ライフサイエンスコーパス: ACLF

1 ACLF displays key features of systemic inflammation and

2 ACLF grade and white cell count, were independent predic

3 ACLF is especially severe in patients with no prior hist

4 ACLF mortality is associated with loss of organ function

5 ACLF resolved or improved in 49.2%, had a steady or fluc

6 ACLF was defined as two or more extrahepatic organ failu

7 ACLF was more common in the younger patients and in thos

8 rrhosis with (n = 178) and without (n = 101) ACLF from the CANONIC study of the CLIF consortium.

9 ients without (80%) than in those with (20%) ACLF.

10 In patients without a prior history of AD, ACLF was unexpectedly characterized by higher numbers of

11 Both SNPs were protective against ACLF; IL-1beta (odds ratio [OR], 0.34, 95% confidence in

12 On multivariate analysis, ACLF was not significantly associated with eGFR less tha

13 HRS (odds ratio, 4.2; 95% CI, 1.2-14.8), and ACLF (odds ratio, 5.9; 95% CI, 1.3-25.9).

14 in (Tf) and ceruloplasmin levels in ACLF and ACLF-MOF, compared to patients with cirrhosis and contro

15 Cirrhosis and ACLF represent a substantial and increasing health and e

16 in patients with decompensated cirrhosis and ACLF, with special emphasis on the principal features of

17 Baseline CysC is a biomarker of RD, HRS, and ACLF and an independent predictor of mortality in patien

18 fails to predict development of RD, HRS, and ACLF.

19 OFs, 33.7% (300 patients) were diagnosed as ACLF.

20 We assessed ACLF grades at different time points to define disease r

21 ver failure (total bilirubin >/=12 mg/dL) at ACLF diagnosis.

22 mortality, and identify differences between ACLF and AD.

23 (28-day) and mid-term (90-day) mortality by ACLF grade at 3-7 days.

24 y patients; and the prognostic score (CLIF-C ACLF score) could be used to provide prognostic informat

25 center European Chronic Liver Failure (CLIF) ACLF in Cirrhosis study.

26 tors of course severity were CLIF Consortium ACLF score (CLIF-C ACLFs) and presence of liver failure

27 e organ failure and mortality data to define ACLF grades, assess mortality, and identify differences

28 had ACLF when the study began, 112 developed ACLF, and 928 did not have ACLF.

29 y began was 33.9%, among those who developed ACLF was 29.7%, and among those who did not have ACLF wa

30 Patients had either ACLF (n = 41), acute decompensation of cirrhosis without

31 Acute-on-chronic liver failure (ACLF) develops in patients with chronic liver disease an

32 who develop acute-on-chronic liver failure (ACLF) have poor outcomes after liver transplantation.

33 Acute-on-chronic liver failure (ACLF) in cirrhosis is an increasingly recognized syndrom

34 Acute-on-chronic liver failure (ACLF) in cirrhosis is characterized by acute decompensat

35 velopment of acute-on-chronic liver failure (ACLF) in patients with liver cirrhosis is associated wit

36 irrhosis and acute-on-chronic liver failure (ACLF) include susceptibility to infection, immuneparesis

37 Acute-on-chronic liver failure (ACLF) is a frequent cause of death in cirrhosis.

38 Acute-on-chronic liver failure (ACLF) is an ailment with high incidence of multiorgan fa

39 Acute on chronic liver failure (ACLF) is associated with multisystem organ failure and p

40 Acute-on-chronic liver failure (ACLF) is characterized by acute decompensation (AD) of c

41 The acute-on-chronic liver failure (ACLF) syndrome is characterized by acute decompensation

42 criteria of acute-on-chronic liver failure (ACLF) were developed in patients with no Hepatitis B vir

43 ered to have acute-on-chronic liver failure (ACLF).

44 2%) in those with severe early course (final ACLF-2 or -3) independently of initial grades.

45 Eighty-one percent had their final ACLF grade at 1 week, resulting in accurate prediction o

46 fatality rates decreased from 65% to 50% for ACLF and from 10% to 7% for cirrhosis.

47 nd 5-fold ($320 million to $1.7 billion) for ACLF.

48 and AD to establish diagnostic criteria for ACLF and showed that it is distinct from AD, based not o

49 We established diagnostic criteria for ACLF based on analyses of patients with organ failure (d

50 e are no established diagnostic criteria for ACLF, so little is known about its development and progr

51 In 2011, the cost per hospitalization for ACLF was 3.5-fold higher than that for cirrhosis ($53,57

52 significantly different between the groups (ACLF 28.77 vs. non-ACLF 21.23, P<0.0001).

53 Of the patients assessed, 303 had ACLF when the study began, 112 developed ACLF, and 928 d

54 received dual organs, 10 of them (29.4%) had ACLF.

55 undred fifty-seven patients in the study had ACLF and 175 patients had no ACLF (non-ACLF) pretranspla

56 sed clinical courses of 388 patients who had ACLF at enrollment, from February through September 2011

57 28-day mortality rate among patients who had ACLF when the study began was 33.9%, among those who dev

58 was 29.7%, and among those who did not have ACLF was 1.9%.

59 an, 112 developed ACLF, and 928 did not have ACLF.

60 ysfunction (RD), hepatorenal syndrome (HRS), ACLF, and mortality.

61 I-ACLF was defined as >/= 2 organ failures given the signi

62 on-related acute-on-chronic liver failure (I-ACLF) derived from multicenter studies are required in o

63 decompensated infected cirrhosis patients, I-ACLF defined by the presence of two or more organ failur

64 nt predictors of poor 30-day survival were I-ACLF, second infections, and admission values of high ME

65 nd hepcidin levels were lower (P < 0.001) in ACLF patients with MOF than those without and other grou

66 of organ failure were predictors of death in ACLF.

67 olism and transport are severely deranged in ACLF patients and more so in those with MOF.

68 ercentage Tf saturation (%SAT) was higher in ACLF-MOF (39.2%; P < 0.001) and correlated with poor out

69 transferrin (Tf) and ceruloplasmin levels in ACLF and ACLF-MOF, compared to patients with cirrhosis a

70 in the subsets of circulating macrophages in ACLF-MOF, compared to other groups (P < 0.01).

71 F and can predict 15- or 30-day mortality in ACLF patients.

72 significant organ dysfunction that occurs in ACLF.

73 T could be used for early prognostication in ACLF patients.

74 tosis, and inflammation were up-regulated in ACLF patients, compared to patients with cirrhosis.

75 ystemic inflammation plays a primary role in ACLF progression.

76 The organ failure trends in ACLF showed an increasing proportion of cardiovascular a

77 tients with nonsevere early course (final no ACLF or ACLF-1) and high-to-very high (42%-92%) in those

78 n the study had ACLF and 175 patients had no ACLF (non-ACLF) pretransplant.

79 y had ACLF and 175 patients had no ACLF (non-ACLF) pretransplant.

80 erence in mean eGFR between the ACLF and non-ACLF cohorts at 3 years posttransplant (56.35 mL/min vs.

81 0-day mortality was extremely low in the non-ACLF patients compared with ACLF patients (4.6% vs 50%,

82 erent between the groups (ACLF 28.77 vs. non-ACLF 21.23, P<0.0001).

83 Assessment of ACLF patients at 3-7 days of the syndrome provides a too

84 ated; and (4) the strength of association of ACLF with SI was higher than with SCD.

85 The course of SI and the course of ACLF (improvement, no change, or worsening) during hospi

86 We aimed to identify diagnostic criteria of ACLF and describe the development of this syndrome in Eu

87 ne independent predictors for development of ACLF were nosocomial infections, Model for Endstage Live

88 flammatory process related to development of ACLF.

89 ese data support SI as the primary driver of ACLF in cirrhosis.

90 dy of 332 patients to evaluate the effect of ACLF, defined as an acute rise in the Model for End-Stag

91 nostic scores and probably the management of ACLF should base on similar principles.

92 demiology, economic burden, and mortality of ACLF in the United States.

93 The prevalence of ACLF among those hospitalizations increased from 1.5% (n

94 severity of SI and frequency and severity of ACLF at enrollment were strongly associated.

95 les were identified according to the type of ACLF precipitating event (active alcoholism/acute alcoho

96 ith nonsevere early course (final no ACLF or ACLF-1) and high-to-very high (42%-92%) in those with se

97 Patients without RD or ACLF at inclusion but with development of either had sig

98 So far there are no biomarkers predicting ACLF.

99 (systemic inflammation [SI] hypothesis) that ACLF is the expression of an acute exacerbation of the S

100 Current study indicates that ACLF is a clinically and pathophysiology distinct even i

101 e was no difference in mean eGFR between the ACLF and non-ACLF cohorts at 3 years posttransplant (56.

102 ients with decompensated cirrhosis (237 with ACLF) and 40 healthy subjects.

103 1beta and IL-1ra) in strong association with ACLF.

104 leukocyte count, and mortality compared with ACLF in patients with a prior history of AD.

105 y low in the non-ACLF patients compared with ACLF patients (4.6% vs 50%, p < 0.0001).

106 on survival of MARS therapy in patients with ACLF could not be demonstrated.

107 Seventy-six percent of the patients with ACLF had acute kidney injury as their reason for decompe

108 Patients with ACLF have increased numbers of immunoregulatory monocyte

109 Patients with ACLF showed significantly higher levels of these markers

110 In all, 189 patients with ACLF were randomized either to MARS (n=95) or to standar

111 Consecutive patients with ACLF were randomly assigned to groups given 5 mug/kg G-C

112 Patients with ACLF were younger and more frequently alcoholic, had mor

113 than doubles the percentage of patients with ACLF who survive for 2 months; it also significantly red

114 One hundred twenty patients with ACLF, 20 patients with compensated cirrhosis, and 20 hea

115 cytokines by immune cells from patients with ACLF, and might be developed to increase the innate immu

116 on, livers, and lymph nodes of patients with ACLF, compared with patients with stable cirrhosis and c

117 c information in HBV cirrhotic patients with ACLF.

118 ent predictors of mortality in patients with ACLF.

119 his study were: (1) Patients with AD without ACLF showed very high baseline levels of inflammatory cy

120 ), acute decompensation of cirrhosis without ACLF (n = 9), cirrhosis without decompensation (n = 17),

121 of C-reactive protein than patients without ACLF (P < .001).

122 r levels of these markers than those without ACLF; (2) different cytokine profiles were identified ac