ライフサイエンスコーパス: TRALI

1 TRALI has primarily been attributed to passive infusion

2 TRALI induction by intact antibody was completely abroga

3 TRALI invokes an acute immune response dominated by neut

4 TRALI is the third leading cause of transfusion-related

5 TRALI is thought to be primarily mediated by donor antib

6 TRALI requires an immune priming step followed by transf

7 TRALI was associated with older platelets (P =.014).

8 TRALI was frequently underdiagnosed and underreported in

9 TRALI, like the acute respiratory distress syndrome, may

10 TRALI, like the adult respiratory distress syndrome, may

11 We report a series of 90 TRALI reactions in 81 patients secondary to transfusion

12 the roles of the F(ab')2 and Fc regions of a TRALI-inducing immunoglobulin G anti-major histocompatib

13 o induce TRALI from RBCs and may represent a TRALI mitigation step.

14 tion even when administered 90 minutes after TRALI onset.

15 elationship between leukocyte antibodies and TRALI is more compelling if concordance between the anti

16 tion, and treatment with ATL in both LPS and TRALI models protected from ALI.

17 al and radiologic manifestations of TACO and TRALI are similar.

18 TACO and TRALI have emerged as important causes of posttransfusio

19 ciated with antibodies have been reported as TRALI and an association with passive infusion of lipids

20 associated with multiple transfusions can be TRALI, because each unit of blood or blood component can

21 First, at the bedside, TRALI causes hypoxia and noncardiogenic pulmonary edema,

22 All blood products can cause TRALI, and no specific treatment is available.

23 exposure to blood components that may cause TRALI are also discussed.

24 a donor whose blood products may have caused TRALI in several transfusion recipients.

25 TRALI syndrome." DATA SYNTHESIS: The classic TRALI syndrome is an uncommon condition characterized by

26 In both experimental and clinical TRALI, an immune priming step is generally necessary to

27 PS) as the priming step, whereas in clinical TRALI the specific priming events are currently being de

28 es is necessary before initiation of complex TRALI workup.

29 s to what should be considered to constitute TRALI.

30 Both the classic and delayed TRALI syndromes are among the most important complicatio

31 e management of both the classic and delayed TRALI syndromes is essentially supportive.

32 and to define the newly recognized "Delayed TRALI syndrome." DATA SYNTHESIS: The classic TRALI syndr

33 While the delayed TRALI syndrome can develop after the transfusion of a si

34 This "delayed TRALI syndrome" is common, occurring in up to 25% of cri

35 To determine TRALI incidence by prospective, active surveillance and

36 re is no sentinel feature that distinguishes TRALI from TACO.

37 e suggest that NETs form in the lungs during TRALI, contribute to the disease process, and thus could

38 In the experimental TRALI model, targeting platelet activation with either a

39 A common theme among the experimental TRALI models is the central importance of neutrophils in

40 s than in red blood cell products (the fatal TRALI incidence for plasma is 1:2-300 000 products; plat

41 s inflammation are known to be important for TRALI initiation.

42 Since 2004, preventive measures for TRALI and TAS have been implemented, but their implement

43 Two proposed pathophysiologic mechanisms for TRALI have received the most attention: the antibody hyp

44 nd DNase1, both of which protected mice from TRALI.

45 I mAb, there was significant protection from TRALI compared with nonbarrier mice.

46 interleukin-8, a known risk factor for human TRALI.

47 tected NETs in the lungs and plasma of human TRALI and in the plasma of patients with acute lung inju

48 ies has replicated several features of human TRALI, focusing prominently on the role of neutrophils.

49 Recent developments in TRALI secondary to antibodies to HNA-3a antigen span dia

50 in platelet concentrates (PCs) implicated in TRALI or control PCs that did not elicit a transfusion r

51 PCs implicated in TRALI reactions contained significantly higher sCD40L le

52 a containing HNA-3a antibodies implicated in TRALI, and their ability to prime the oxidase was measur

53 ibodies to HNA-3a are commonly implicated in TRALI.

54 i-HNA-3a antibodies previously implicated in TRALI.

55 to biologic response modifiers implicated in TRALI.

56 In this study, the role of these lipids in TRALI was investigated using an isolated, perfused rat l

57 roup to identify areas of research needed in TRALI.

58 e we show that NET biomarkers are present in TRALI patients' blood and that NETs are produced in vitr

59 , which, in a susceptible patient, result in TRALI (2-hit hypothesis).

60 uct-derived factors and appears to result in TRALI by binding directly to pulmonary endothelium as we

61 lammatory activity and the ability to induce TRALI from RBCs and may represent a TRALI mitigation ste

62 priming activity, and the ability to induce TRALI in an animal model were measured.

63 ng of transfusion related acute lung injury (TRALI) and transfusion associated circulatory overload (

64 Transfusion-related acute lung injury (TRALI) is a form of posttransfusion acute pulmonary insu

65 Transfusion-related acute lung injury (TRALI) is a life-threatening complication of hemotherapy

66 Transfusion-related acute lung injury (TRALI) is a serious complication of hemotherapy.

67 Transfusion-related acute lung injury (TRALI) is a syndrome of respiratory distress triggered b

68 Transfusion-related acute lung injury (TRALI) is a syndrome that includes dyspnea, hypotension,

69 Transfusion-related acute lung injury (TRALI) is now the leading cause of transfusion-associate

70 Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion death.

71 Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-associated mo

72 Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related death

73 Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related morta

74 Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related morta

75 Transfusion-related acute lung injury (TRALI) is the leading cause of transfusion-related morta

76 Transfusion-related acute lung injury (TRALI) is the most common cause of transfusion-related m

77 Transfusion-related acute lung injury (TRALI) remains a significant cause of transfusion-relate

78 rding transfusion-related acute lung injury (TRALI) through the bedside to bench and back to the beds

79 term transfusion-related acute lung injury (TRALI) was coined in 1983 to describe a constellation of

80 Transfusion-related acute lung injury (TRALI), a form of noncardiogenic pulmonary edema that de

81 el of transfusion-related acute lung injury (TRALI), a life-threatening complication of transfusions

82 el of transfusion-related acute lung injury (TRALI), Boc2 also reversed ASA protection, and treatment

83 e US, transfusion-related acute lung injury (TRALI), hemolytic transfusion reactions (HTRs), and tran

84 ions, transfusion-related acute lung injury (TRALI), transfusion-associated graft-versus-host disease

85 s) in transfusion-related acute lung injury (TRALI), which is the leading cause of death after transf

86 ed in transfusion-related acute lung injury (TRALI).

87 to as transfusion-related acute lung injury (TRALI).

88 event transfusion-related acute lung injury (TRALI).

89 fatal transfusion-related acute lung injury (TRALI).

90 is of transfusion-related acute lung injury (TRALI).

91 to as transfusion-related acute lung injury (TRALI).

92 Only additional research into TRALI prevention will provide the answers on how to best

93 ng male predominant plasma programs to limit TRALI, and preliminary evidence suggests that this is a

94 whether CRP affects murine antibody-mediated TRALI induced by the anti-major histocompatibility compl

95 est a two-step process for antibody-mediated TRALI induction: the first step involves antibody bindin

96 A murine antibody-mediated TRALI model was used to elucidate the roles of the F(ab'

97 y predispose recipients to antibody-mediated TRALI reactions and support the notion that modulating C

98 reviewed and contrasted to antibody-mediated TRALI.

99 veoli of mice experiencing antibody-mediated TRALI.

100 reviously, we established an immune-mediated TRALI mouse model, wherein mice with cognate antigen wer

101 of lipid priming activity and lipid-mediated TRALI.

102 ces in pulmonary and critical care medicine, TRALI is now considered to be one of the leading causes

103 Thus, steps to mitigate TRALI are in place, but a complete mechanistic understan

104 Experimental studies have modeled TRALI by using anti-major histocompatibility complex ant

105 Superimposed illness prevented assessment of TRALI in 14 patients.

106 ld to develop and standardize definitions of TRALI so that epidemiologic and research aspects of this

107 Because development of TRALI is associated with donor antibodies (Abs) reactive

108 Second, the development of TRALI requires a hit from the patient and from the produ

109 To examine the epidemiology of TRALI, we completed a nested case-control study of the f

110 pted clinical (mainly pulmonary) features of TRALI, the treatment options, and the excellent long-ter

111 The two major hypotheses of TRALI, passively transfused neutrophil and human leukocy

112 be effective in decreasing the incidence of TRALI and which could have significant drawbacks.

113 early promise in decreasing the incidence of TRALI from high plasma volume blood products.

114 n explanation for the increased incidence of TRALI in patients with immune priming conditions, and we

115 antibodies, have decreased the incidence of TRALI.

116 review are to summarize current knowledge of TRALI with an emphasis on issues pertinent to the intens

117 These data suggest a 2-step mechanism of TRALI: priming of hematopoietic cells, followed by vascu

118 all of the proposed pathogenic mechanisms of TRALI is increased pulmonary capillary permeability, whi

119 s in the pathogenesis of this mouse model of TRALI and show ultrastructural evidence of pulmonary vas

120 A new in vivo mouse model of TRALI based on major histocompatibility complex (MHC) I

121 The proposed two-hit model of TRALI is also supported by animal studies.

122 rux and Sachs clarified the two-hit model of TRALI pathogenesis.

123 In a mouse model of TRALI that is neutrophil and platelet dependent, NETs ap

124 a clinically relevant in vivo mouse model of TRALI using an MHC I mAb, the mechanism of lung injury w

125 The two-event model of TRALI, which is identical to the pathogenesis of the acu

126 second event in a 2-event in vitro model of TRALI.

127 n was evaluated in a 2-event animal model of TRALI.

128 g injury is common to all existing models of TRALI.

129 anistic understanding of the pathogenesis of TRALI and of which patients are at highest risk remains

130 To explore the pathogenesis of TRALI, we developed an in vivo mouse model based on the

131 have been implicated in the pathogenesis of TRALI.

132 for establishing the pretest probability of TRALI as opposed to TACO.

133 o, are discussed as well as human studies of TRALI.

134 port both the antibody and lipid theories of TRALI.

135 ications for the prevention and treatment of TRALI.

136 but because of gaps in our understanding of TRALI, blood-bankers do not know how beneficial these in

137 between hydrostatic (TACO) and permeability (TRALI) pulmonary edema after transfusion is difficult, i

138 MNs, causing endothelial damage and possibly TRALI in predisposed patients.

139 red blood cell (RBC) supernatant and prevent TRALI.

140 rtality, and thus determining how to prevent TRALI is extremely important.

141 Preventing TRALI poses a difficult challenge for blood-banking expe

142 an effective therapeutic strategy to reduce TRALI severity.

143 om female donors was concurrent with reduced TRALI incidence: 2.57 (95% CI, 1.72-3.86) in 2006 versus

144 s report, clinicians can diagnose and report TRALI cases to the blood bank; importantly, researchers

145 vide potential targets for reducing residual TRALI.

146 ), and compared with pretransfusion samples, TRALI patients' plasma demonstrated increases in both in

147 We conclude that TRALI is the result of 2 events with the second events c

148 We conclude that TRALI may be more frequent than previously recognized an

149 consensus conference helped demonstrate that TRALI is likely underreported.

150 We hypothesize that TRALI requires 2 events: (1) the clinical condition of t

151 The major concept is that TRALI is defined as new acute lung injury occurring duri

152 The TRALI definition developed at the 2004 consensus confere

153 response modifiers responsible for 51 of the TRALI cases, including human leukocyte antigen (HLA) cla

154 The biologic processes contributing to TRALI are poorly understood.

155 ens in the recipient does not always lead to TRALI.

156 ids in components may predispose patients to TRALI.

157 with 34-1-2s or CRP alone were resistant to TRALI, however mice injected with 34-1-2s together with

158 d thus could be targeted to prevent or treat TRALI.

159 A typical TRALI serologic workup consists of tests for HLA class I

160 well as mitigating antibody-mediated in vivo TRALI.

161 e conferences have set out criteria by which TRALI is distinguished from other causes of acute lung i

162 HC), a mouse model has been studied in which TRALI-like disease is caused by injecting mice with anti

163 s were sequestered in the lungs of mice with TRALI, and retention of platelets was neutrophil depende

164 -control study of the first 46 patients with TRALI compared with 225 controls who had received transf