ライフサイエンスコーパス: plasma exchange

1 Three patients also received plasma exchange.

2 ficult cases or before thymectomy in lieu of plasma exchange.

3 hout plasma exchange treatment, and risks of plasma exchange.

4 gs, danazol, intravenous immunoglobulin, and plasma exchange.

5 ith this disorder need urgent treatment with plasma exchange.

6 in is equivalent to but more convenient than plasma exchange.

7 -eight percent were refractory to first-line plasma exchange.

8 e-pass albumin dialysis, blood exchange, and plasma exchange.

9 vant clinical indications and precautions of plasma exchange.

10 ited efficacy, include immunosuppression and plasma exchange.

11 ncreases observed in TTP patients treated by plasma exchange.

12 gnosed clinically with PTMA and treated with plasma exchange.

13 ough 10 of the 11 patients had a response to plasma exchange, 2 required 20 or more exchanges before

14 cyclophosphamide and corticosteroids (83%), plasma exchange (9%), and biologic agents (after 2002; 1

15 d dramatically with the initiation of prompt plasma exchange, a treatment routinely used without any

16 torical survivors who were given therapeutic plasma exchange alone or with vincristine.

17 ld determine whether adjuvant rituximab with plasma exchange also is beneficial at first diagnosis.

18 ety-seven patients (91.5%) were treated with plasma exchange and 50 patients (47.2%) received eculizu

19 Upfront treatment of acute TTP includes plasma exchange and corticosteroids.

20 resolved upon the remission that accompanied plasma exchange and discontinuation of ticlopidine thera

21 caplacizumab (10 mg daily) or placebo during plasma exchange and for 30 days afterward.

22 scontinuation of the drug and treatment with plasma exchange and has not recurred during 10 months of

23 dium succinate and alternate treatment using plasma exchange and immunoabsorption as well as subseque

24 Daily plasma exchange and immunosuppressive therapies induce r

25 investigated whether NAC, without concurrent plasma exchange and immunosuppressive therapy, is effect

26 hylaxis with eculizumab or standard of care (plasma exchange and intravenous Ig) at ten international

27 Variable regimes of steroids, plasma exchange and intravenous immunoglobulin were asso

28 rials have shown equivalent efficacy of both plasma exchange and intravenous immunoglobulin, but not

29 Plasma exchange and IVIG were both effective in lessenin

30 ith acquired TTP respond to a combination of plasma exchange and rituximab, but some die or acquire i

31 purpura who responded poorly to therapeutic plasma exchange and who were treated with rituximab had

32 igh-dose intravenous steroids in addition to plasma exchange and/or intravenous immunoglobulin.

33 Despite the use of plasma exchanges and intravenous immunoglobulins, Guilla

34 nflammatory syndrome (IRIS), 11 patients had plasma exchange, and 2 had immunoabsorption.

35 ed with methylprednisolone sodium succinate, plasma exchange, and azathioprine and has remained in re

36 fication techniques including hemoperfusion, plasma exchange, and hemofiltration with hemoperfusion w

37 corticosteroids, intravenous immunoglobulin, plasma exchange, and immunosuppressants) and ambulatory

38 The role of stem cell transplantation, plasma exchange, and kidney transplantation in the manag

39 abilized under therapy with corticosteroids, plasma exchange, and mitoxantrone, severe cognitive impa

40 are investigating the roles of methotrexate, plasma exchange, and pulse cyclophosphamide in acute dis

41 0 with high-dose intravenous immunoglobulin, plasma exchanges, and eventually rituximab.

42 presentations of TTP, which are treated with plasma exchange, anticoagulation is the most important t

43 icosteroids, intravenous immunoglobulin, and plasma exchange are the most commonly used treatments fo

44 Response rates to current therapies (mainly plasma exchange) are unsatisfactory.

45 essive agents often used in combination with plasma exchange, are less well defined.

46 ticoids, intravenous immunoglobulins, and/or plasma exchange at some point in their illness.

47 Treatment with plasma exchange, available for more than 20 years, has d

48 ther immunosuppressive agents in addition to plasma exchange but who have a high risk for relapse.

49 e that often could be treated effectively by plasma exchange, but without real understanding of the u

50 Plasma exchange can be helpful in selected patients.

51 ence in the diagnosis to justify the risk of plasma exchange complications.

52 Therapeutic plasma exchange continues to be indicated for idiopathic

53 Therapeutic plasma exchange continues to be reported sporadically in

54 Treatments have usually consisted of plasma exchange, corticosteroids, intravenous immunoglob

55 ines the literature published on therapeutic plasma exchange during 2002.

56 In the acute situation plasma exchange, fat-free parenteral nutrition and acute

57 drome, were randomly assigned treatment with plasma exchange (five single-volume exchanges over 2 wee

58 py and chronic intravenous immunoglobulin or plasma exchange for 12 months without symptom control.

59 for a clinical trial testing the efficacy of plasma exchange for children with septic shock and TAMOF

60 The literature confirms the use of plasma exchange for Guillain-Barre syndrome but suggests

61 he period, reviews of the use of therapeutic plasma exchange for managing Guillain-Barre syndrome and

62 Finally, plasma exchange for Wegener granulomatosis with severe r

63 and 51 (73%) of 70 and 35 of (50%) 70 in the plasma exchange group, respectively.

64 At 1 month, the IVIG and plasma exchange groups showed striking improvements in o

65 Plasma exchange has a confirmed place in therapy.

66 Plasma exchange has been proved to be the most important

67 Plasma exchange has improved survival rates from 10% to

68 ve studies of intravenous immunoglobulin and plasma exchange have not been performed.

69 These patients require plasma exchange, i.e., concurrent replacement of the inh

70 Plasma exchange improves renal recovery rates in severe

71 estions about the rationale for and value of plasma exchange in ADAMTS13 nondeficient patients.

72 cytotoxic drug therapy with the addition of plasma exchange in disease induced by antibody to glomer

73 supportive care, but also immunosuppression, plasma exchange in severe cases and dialysis as needed.

74 vided a compelling rationale for therapeutic plasma exchange in some patients with thrombotic thrombo

75 1978, after performing the first studies on plasma exchange in that disease, he established a myasth

76 The proper role of therapeutic plasma exchange in the treatment of autoimmune hemolytic

77 Recent reports on the value of plasma exchange in the treatment of severe antineutrophi

78 Finally, a large case series of the use of plasma exchange in Wegener granulomatosis was published.

79 Discontinuation of cyclosporine and daily plasma exchange increased the ADAMTS13 activity, which w

80 Plasma exchange increased the rate of renal recovery in

81 t patients, regardless of mutational status, plasma exchange/infusion use, platelet count, or lactate

82 and receiving standard treatment, including plasma exchange, intravenous Ig, and rituximab.

83 Plasma exchange, intravenous immunoglobulin and corticos

84 Syndrome (GBS) enrolled in a trial comparing plasma exchange, intravenous immunoglobulin, and both tr

85 Therapeutic plasma exchange is an effective empiric treatment for th

86 A major unanswered question is whether plasma exchange is effective for the subset of patients

87 ally similar syndromes for which therapeutic plasma exchange is not or may not be beneficial.

88 Treatment with plasma exchange is often effective but does not address

89 Plasma exchange is the most effective initial therapy fo

90 Treatment with intravenous immunoglobulin or plasma exchange is the optimal management approach, alon

91 The role of plasma exchange is uncertain, but this treatment is appr

92 Plasma exchange leads to functionally important neurolog

93 er than 5% but no inhibitor at presentation, plasma exchange led to complete clinical remission and a

94 of patients with severe sepsis suggests that plasma exchange may benefit a subset of patients, those

95 symptoms were also significantly improved by plasma exchange (mean change on Tourette syndrome unifie

96 lism in patients with myeloma indicated that plasma exchange might remove only 25% of the total amoun

97 lopidine or clopidogrel therapy, therapeutic plasma exchange must be promptly instituted to enhance l

98 7), intravenous immunoglobulin (n = 3), and plasma exchange (n = 1).

99 /dl) were randomly assigned to receive seven plasma exchanges (n = 70) or 3000 mg of intravenous meth

100 Ten received plasma exchange, nine IVIG, and ten placebo.

101 ed on plasma infusion for congenital TTP, or plasma exchange, often in combination with immunosuppres

102 of more than 25% for at least 8 weeks during plasma exchange or infusion (in trial 2) were recruited.

103 Plasma exchange or infusion may transiently maintain nor

104 o decrease in the platelet count of >25%, no plasma exchange or infusion, and no initiation of dialys

105 spond to immunomodulatory treatments such as plasma exchange or intravenous immunoglobulin (IVIG).

106 We studied whether plasma exchange or IVIG would be better than placebo (sh

107 imab and cyclosporine in cases refractory to plasma exchange or resistant to the tapering of plasma e

108 ids; 43, intravenous immunoglobulin; and 13, plasma exchange; or a combination of these treatments.

109 ected adult participants, those treated with plasma exchange (PE) improved significantly more on this

110 The effect of plasma exchange (PE) on clinical outcome, suPAR levels,

111 rejection (AMR) is based on a combination of plasma exchange (PE), IVIg, corticosteroids (CS), and ri

112 ing high-dose corticosteroids, mitoxantrone, plasma exchange (PE), rituximab (anti-CD20), and alemtuz

113 ld enhance the efficacy of DSA removal using plasma exchange (PE).

114 Plasma exchange (PE, four to seven treatments per patien

115 h-dose intravenous steroids (HD-S; n = 810), plasma exchange (PE; n = 192), immunoadsorption (IA; n =

116 Initial treatment consisted of plasma exchanges (PE), high doses of calcineurin inhibit

117 ed thrombotic microangiopathy, and intensive plasma exchange (PEx) both replenishes ADAMTS-13 and imp

118 Sixteen of 19 patients were treated with plasma exchange (PEX) therapy, with 6/16 (38%) respondin

119 The article reviews the use of plasma exchange (PLEX) in the management of the antineut

120 Management of PML has routinely used plasma exchange (PLEX) or immunoabsorption to hasten cle

121 with I+R (n = 25), or, in more severe ABMR, plasma exchange (PLEX)+I+R (n = 20).

122 To retrospectively analyze the effect of plasma exchange (PLEX; yes = PLEX(+) , no = PLEX(-) ) an

123 re intensive therapies including twice-daily plasma exchange; pulses of cyclophosphamide, vincristine

124 Plasma exchange reduced circulating levels of soluble B7

125 Plasma exchange reduces levels of B7 in sera from patien

126 Early treatment by plasma exchange reduces serum FLC concentrations, but ra

127 unresponsive to standard therapy (including plasma exchange), renal replacement therapy was successf

128 ion, and/or plasmapheresis with fresh-frozen plasma exchange, resolved TMA in most patients (57%).

129 ticosteroids, intravenous immunoglobulin, or plasma exchange) respond faster to treatment and less fr

130 , 0.50-0.80]; p<0.001; 10 trials, n=557) and plasma exchange (risk ratio, 0.63 [95% CI, 0.42-0.96]; p

131 r antirejection treatment: group I (n = 10), plasma exchange-Rituximab; group II (n = 8), Bortezomib;

132 and after each renal-replacement therapy or plasma exchange session.

133 " improved over baseline (seven of eight for plasma exchange, seven of nine for IVIG).

134 Evidence suggests that plasma exchange should be added to those with more sever

135 Plasma exchange should be promptly initiated before cyto

136 One patient died despite undergoing plasma exchange soon after diagnosis.

137 TTP, and discuss use of rituximab, increased plasma exchange, splenectomy, and immunosuppressive opti

138 relapsing thrombotic microangiopathy despite plasma exchange; splenectomy; and therapy with vincristi

139 for acute TTP is based on daily therapeutic plasma exchange supplying deficient ADAMTS13, with or wi

140 rovement of some affected children following plasma exchange that removed circulating GluR3 antibodie

141 Despite the success of plasma exchange the risk of relapse is high.

142 ide a rationale for the previously empirical plasma exchange therapy (removal of the inhibitory antib

143 universally fatal until the introduction of plasma exchange therapy in the 1970s.

144 3 activity in the context of the response to plasma exchange therapy to identify patients whose diagn

145 nt prolonged or inappropriate treatment with plasma exchange therapy when it is less likely to be suc

146 sma exchange or resistant to the tapering of plasma exchange therapy.

147 imal anticoagulation, immunosuppression, and plasma exchange therapy.

148 icosteroids, intravenous immunoglobulin, and plasma exchange; there is a clear need to test new agent

149 Here we utilize miniaturized plasma exchange to deliver labeled albumin to tissues in

150 A large randomized trial of the use of plasma exchange to treat sepsis also appeared.

151 n were preemptively treated with therapeutic plasma exchange (tPE) and a single dose of Rituximab.

152 Repeated therapeutic plasma exchange (TPE) has been advocated to remove hepar

153 Therapeutic plasma exchange (TPE) has been successfully used to trea

154 P >2 weeks after thienopyridine, therapeutic plasma exchange (TPE) increased likelihood of survival (

155 Therapeutic plasma exchange (TPE) is a useful adjunct in the managem

156 underwent one or two courses of therapeutic plasma exchange (TPE) with subsequent complete resolutio

157 US/TTP during this outbreak with therapeutic plasma exchange (TPE).

158 failure underwent a total of 243 therapeutic plasma exchanges (TPE).

159 udies have suggested the lack of efficacy of plasma exchange treatment and have identified other tran

160 ADAMTS13 was measured before beginning plasma exchange treatment in 142 (88%) of 161 consecutiv

161 diagnostic criteria, high mortality without plasma exchange treatment, and risks of plasma exchange.

162 The diagnosis of TTP is an indication for plasma exchange treatment, but beginning treatment requi

163 iagnosed with TTP-HUS and who may respond to plasma exchange treatment.

164 activity categories apparently responded to plasma exchange treatment.

165 at has not changed since the introduction of plasma exchange treatment.

166 severe ADAMTS13 deficiency may benefit from plasma exchange treatment; in addition, some patients wi

167 ompared with intravenous methylprednisolone, plasma exchange was associated with a reduction in risk

168 Plasma exchange was effective in reducing VGKC antibody

169 s study investigated whether the addition of plasma exchange was more effective than intravenous meth

170 During cardiopulmonary bypass, plasma exchange was performed.

171 ic administration of NAC, without concurrent plasma exchange, was effective in preventing severe TTP

172 less so with intravenous immunoglobulins and plasma exchange-was associated with the most marked redu

173 dnisolone compared with 48 (69%) or 70 after plasma exchange were alive and independent of dialysis (

174 patients desensitized with IVIG+rituximab+/-plasma exchange were enrolled and randomized 1:1 to rece

175 urs, to perform renal-replacement therapy or plasma exchange, were randomly allocated (1:1) to receiv

176 enefit from immunosuppressive therapy and/or plasma exchange, whereas patients with HIT need an alter

177 ugh approximately 80% of patients respond to plasma exchange, which removes autoantibody and replenis

178 ing, or use of intravenous immunoglobulin or plasma exchange within 4 weeks before randomisation, or

179 zed, sham-controlled, double-masked study of plasma exchange without concomitant immunosuppressive tr