ライフサイエンスコーパス: multiple organ failure

1 pre-existing injury, potentially leading to multiple organ failure).

2 vidence of a "second-hit"-induced late-onset multiple organ failure.

3 ratory failure that is often associated with multiple organ failure.

4 intravascular coagulation, septic shock, and multiple organ failure.

5 mild to severe and possibly lead to death by multiple organ failure.

6 hallenge in a baboon model of sepsis-induced multiple organ failure.

7 ntribute to the development of shock-induced multiple organ failure.

8 rculation to distant organs, where it causes multiple organ failure.

9 e coexisting conditions including sepsis and multiple organ failure.

10 independent predictor of excess mortality in multiple organ failure.

11 ntrinsically involved in the pathogenesis of multiple organ failure.

12 systemic inflammatory response syndrome and multiple organ failure.

13 ibutes to the pathological manifestations of multiple organ failure.

14 in response to inflammation, infection, and multiple organ failure.

15 a may affect the severity and progression of multiple organ failure.

16 barrier, predisposing patients to sepsis and multiple organ failure.

17 lay an important role in the pathogenesis of multiple organ failure.

18 ose and (except one) died within 58 hrs with multiple organ failure.

19 appaB activation, in experimental sepsis and multiple organ failure.

20 extracorporeal life support while in severe multiple organ failure.

21 ve state serve to trigger the development of multiple organ failure.

22 tion and appropriate treatment of sepsis and multiple organ failure.

23 ailure, and possibly a delayed recovery from multiple organ failure.

24 pal mediator of sepsis, often with resulting multiple organ failure.

25 NE in inflammatory disorders such as ALI and multiple organ failure.

26 nduce uncontrolled systemic inflammation and multiple organ failure.

27 ths from exsanguination and late deaths from multiple organ failure.

28 s to acute respiratory distress syndrome and multiple organ failure.

29 cell activation and inflammation, as well as multiple organ failure.

30 on the role of the gut in the generation of multiple organ failure.

31 a due to excessive systemic inflammation and multiple organ failure.

32 inant meningococcemia, refractory shock, and multiple organ failure.

33 ents considered to be at risk for developing multiple organ failure.

34 se in tissue injury, a presumed harbinger of multiple organ failure.

35 ng parenchymal lymphocytic infiltration with multiple organ failure.

36 e associated with venous thromboembolism and multiple organ failure.

37 ne associations between genetic variants and multiple organ failure.

38 ysregulated inflammatory response leading to multiple organ failure.

39 lant and antifibrinolytic state and eventual multiple organ failure.

40 rfusion, systemic inflammatory response, and multiple organ failure.

41 sponse to infection that often culminates in multiple organ failure.

42 ents with acute-on-chronic liver failure and multiple organ failure.

43 Most deaths occurred early after multiple organ failure.

44 ic ischemia, and the patient rapidly died of multiple organ failure.

45 nduces hyperinflammation, ultimately causing multiple organ failure.

46 er OHCA, cyclosporine does not prevent early multiple organ failure.

47 of systemic inflammatory response underlying multiple organ failure.

48 pital mortality, venous thromboembolism, and multiple organ failure.

49 can be challenging to manage and can lead to multiple organ failure.

50 iver abscess, (7) endophthalmitis, , and (8) multiple organ failure.

51 the pathogenesis of critical illness-induced multiple organ failure.

52 n previously shown to be more susceptible to multiple organ failure.

53 severe trauma, which predisposes patients to multiple organ failure.

54 a role in the pathophysiology of sepsis and multiple organ failure.

55 econdary conditions such as septic shock and multiple-organ failure.

56 oscopic necrosectomy did not cause new-onset multiple organ failure (0% vs 50%, RD, 0.50; 95% CI, 0.1

57 t in acute respiratory distress syndrome and multiple organ failure(1-4), but little is known about i

58 te of deaths from exsanguination (9% to 1%), multiple organ failure (12% to 1%), and death within 24

59 atio, 0.15; 95% CI, 0.03-0.60) and new-onset multiple-organ failure (15.6% vs 39.1%; P = .008; risk r

60 Multiple organ failure (16.1%) and sepsis (9.6%) were th

61 f death in both trial groups were sepsis and multiple organ failure (31 [10%] vs 30 [10%]), and the m

62 rsus-host disease, and the patient died from multiple organ failure 4 months after transplantation.

63 died within 14 days, primarily of refractory multiple organ failure (62%).

64 ent; p = 0.004), especially in patients with multiple organ failure (acute-on-chronic liver failure g

65 th complex conditions such as sepsis-induced multiple organ failure, acute liver failure, and thrombo

66 rminated EVT, three patients died because of multiple organ failure, acute respiratory distress syndr

67 h increased risk of cardiovascular death and multiple-organ failure (adjusted hazard ratio, 2.07 [1.3

68 tients who have a hematologic malignancy and multiple organ failure admitted to the ICU.

69 c hypotension, in order to prevent "delayed" multiple organ failure after hemostasis and all-out resu

70 nce and pattern of systemic inflammation and multiple organ failure after major trauma.

71 vation may contribute to the pathogenesis of multiple organ failure among children with indirect acut

72 icantly smaller risk of lung dysfunction and multiple organ failure among the group receiving antipla

73 re following liver transplantation will have multiple organ failure and a high rate of mortality unle

74 leukocytes and has been associated with the multiple organ failure and adult respiratory distress sy

75 Between causes of death, multiple organ failure and brain death affected respecti

76 as a consequence of the rapid development of multiple organ failure and cerebral edema.

77 ciated with severe disease pathology such as multiple organ failure and cerebral malaria.

78 hereby uncontrolled inflammation can lead to multiple organ failure and death of the infected host.

79 complement cascades that could contribute to multiple organ failure and death.

80 atients, this inflammatory response leads to multiple organ failure and death.

81 re to develop sepsis, which may culminate in multiple organ failure and death.

82 uncontrolled immune activation resulting in multiple organ failure and death.

83 bolism that delays recovery or even leads to multiple organ failure and death.

84 nd chemokine interactions, which might limit multiple organ failure and decrease mortality in hemorrh

85 Multiple organ failure and early cardiogenic shock seem

86 drug-induced T cell activation and can cause multiple organ failure and even death.

87 sociated with a significantly higher risk of multiple organ failure and fewer ventilator-free days.

88 % of those with a score of > or =2 developed multiple organ failure and half of them died from sepsis

89 ory response to bacterial infection, causing multiple organ failure and high mortality.

90 a complication of cirrhosis characterized by multiple organ failure and high short-term mortality.

91 e phase with IGF-1/BP-3 response may prevent multiple organ failure and improve clinical outcomes aft

92 omen, with increased age, in the presence of multiple organ failure and in patients with intra-abdomi

93 bundles has fortunately led to a decline in multiple organ failure and in-hospital mortality.

94 formation, and hypotension that can lead to multiple organ failure and lethal shock, as well as desq

95 ns may be associated with a decrease in late multiple organ failure and morbidity.

96 gulopathy and later propensity to infection, multiple organ failure and mortality are associated with

97 Multiple organ failure and mortality rates were 34.8% an

98 is associated with poor outcomes, including multiple organ failure and mortality.

99 endent protective effect of female gender on multiple organ failure and nosocomial infection rates re

100 associated with a 43% and 23% lower risk of multiple organ failure and nosocomial infection, respect

101 died during induction 1 (n = 130), two from multiple organ failure and one from hemorrhage, and none

102 he highest TNF-alpha concentration developed multiple organ failure and required continuous venovenou

103 kidney injury often occurs in the context of multiple organ failure and sepsis.

104 One recipient died of multiple organ failure and sepsis.

105 tion from which numerous patients die due to multiple organ failure and septic shock.

106 eralized inflammatory state that can lead to multiple organ failure and shock.

107 candidemic septic shock sustained persistent multiple organ failure and showed delayed recovery from

108 major secondary causative agents of delayed multiple organ failure and subsequent death after OPW ex

109 comial infection did not increase subsequent multiple organ failure and there was no evidence of a "s

110 hospital-acquired septic shock that leads to multiple organ failures and ultimately ends with death.

111 dict those individuals at increased risk for multiple-organ failure and death and therefore assist in

112 all, 63% developed lung dysfunction, 19% had multiple organ failure, and 21% died.

113 natomical severity of injury, development of multiple organ failure, and 30-day survival were determi

114 in rats and was associated with hypotension, multiple organ failure, and 50% mortality.

115 as well as more frequent infections, sepsis, multiple organ failure, and death (p < 0.05).

116 condition that can manifest as septic shock, multiple organ failure, and death.

117 cessive activation leads to cytokine storms, multiple organ failure, and even death.

118 knockout mice develop severe hypotension and multiple organ failure, and exhibit a remarkable increas

119 d metabolic responses, prevalence of sepsis, multiple organ failure, and mortality than burn patients

120 Overall mortality, multiple organ failure, and nosocomial infection rates f

121 evaluate the effects of gender on mortality, multiple organ failure, and nosocomial infection, after

122 cations, but mostly due to the occurrence of multiple organ failure, and occurred after a median time

123 tality rate, a high likelihood of associated multiple organ failure, and possibly a delayed recovery

124 d with a decreased risk of lung dysfunction, multiple organ failure, and possibly mortality in high-r

125 ection characterized by marked coagulopathy, multiple organ failure, and rapid tissue destruction and

126 h - severe anaemia, coma (cerebral malaria), multiple organ failure, and respiratory distress.

127 acis, leading to extreme bacteremia, sepsis, multiple organ failure, and, ultimately, death.

128 results in a systemic inflammatory response, multiple-organ failure, and death.

129 rimarily driven by cardiovascular causes and multiple-organ failure, and may thus identify a vulnerab

130 ation support was withdrawn in 70 (70%) with multiple organ failure as the indication in 58 (83%) pat

131 nthetic RvD1 on resuscitation attenuated the multiple organ failure associated with HS by a mechanism

132 nthetic RvD1 on resuscitation attenuated the multiple organ failure associated with HS by a mechanism

133 play an important role in the development of multiple organ failure associated with severe sepsis.

134 age II group, 9 died (8% of all deaths) from multiple organ failure associated with their underlying

135 nts with candidemia and septic shock were in multiple organ failure at days 3, 7, and 14; patients wi

136 ilure of three of more organs and sequential multiple organ failure but not mortality.

137 Ebola virus disease complicated by multiple organ failure can be survivable with the applic

138 arenchymal cell apoptosis is contributing to multiple organ failure cannot be determined from the pre

139 d acute liver failure patients compared with multiple organ failure, chronic liver disease, and healt

140 gan failure and showed delayed recovery from multiple organ failure compared with patients with bacte

141 ital-free days (P < 0.05), with no change in multiple organ failure deaths.

142 ia, acute respiratory distress syndrome, and multiple organ failure (Denver 2 score>3) for both child

143 by the Denver multiple organ failure score), multiple organ failure (Denver multiple organ failure sc

144 Hemorrhagic shock often progresses to multiple organ failure despite conventional resuscitatio

145 Overall, 29% of patients had multiple organ failure develop.

146 Multiple organ failure developed in 14% of the survivors

147 Multiple organ failure developed in 31% of patients with

148 ondary endpoints included the development of multiple organ failure, duration of mechanical ventilati

149 lay a fundamental role in the development of multiple organ failure during sepsis.

150 injury in rodent models of inflammation and multiple organ failure elicited by intraperitoneal injec

151 species colonization at multiple sites, and multiple organ failure, empirical treatment with micafun

152 ccompanied by diarrhea and often followed by multiple organ failure, especially of the respiratory an

153 uired sepsis, multiple Candida colonization, multiple organ failure, exposed to broad-spectrum antiba

154 Multiple organ failure following a variety of insults, i

155 ischemia-reperfusion (IR) injury leading to multiple organ failure; however, few studies have focuse

156 olonged response, however, may contribute to multiple organ failure, hypermetabolism, complications,

157 est for associations between soluble Fas and multiple organ failure, identify protein quantitative tr

158 Cause of death was neurologic in 60.0% and multiple organ failure in 34.3% of pediatric acute respi

159 lative protection from acute lung injury and multiple organ failure in children.

160 Multiple organ failure in critically ill patients is ass

161 tion of microvascular thrombi contributes to multiple organ failure in human cases of gram-negative b

162 y innate immune cells is thought to initiate multiple organ failure in murine models of sepsis.

163 42% (11/26); causes of death were sepsis or multiple organ failure in nine and hemorrhage in two pat

164 tions are associated with the development of multiple organ failure in pediatric sepsis.

165 The incidence of multiple organ failure in pediatric trauma victims is lo

166 t they also contribute to the development of multiple organ failure in sepsis.

167 microvasculature from injury and preventing multiple organ failure in sepsis.

168 ocytes are implicated in the pathogenesis of multiple organ failure in sepsis.

169 y injured patients to sepsis and the ensuing multiple organ failure in the clinical situation.

170 e Staphylococcus haemolyticus, septic shock, multiple organ failure including acute respiratory distr

171 nt patients, complicated by septic shock and multiple organ failure, including acute renal injury and

172 Male sex, multiple organ failure, increasing percentage of pancrea

173 ogy and Chronic Health Evaluation II scores, Multiple Organ Failure index, and Glasgow Coma Score, in

174 We propose that, first, multiple organ failure induced by critical illness is pr

175 end point of major complications (new-onset multiple organ failure, intra-abdominal bleeding, entero

176 Sepsis followed by multiple organ failure is a leading cause of death in no

177 Multiple organ failure is a major threat to the survival

178 There is moderate evidence that multiple organ failure is a risk factor for delirium.

179 Multiple organ failure is associated with subsequent nos

180 Sepsis-induced multiple organ failure is the major cause of mortality a

181 ged widely, from mild respiratory disease to multiple organ failure leading to death.

182 included respiratory infection, sepsis, and multiple organ failure, length of stay and mortality; ad

183 ions that include fever and rash, as well as multiple organ failure (liver, kidney, lungs, and/or hea

184 Secondary outcomes were multiple organ failure, lung injury, and sepsis.

185 Patients with multiple organ failure may be at risk for unusual pigmen

186 er understanding of the role of adenosine in multiple organ failure may facilitate the development of

187 olic hepatitis (AH) frequently progresses to multiple organ failure (MOF) and death.

188 Postinjury multiple organ failure (MOF) may result from overwhelmin

189 Although there was no difference in multiple organ failure (MOF) rates across injury mechani

190 Outcomes measured were mortality, multiple organ failure (MOF), venous thromboembolism, in

191 ry is the strongest independent predictor of multiple organ failure (MOF).

192 emia occur in children dying with sepsis and multiple organ failure (MOF).

193 without new onset thrombocytopenia but with multiple organ failure (MOF).

194 Outcomes of interest included multiple organ failure (MOF, Marshall MOD score > 5) and

195 ced acute liver failure (n = 13), nonhepatic multiple organ failure (n = 28), chronic liver disease (

196 ncluded postcardiac surgery (n = 58), sepsis/multiple organ failure (n = 32), respiratory disease (n

197 composite of major complications (new-onset multiple organ failure, new-onset systemic dysfunction,

198 important to apply mechanical support before multiple organ failure occurs.

199 e system participate in the life-threatening multiple-organ failure of endotoxic shock.

200 nfidence interval (CI): 0.09-0.55; P <0.01), multiple organ failure (OR = 0.15; 95% CI: 0.04-0.62; P

201 2.167, 95% CI: 1.234-13.140, p = 0.005), and multiple organ failure (OR = 3.067, 95% CI: 1.184-15.150

202 s thromboembolism (OR, 1.73; p < 0.001), and multiple organ failure (OR, 1.38; p = 0.02).

203 Females had less multiple organ failure [OR: 1.18 (95% CI, 1.05-1.33); P

204 t receiving it (lung dysfunction p = 0.0116, multiple organ failure p = 0.0291).

205 p < 0.001), endophthalmitis (p = 0.003), and multiple organ failure (p < 0.001).

206 erative intensive care stay (P = 0.014), and multiple organ failure (P < 0.001); operation before 200

207 with a potential torpid evolution comprising multiple organ failure, pancreatic necrosis, infected co

208 ng high-dose catecholamines and had signs of multiple organ failure: pH 7.16 (6.68-7.39), blood lacta

209 Network Phenotyping Pediatric Sepsis-Induced Multiple Organ Failure (PHENOMS) study who had not previ

210 y for predicting subsequent mortality and/or multiple organ failure, plasma lactate >or=3.85 mmol/L w

211 nosocomial infection, whereas persistence of multiple organ failure predicted mortality.

212 arrow, heart, and liver transplants, died of multiple organ failure, probably unrelated to TMA.

213 Overall, the multiple organ failure rate was 27%.

214 Multiple organ failure remains common after severe injur

215 ulnerable obese population, evolved toward a multiple organ failure, required prolonged mechanical ve

216 these critically ill patients with impending multiple organ failure requires a team approach with exp

217 tion of patients with cirrhosis manifests as multiple organ failure requiring admission to an intensi

218 deteriorate and within 3 weeks had developed multiple organ failure requiring ventilation, haemofiltr

219 ntially supportive with management of severe multiple organ failure resulting from immune-mediated ce

220 ilure score), multiple organ failure (Denver multiple organ failure score >3), and mortality.

221 c Health Evaluation II score (P = 0.03), the Multiple Organ Failure score (P = 0.01), or presence of

222 red blood cells within 24 hours, and Denver multiple organ failure score at 72 hours as independent

223 MODS was defined as a Denver Multiple Organ Failure score of 4 or greater.

224 unction (defined as grades 2-3 by the Denver multiple organ failure score), multiple organ failure (D

225 005), greater organ failure severity (Denver multiple organ failure score, 3.5 +/- 2.4 vs 0.8 +/- 1.1

226 on persisted after adjustment for APACHE II, Multiple Organ Failure score, or the combined covariates

227 ultiple organ dysfunction score and with the multiple organ failure score.

228 KIM-1 increased in tandem with APACHE II and Multiple Organ Failure scores.

229 ons, acute respiratory distress syndrome, or multiple organ failure scores.

230 nd developed for severe critical illness and multiple organ failure secondary to Ebola virus infectio

231 cascade of complications of septic shock and multiple organ failure seen in Gram-negative bacterial i

232 Males are more susceptible to multiple organ failure, sepsis, and mortality after trau

233 ent modalities, length of stay, and outcome (multiple organ failure, sepsis, mortality rates) were as

234 Our results suggest that multiple organ failure should not be used as a criterion

235 ardiovascular, renal and liver injury or/and multiple organ failure, suggesting a spread of the SARS-

236 rdiovascular, renal and liver injury, and/or multiple organ failure, suggesting a spread of the sever

237 hondrial damage is an important component of multiple organ failure syndrome, a highly lethal complic

238 gut ischemia leading to the exacerbation of multiple organ failure syndrome.

239 Thrombocytopenia-associated multiple organ failure (TAMOF) is a poorly understood sy

240 septic shock and thrombocytopenia-associated multiple organ failure (TAMOF), and in those without new

241 nces, cause cell and tissue damage and hence multiple organ failure, the clinical hallmark of sepsis.

242 n of mitochondrial biogenesis as a potential multiple organ failure therapy.

243 erapies to sustain patients with diverse and multiple organ failures, thus providing patients with a

244 apoptosis of neutrophils is associated with multiple organ failure under those conditions.

245 He was in a septic shock with multiple organ failure up on presentation to emergency r

246 cluding acute respiratory distress syndrome, multiple organ failure, venous thromboembolism, sepsis,

247 (30-day and 90-day mortality, development of multiple organ failure, ventilator-free days, renal fail

248 Multiple organ failure was a frequent cause of death dur

249 n size for mortality, sepsis, infection, and multiple organ failure was approximately 60% total body

250 exchange use in thrombocytopenia-associated multiple organ failure was associated with a decrease in

251 e, hepatic failure, and hemodynamic failure; multiple organ failure was defined as failure of two or

252 Development of multiple organ failure was early (median time, 2 days),

253 Multiple organ failure was inversely associated with lon

254 Multiple organ failure was significantly less likely to

255 ree distinct subphenotypes of CA; those with multiple organ failure were associated with a significan

256 characteristics, 28-day mortality rates, and multiple organ failure were compared for the two cohorts

257 decreased incidence and different pattern of multiple organ failure when compared with adults.

258 Patients with multiple organ failure who have undergone hepatectomy re

259 g with Candida infections, two patients with multiple organ failure who received high-dose fluconazol

260 in children with thrombocytopenia-associated multiple organ failure who received therapeutic plasma e

261 as having capillary leak syndrome (n = 24), multiple organ failure with death from sepsis (n = 37),

262 One study observed an increase in multiple organ failure with higher ratios, whereas no st

263 zed endothelial dysfunction, contributing to multiple organ failure with increased morbidity and mort

264 failure with death from sepsis (n = 37), or multiple organ failure with recovery (n = 57) or as well

265 icant tissue damage and frequently result in multiple organ failure, with >70% mortality.