetaminophen (APAP) hepatotoxicity is associated with a

59 The role of lysosomes in acetaminophen (APAP) hepatotoxicity is poorly understood

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

61 Acetaminophen (APAP) is an effective antipyretic and one

62 Acetaminophen (APAP) is one of the most widely used anal

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

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

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

66 Although necrosis in the acetaminophen (APAP) model is known to be regulated by c

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

68 Acetaminophen (APAP) overdose is a frequent cause of dru

69 Acetaminophen (APAP) overdose is a major cause of acute

70 matically elevated in the plasma or serum of acetaminophen (APAP) overdose patients.

71 Acetaminophen (APAP) overdoses are of major clinical con

72 In agreement with in vivo studies, acetaminophen (APAP) toxicity was most profound in HUVEC

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

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

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

76 Acetaminophen (APAP)-induced acute liver injury (AILI) i

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

78 ase-activated receptor (PAR)-4 contribute to acetaminophen (APAP)-induced liver damage.

79 Acetaminophen (APAP)-induced liver injury in humans is a

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

81 sease progression and poor outcomes in acute acetaminophen (APAP)-related liver failure.

82 cute liver failure 12 h after application of acetaminophen (APAP).

83 as induced in BALB/c mice by a toxic dose of acetaminophen (APAP).

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

85 Acetaminophen (APAP, paracetamol) poisoning is a leading

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

87 Acetaminophen (APAP; ie, Paracetamol or Tylenol) is gene

88 Acute kidney injury in the context of acetaminophen (APAP; paracetamol)-induced liver injury i

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

90 Opiates and acetaminophen are preferred analgesic agents, and gabape

91 differences in gastric emptying of liquids (acetaminophen area under the concentration [AUC] vs time

92 dence base supports a stepwise approach with acetaminophen as first-line therapy.

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

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

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

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

97 Removal of acetaminophen, ciprofloxacin, trimethoprim, propranolol,

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

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

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

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

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

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

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

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

106 Acetaminophen, diclofenac, codeine, ampicillin, tetracyc

107 Acetaminophen DILI yielded lower risks of mortality (HR

108 Acetaminophen diminished NPSH in nasal, thoracic extrapu

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

110 verse mouse strains following a single toxic acetaminophen dose.

111 Children whose mothers used acetaminophen during pregnancy were at higher risk for r

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

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

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

115 We categorized prenatal acetaminophen exposure as the maximum intake (never, 1-9

116 Mice were given acetaminophen gavage or intravenous injections of fluore

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

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

119 dary outcome, was significantly lower in the acetaminophen group (1.0 mg/dL; interquartile range, 0.6

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

121 significantly reduced on study day 2 in the acetaminophen group (24 pg/mL; interquartile range, 19-3

122 3.9 (95% CI, 3.2 to 4.5) in the codeine and acetaminophen group (P = .053).

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

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

125 28 did not differ significantly between the acetaminophen group and the placebo group: 23 days (inte

126 The acetaminophen group had significantly lower adjusted tim

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

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

129 obenzaprine group, and 11.1 in the oxycodone/acetaminophen group.

130 (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

131 .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

132 .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

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

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

135 We show that adaptation to acetaminophen has a spatial component, involving a shift

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

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

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

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

140 In acetaminophen-hepatotoxicity, the mechanism by which tis

141 nd multiple low-abundance metabolites (e.g., acetaminophen hydroxy- and methoxysulfate) that are rare

142 ation half-life (DT50) as short as 1.8 days (acetaminophen, ibuprofen) to not degradable (chlorthalid

143 mage in humans, whereas repeated exposure to acetaminophen in humans and animal models results in aut

144 This trial evaluated the efficacy of acetaminophen in reducing oxidative injury, as measured

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

146 Acetaminophen-induced acute liver failure (AALF) is char

147 tober 2013, as well as from 78 patients with acetaminophen-induced acute liver failure admitted to th

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

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

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

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

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

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

154 9 expression increased upon stimulation with acetaminophen-induced acute liver failure plasma, which

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

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

157 In patients with acetaminophen-induced acute liver failure, a low serum l

158 son-years) compared with 3 patients with non-acetaminophen-induced ALF (21.4%; 0.18/1,000,000 person-

159 One patient with acetaminophen-induced ALF died (5.6%; 0.06 events/1,000,

160 e rates of any definite drug-induced ALF and acetaminophen-induced ALF were 1.61 events/1,000,000 per

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

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

163 2 channels are essential in the mechanism of acetaminophen-induced hepatocellular death.

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

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

170 mmunity in mice after partial hepatectomy or acetaminophen-induced injury, with resident hepatic macr

171 while hepatic Fra-1 expression protects from acetaminophen-induced liver damage, a paradigm for gluta

172 In TRPM2 knockout mice, acetaminophen-induced liver damage, assessed by the bloo

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

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

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

176 were also observed in the alpha-amanitin and acetaminophen-induced liver injury mouse models.

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

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

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

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

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

182 of acetaminophen overdose, its importance in acetaminophen-induced liver toxicity is not well underst

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

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

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

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

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

188 zable) to mice after partial hepatectomy and acetaminophen intoxication, and measured regenerative pa

189 n resulted in 100% survival following lethal acetaminophen intoxication.

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

191 In a rat model, we show the response to acetaminophen involves the expression of 30% of all prot

192 Acetaminophen is a common therapy for fever in patients

193 Research data suggest that acetaminophen is a hormone disruptor, and abnormal hormo

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

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

196 tion of phenolic compounds such as phenol or acetaminophen leads to the generation of the reactive in

197 trient liquid meal was assessed by measuring acetaminophen levels predose and at 0.25, 0.5, 0.75, 1,

198 miRNA specificity was determined in non-acetaminophen liver injury and murine models.

199 r model (miR-382-5p) accurately reported non-acetaminophen liver injury and were unaffected by kidney

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

201 trophils up-regulated TLR9 expression during acetaminophen-mediated necrosis, and these cells sensed

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

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

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

205 that four pharmaceuticals (efavirenz (EFV), acetaminophen, mirtazapine, and galantamine) prescribed

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

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

208 ma risk in early childhood for higher infant acetaminophen (odds ratio [OR], 1.21; 95% CI 1.04-1.41)

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

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

211 and 14 hours after administration of 1000 mg acetaminophen on Days 0 and 10.

212 Effects of acetaminophen on oxidant and irritant respiratory tract

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

214 d with nonsteroidal anti-inflammatory drugs, acetaminophen, opioids, or skeletal muscle relaxants, of

215 After acute acetaminophen or carbon tetrachloride injury no contribu

216 inhibits activation of the current by either acetaminophen or H2O2.

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

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

219 inally in mice after systemic challenge with acetaminophen or isoniazid.

220 fection to receive either 1 g of intravenous acetaminophen or placebo every 6 hours until ICU dischar

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

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

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

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

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

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

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

228 Acetaminophen overdose causes a multitude of interrelate

229 Acetaminophen overdose is the leading cause of acute liv

230 At the same time, acetaminophen overdose is the most common cause of acute

231 sponsible for Ca(2+) entry in hepatocytes in acetaminophen overdose is the Transient Receptor Potenti

232 oscopy, we revealed that liver injury due to acetaminophen overdose led to a directional migration of

233 ion in hepatocytes is a known consequence of acetaminophen overdose, its importance in acetaminophen-

234 ing the circulating miRNome in patients with acetaminophen overdose.

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

236 Acetaminophen (paracetamol) is a widely used analgesic a

237 Acetaminophen (paracetamol) is the most commonly used me

238 Acetaminophen (paracetamol) is the most frequently used

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

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

241 s the use of anti-inflammatory drugs such as acetaminophen/paracetamol and nonsteroidal anti-inflamma

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

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

244 placement did not impact 21-day mortality in acetaminophen patients (p = 0.89).

245 f liquids in healthy subjects as measured by acetaminophen pharmacokinetics.

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

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

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

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

250 clamping that treatment of hepatocytes with acetaminophen results in activation of a cation current

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

252 All treatments except acetaminophen showed clinically significant improvement

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

254 When stratifying by acetaminophen status and adjusting for confounders, intr

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

256 Applied to acetaminophen, this electrochemical immunosensor present

257 IV acetaminophen thus produces modest fever reduction in cr

258 1 subfamily A member 2 (CYP1A2) that convert acetaminophen to highly reactive N-acetyl-p-benzoquinone

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

260 the ED, adding cyclobenzaprine or oxycodone/acetaminophen to naproxen alone did not improve function

261 Early administration of acetaminophen to treat fever due to probable infection d

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

263 is limited to select proteins implicated in acetaminophen toxicity and cellular defence.

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

265 Profiling of acetaminophen toxicity identified multiple miRNAs that r

266 Acetaminophen toxicity is a leading cause of acute liver

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

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

269 of Nrf2 signaling to rescue mice from acute acetaminophen toxicity.

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

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

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

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

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

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

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

277 ends were found with increasing frequency of acetaminophen use during gestation for all outcomes (ie,

278 Maternal acetaminophen use during pregnancy is associated with a

279 Acetaminophen use during pregnancy was assessed prospect

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

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

282 Exposures: Acetaminophen use was assessed by questionnaire completi

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

284 More than half of all mothers reported acetaminophen use while pregnant.

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

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

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

288 d by unmeasured behavioral factors linked to acetaminophen use.

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

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

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

292 CI, -1.5 to 4.1; P = .28), and for oxycodone/acetaminophen vs cyclobenzaprine, 0.9 (98.3% CI, -2.1 to

293 .3% CI, -2.6 to 3.2; P = .77), for oxycodone/acetaminophen vs placebo, 1.3 (98.3% CI, -1.5 to 4.1; P

294 Prenatal acetaminophen was associated with increased asthma (OR,

295 Acetaminophen was implicated in 18 events (56.3%), dieta

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

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

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

299 There is limited evidence to support using acetaminophen with stronger opioids.

300 plasma cell-free hemoglobin, treatment with acetaminophen within 24 hours of ICU admission may reduc