ライフサイエンスコーパス: IVIG

1 IVIG (400 mg/kg) was given every 3 weeks from week 12 to

2 IVIG at the dose and frequency used in this study was no

3 IVIG can alter the viability of human neutrophils via ag

4 IVIG cases were propensity-matched and risk-adjusted.

5 IVIG is also a recently recognized modifier of complemen

6 IVIG is used to prevent cardiovascular complications rel

7 IVIG may provide at least some level of protection for i

8 IVIG or albumin control was administered 24 hours before

9 IVIG preparations contain broadly cross-reactive ADCC me

10 IVIG products are also effective in the treatment of aut

11 IVIG resistance was associated with higher levels of IL-

12 IVIG resulted in a reduction in IL-6 and IL-17A at both

13 IVIG subjects were younger with lower comorbidity indice

14 IVIG therapy appears to be effective in the short term i

15 IVIG therapy in this subgroup may improve survival and m

16 IVIG therapy of OVA-sensitized and OVA-challenged mice i

17 IVIG therapy resulted in increased expression of Treg-re

18 IVIG was administered at a dose of 400 mg/kg at weeks 12

19 IVIG was protective in the nonreperfusion model of murin

20 .001) or after (29 [54.7%] of 53, P < .001) IVIG treatment, inability to walk unaided (21 [35.0%] of

21 Patients received a mean of 2.7 +/- 2.1 IVIG courses (1.3 +/- 0.5 g/kg/course).

22 H1N1 swine-origin influenza pandemic and 10 IVIG preparations made after 2010 for their ability to m

23 amnestic MCI were administered 0.4 g/kg 10% IVIG or 0.9% saline every 2 weeks for a total of 5 infus

24 KD patients, a total of 150 KD patients (126 IVIG responders and 24 IVIG nonresponders) were recruite

25 150 KD patients (126 IVIG responders and 24 IVIG nonresponders) were recruited for this study.

26 ion of patients was noted (IVIG+placebo N=7, IVIG+rituximab N=6).

27 We tested 8 IVIG preparations prior to the 2009 H1N1 swine-origin in

28 Adjunctive IVIG was administered infrequently in NF with shock and

29 cument the clinical efficacy of administered IVIG therapy in a comparative observational study of wel

30 Serum samples were obtained before and after IVIG treatment at 4 standardized time points from 174 pa

31 levels increased significantly 3 days after IVIG therapy (2.28 +/- 0.34 vs 0.88 +/- 0.14, P < 0.001)

32 IL-6 and IL-17A at both 3 and 21 days after IVIG therapy.

33 herapy, followed by 3 days and 21 days after IVIG therapy.

34 all recover ITP with similar dynamics after IVIG (1 g/kg) treatment; however, this was not the case

35 n of KD patients have persistent fever after IVIG treatment and are defined as IVIG resistant.

36 mediated by tolerogenic DCs generated after IVIG exposure.

37 ism of intravenous anti-D and IVIG, although IVIG may also enhance thrombopoiesis.

38 or identifying true NF and debridement among IVIG cases using our algorithms were 97% and 89%, respec

39 and vasopressor intensity were higher among IVIG cases, as was coding for TSS and GAS.

40 IIB neutrophil antigen 1 (NA1) variant among IVIG nonresponders (P=0.0002) and specifically to white

41 nt of IVIG and helps guide development of an IVIG replacement with improved activity and availability

42 .007), clindamycin (OR, 8.6; P = .007), and IVIG (OR, 5.6; P = .030).

43 f new functions of monoclonal antibodies and IVIG.

44 ngineering of intact monoclonal antibody and IVIG.

45 Corticosteroid and IVIG treatment was completely stopped.

46 primary mechanism of intravenous anti-D and IVIG, although IVIG may also enhance thrombopoiesis.

47 eatly surpassed AAV-2 in livers of naive and IVIG-immunized mice.

48 er PRA, and received more plasmapheresis and IVIG at the time of transplant.

49 dy provides class III evidence that PLEX and IVIG both have high response rates as maintenance therap

50 Both PLEX and IVIG had high response rates.

51 ever after IVIG treatment and are defined as IVIG resistant.

52 tients coded for TSS, GAS, and/or S. aureus, IVIG use was still unusual (59/868 [6.8%]) and lacked be

53 e tested five lots of commercially available IVIG preparations from two different suppliers for polyo

54 hildren with Kawasaki disease at 24 h before IVIG therapy, followed by 3 days and 21 days after IVIG

55 Median LOS was similar between IVIG and non-IVIG groups (26 [13-49] vs 26 [11-43]; P =

56 ntified STSS patients demonstrates that both IVIG and clindamycin therapy contribute to a significant

57 ession of either CAbIA or K/BxN arthritis by IVIG.

58 ions that lead to induction of Treg cells by IVIG.

59 t changes in blood clearance were induced by IVIG.

60 resent the initial step that is triggered by IVIG to suppress inflammation.

61 Certain IVIG products tested positive for GM-EIA and there were

62 ore antibody among patients newly commencing IVIG.

63 Different commercial IVIG preparations similarly induced cytokine-dependent d

64 CONCLUSIONS.: IVIG and rituximab seems to offer significant benefits i

65 Among those who received concurrent IVIG, the fatality rate was lower still (7%).

66 induced mast cell activation/degranulation, IVIG attenuated post-ICH mast cell activation.

67 High-dose IVIG (1-2 g/kg body weight) suppressed inflammatory arth

68 oing chronic graft damage, whereas high-dose IVIG may reduce the risk of chronic graft dysfunction in

69 High-dose IVIG resulted in modest DSA MFI reductions in patients w

70 Early IVIG (</=2 days) did not alter this effect (P = .99).

71 varied, with the authors generally favoring IVIG and/or corticosteroids as first-line agents.

72 moglobin level was corrected after the first IVIG course in 124 patients (93%); disease relapsed in 4

73 the 2 groups and identified risk alleles for IVIG resistance.

74 d 12 months showed a significant benefit for IVIG+rituximab (P=0.04).

75 difficult to detect or that serum pooled for IVIG purification may include asymptomatic persons with

76 eing explored as biomimetic replacements for IVIG therapy, which is deployed to manage many diseases

77 f Kawasaki disease patients at high risk for IVIG resistance found that the group receiving steroids,

78 Furthermore, IVIG-primed DCs can stimulate Treg cell differentiation

79 we showed that intravenous immunoglobulin G (IVIG) treatment significantly reduced endotoxemia and th

80 stosis following intravenous gamma globulin (IVIG) and corticosteroid therapy.

81 sitization with intravenous immune globulin (IVIG) and rituximab improves transplantation rates.

82 sitization with intravenous immune globulin (IVIG) and rituximab improves transplantation rates.

83 now report that intravenous immune globulin (IVIG) derived from pools of human plasma contains IgGs t

84 Intravenous immune globulin (IVIG) suppresses autoantibody-mediated inflammation by i

85 that high-dose intravenous immune globulin (IVIG; 2 g/kg x2 doses)+rituximab (1 g x2 doses) was effe

86 clearance rates among the intravenous group, IVIG group, and HAI group, nor was there any difference

87 However, IVIG at low doses consistent with replacement does not p

88 However, IVIG+rituximab appeared more effective in preventing DSA

89 Human IVIG preparations contain BKV neutralizing antibodies.

90 several samples of clinically approved human IVIG (IgG).

91 nti-inflammatory activity of intravenous Ig (IVIG) results from a minor population of the pooled IgG

92 High-dose i.v. Ig (IVIG) is used to treat various autoimmune and inflammato

93 Here we show that i.v. Ig (IVIG) treatment, which scavenges complement fragments, p

94 ts from clinically approved intravenous IgG (IVIG) and used at higher concentrations to suppress grow

95 How high doses of intravenous IgG (IVIG) suppress autoimmune diseases remains unresolved.

96 when a large dose of human intravenous IgG (IVIG) was administered to manipulate the Fc receptor or

97 lowing antenatal intravenous immunoglobulin (IVIG) +/- prednisone therapy demonstrated a significant

98 Intravenous immunoglobulin (IVIG) and aspirin is the standard initial therapy in the

99 using high-dose intravenous immunoglobulin (IVIG) and rituximab to improve transplantation rates in

100 e the effects of intravenous immunoglobulin (IVIG) and rituximab treatment.

101 Intravenous immunoglobulin (IVIG) are purified IgG preparations made from the pooled

102 8 responding to intravenous immunoglobulin (IVIG) did not have corresponding increases in A-IPF, but

103 term efficacy of intravenous immunoglobulin (IVIG) for the treatment of CIDP and the US Food and Drug

104 Intravenous immunoglobulin (IVIG) has been shown to have a beneficial effect in syst

105 peutic action of intravenous immunoglobulin (IVIG) in immune thrombocytopenia (ITP) involves up-regul

106 clindamycin and intravenous immunoglobulin (IVIG) in treatment of invasive group A streptococcal (iG

107 Intravenous immunoglobulin (IVIG) is a FDA-approved drug containing IgG.

108 Intravenous immunoglobulin (IVIG) is a frequently used disease-modifying therapy for

109 Intravenous immunoglobulin (IVIG) is a purified pool of human antibodies from thousa

110 tory activity of intravenous immunoglobulin (IVIG) is dependent on the presence of sialic acid in the

111 Intravenous immunoglobulin (IVIG) is sometimes administered for presumptive toxic sh

112 Intravenous immunoglobulin (IVIG) is the treatment of choice in Kawasaki disease (KD

113 bulin (RATG) and intravenous immunoglobulin (IVIG) may allow successful transplant of these high-risk

114 ne the effect of intravenous immunoglobulin (IVIG) on brain atrophy and cognitive function in mild co

115 Intravenous immunoglobulin (IVIG) products are derived from pooled human plasma and

116 n pharmaceutical intravenous immunoglobulin (IVIG) purified from serum pooled from healthy subjects.

117 aRIIB influences intravenous immunoglobulin (IVIG) response in Kawasaki disease (KD), a vasculitis pr

118 atients received intravenous immunoglobulin (IVIG) therapy at 400 mg/kg x 3 to 4 doses.

119 etermine whether intravenous immunoglobulin (IVIG) therapy could prevent the development of CHB in th

120 Intravenous immunoglobulin (IVIG) therapy has been suggested as adjunctive treatment

121 the efficacy of intravenous immunoglobulin (IVIG) therapy in patients with pure red cell aplasia (PR

122 atory responses, intravenous immunoglobulin (IVIG) was evaluated as preventive therapy for CHB.

123 Intravenous immunoglobulin (IVIG), a pooled normal IgG formulation prepared from tho

124 of steroids and intravenous immunoglobulin (IVIG), and ameliorates neurological deficits, compared t

125 s, vitamin D, or intravenous immunoglobulin (IVIG), are discussed, as their dissection might reveal t

126 lbumin (HSA) and intravenous immunoglobulin (IVIG).

127 col of high-dose intravenous immunoglobulin (IVIG).

128 ctivity of human intravenous immunoglobulin (IVIG).

129 ally with P4 and intravenous immunoglobulin (IVIG).

130 heresis (PL) and intravenous immunoglobulin (IVIG).

131 orm of high-dose intravenous immunoglobulin (IVIG).

132 nts treated with intravenous immunoglobulin (IVIG).

133 dministration of intravenous immunoglobulin (IVIG).

134 ients commencing intravenous immunoglobulin (IVIG); and pre- and post-infusion analysis of GM-EIA in

135 ed human plasma [intravenous immunoglobulin (IVIG)] confer anti-inflammatory activity in a variety of

136 human antisera (intravenous immunoglobulin [IVIG]) then led to the selection of a single type 2/type

137 based on IgM-enriched human immunoglobulins (IVIG), repeated every 4 weeks, and a single dose of Ritu

138 Human intravenous immunoglobulins (IVIG) have been used as an empiric therapy without proof

139 80), as well as to evaluate DSA clearance in IVIG-treated patients versus historic patients who had u

140 (HA) and neuraminidase (NA) were detected in IVIG preparations prior to the 2009-H1N1 pandemic.

141 some of the species differences observed in IVIG protection.

142 rologous influenza strains may be present in IVIG preparations.

143 In addition, FcgammaRIII-induced IVIG anti-inflammatory activity in neutrophils was media

144 transplanted using standard RATG induction, IVIG, and maintenance immunosuppression with equal renal

145 weekly maternal IV immunoglobulin infusion (IVIG), with or without additional corticosteroid therapy

146 When using 2.5 g/kg IVIG in FcgammaRIIB(-/-) B6 mice, amelioration of ITP wa

147 bed a standard regimen of high-dose (5 g/kg) IVIG dosed over 6 months.

148 tal mortality did not differ between matched IVIG and non-IVIG groups (crude mortality, 27.3% vs 23.6

149 During pregnancy, maternal IVIG was given in 9 and dexamethasone in 17.

150 tionally, our results indicate that maternal IVIG therapy can effectively prevent this devastating di

151 ve factor for the fetal response to maternal IVIG therapy.

152 FcgammaRIII mediated IVIG-triggered inhibition of leukocyte recruitment, circ

153 ared with albumin-treated, OVA-exposed mice, IVIG-primed DCs express altered Notch ligands, including

154 /BxN serum transfer arthritis model in mice, IVIG suppression of inflammation has been attributed to

155 requiring approximately 2- to 2.5-fold more IVIG than BALB/c.

156 Median LOS was similar between IVIG and non-IVIG groups (26 [13-49] vs 26 [11-43]; P = .84).

157 did not differ between matched IVIG and non-IVIG groups (crude mortality, 27.3% vs 23.6%; adjusted o

158 inded and attribution of patients was noted (IVIG+placebo N=7, IVIG+rituximab N=6).

159 s further clarify the mechanism of action of IVIG in both antibody- and T cell-mediated inflammatory

160 il involvement in the mechanism of action of IVIG therapy.

161 shown that the antiinflammatory activity of IVIG can be attributed to a minor species of IgGs that i

162 impact on the anti-inflammatory activity of IVIG or Fc fragments.

163 abrogated the anti-inflammatory activity of IVIG or sialylated Fc fragments.

164 Our data confirm the therapeutic benefit of IVIG and IgG Fc in Ab-induced arthritis but fail to supp

165 defines the biologically active component of IVIG and helps guide development of an IVIG replacement

166 s with clinically relevant concentrations of IVIG derived from healthy and hepatitis B vaccinated sub

167 ides limited evidence that a short course of IVIG administered in the MCI stage of AD reduces brain a

168 Even a single low dose of IVIG given after stroke was effective.

169 sensitization protocol included two doses of IVIG (2 g/kg, max 120 g each dose) and a single dose of

170 for at least 1 year; however, this effect of IVIG appears to wane by 2 years.

171 plays no role in the mechanism of effect of IVIG in experimental ITP.

172 B and III abrogated the protective effect of IVIG on acute vaso-occlusive crisis caused by neutrophil

173 Indeed, the protective effect of IVIG on leukocyte recruitment and activation was abrogat

174 ammaRIIB, abrogated the inhibitory effect of IVIG on leukocyte recruitment and heterotypic red blood

175 CAbIA model, the anti-inflammatory effect of IVIG was dependent on IgG Fc but not F(ab')2 fragments.

176 The effect of IVIG was evaluated in patients with STSS prospectively i

177 The inhibitory effect of IVIG was mediated at least in part by soluble immune com

178 We investigated the effects of IVIG on cellular responses to interferon-gamma (IFN-gamm

179 In this study, we compared the effects of IVIG on human and mouse neutrophils using different deat

180 ese observations demonstrate that effects of IVIG on neutrophil survival are not adequately reflected

181 The anti-inflammatory effects of IVIG therapy can be mediated by the immunomodulation of

182 Four patients showed side effects of IVIG treatment: acute reversible renal failure (n = 2) a

183 h we demonstrated that beneficial effects of IVIG were mediated, at least partly, via SHIP1/PIP3 path

184 this report was to evaluate the efficacy of IVIG+rituximab on reduction of anti-HLA antibodies to a

185 F(ab')2 but not Fc fragments of IVIG induced death of human neutrophils, whereas neither

186 is not clear because of the heterogeneity of IVIG.

187 Fifteen patients received infusions of IVIG.

188 challenges, however, are the pluripotency of IVIG and its xenogeneicity in animals.

189 butes to the anti-inflammatory properties of IVIG.

190 three patients suggests a potential role of IVIG therapy in controlling active WNV infection, partic

191 This study establishes the safety of IVIG and the feasibility of recruiting pregnant women wh

192 ally, the structure and thermal stability of IVIG were studied, and a comprehensive characterization

193 to determine the optimal dose and timing of IVIG administration.

194 +) T cells ex vivo, and adoptive transfer of IVIG-primed DCs abrogates airway hyperresponsiveness and

195 and Drug Administration approved the use of IVIG (Gamunex) as a treatment for CIDP.

196 ort for investigating the therapeutic use of IVIG in Alzheimer's disease.

197 inical trials seeking to validate the use of IVIG in patients with BKV infection.

198 On IVIG, 79 of 79 tested positive for surface antibody, 37

199 l management strategy applied; FBS, IUPT, or IVIG with or without corticosteroids.

200 Survival of P4-IVIG-treated mice increased from 0% to 60% among those t

201 Combinations that include plasmapheresis, IVIG, cyclophosphamide, and rituximab have been used in

202 with generalized juvenile MG receiving PLEX, IVIG, or both treatments, 7 of 7 patients treated with P

203 Compared to PLEX, IVIG appears of similar clinical (mortality and complica

204 0.31; 95% CI, .09-1.12) and clindamycin plus IVIG-treated patients (0.12; 95% CI, .01-1.29) compared

205 Pre-IVIG, 9 of 80 patients tested positive for HBV surface a

206 g system based on genetic markers to predict IVIG responsiveness in KD patients, a total of 150 KD pa

207 Only group 3 received IVIG at 500 mg/kg daily in three doses.

208 tients via HAI, and 5 patients also received IVIG.

209 nly 164 patients (4%) at 61 centers received IVIG.

210 After birth, 17 infants received IVIG (n = 14) and/or corticosteroids (n = 15).

211 15 HS patients received IVIG (2 g/kg x2 doses)/rituximab (375 mg/m x1) for desen

212 Twenty-three patients received IVIG therapy compared with 44 who did not.

213 133 patients with HPV-B19 PRCA who received IVIG (our 10 patients and 123 from the literature), 63 h

214 The LMCI participants who received IVIG performed better on Alzheimer's Disease Assessment

215 years, while the youngest child who received IVIG was 9 months old.

216 rtery abnormalities than the group receiving IVIG and aspirin alone.

217 positivity are common in patients receiving IVIG and confound diagnostic results.

218 rmacokinetics showed that patients receiving IVIG had a significantly shorter serum half-time (41.6 +

219 analysis of GM-EIA in 37 patients receiving IVIG.

220 ntly more complications than those receiving IVIG (30.06% vs 14.79%, p < 0.001).

221 luding intravenous immunoglobulin/rituximab (IVIG/R) are employed to decrease anti-human leukocyte an

222 FcgammaRIIIB) also influence susceptibility, IVIG treatment response, and coronary artery disease in

223 ay have a more consistent response rate than IVIG in this setting.

224 ciated with bacterial translocation and that IVIG treatment resolves bacterial translocation and rest

225 We conclude that IVIG treatment represents a promising therapeutic approa

226 Recent reports demonstrate that IVIG exerts anti-inflammatory actions by stimulating the

227 c airways disease, we have demonstrated that IVIG markedly improves ovalbumin (OVA)-induced airway hy

228 fluorescence videomicroscopy, we found that IVIG affected specifically the recruitment of neutrophil

229 We hypothesized that IVIG will attenuate the ICH-induced mast cell activation

230 analyses of leukocyte behavior revealed that IVIG significantly increased rolling velocities, indicat

231 Recent investigations suggest that IVIG has a much broader ability to regulate cellular imm

232 The IVIG yielded increased DSA clearance compared with histo

233 an important role in KD pathogenesis and the IVIG antiinflammatory mechanism.

234 se, organ failures, or sex was seen, but the IVIG group was slightly younger and had a higher degree

235 Twenty mothers completed the IVIG protocol before the predetermined stopping rule of

236 conversions from LMCI to AD dementia in the IVIG group (33.3%) when compared with control group (58.

237 hy (p=0.037, adjusted for MCI status) in the IVIG group (5.87%) when compared with placebo (8.14%) at

238 All ABMR episodes occurred in the IVIG+placebo arm and required intense therapy (P=0.06).

239 evere ABMR was seen in three patients in the IVIG+placebo group.

240 No rebound was seen in the IVIG+rituximab group.

241 fter becoming PCR-positive was longer in the IVIG-treated patients (p = 0.03) with a trend toward imp

242 d a highly selective glycoengineering of the IVIG's Fc glycans into a fully sialylated Fc glycoform,

243 The outcomes of the IVIG-treated, PCR-positive patients (n = 20) were compar

244 These results suggest that the IVIG + rituximab desensitization combined with alemtuzma

245 -based single-antigen assays showed that the IVIG/R therapy decreased antibody levels for a period of

246 er 2004, intravenous immunoglobulin therapy (IVIG) was administered to patients with PCR-positive EMB

247 human neutrophils, whereas neither of these IVIG fragments, nor agonistic monoclonal antibodies to h

248 the group receiving steroids, in addition to IVIG and aspirin, had fewer coronary artery abnormalitie

249 on contributing cross-reactive antibodies to IVIG.

250 mice are much less sensitive than BALB/c to IVIG-mediated amelioration of ITP, requiring approximate

251 ibited a different immunoprofile compared to IVIG, also had no effect on mouse cells.

252 erent strains of mice respond differently to IVIG and that FcgammaRIIB plays no role in the mechanism

253 enzymes worked through a similar pathway to IVIG, requiring DC-SIGN, STAT6 signaling, and FcgammaRII

254 Candidates were randomized to IVIG+placebo versus IVIG+rituximab.

255 3 and 4 versus group 1) and the response to IVIG (Fisher's exact P value 4.518x10(-)(03) and 8.224x1

256 r disease activity and treatment response to IVIG in patients with GBS.

257 examined neutrophil behavior in response to IVIG in vivo, using real-time intravital microscopy.

258 tion via recruitment of SHP-1 in response to IVIG.

259 rovide a prediction of the responsiveness to IVIG.

260 evidence for the value of adding steroids to IVIG.

261 ed in 35 patients completely unresponsive to IVIG or high-dose steroid treatment.

262 isorders; however, the mechanisms underlying IVIG's inhibitory effect on neutrophil recruitment and a

263 and graft survival in patients who underwent IVIG-based DSA treatment (group A, n = 57) versus contem

264 Although most practitioners in the USA use IVIG as a second-line therapy for those Kawasaki disease

265 dney transplants after desensitization using IVIG 2 g/kg (days 1 and 30)+rituximab (1 g, day 15).

266 y positive, PRA>80%) were desensitized using IVIG and rituximab.

267 hemic brain injury and the prospect of using IVIG in relatively low doses as an interventional therap

268 dates were randomized to IVIG+placebo versus IVIG+rituximab.

269 rates between patients who received PLEX vs IVIG (P = .04).

270 line antenatal management in FNAIT is weekly IVIG administration, with or without the addition of cor

271 We sought to determine whether IVIG induces antigen-specific Treg cells and to address

272 We studied the mechanisms by which IVIG exerts protection from neutrophil-mediated acute va

273 ponders (P=0.0002) and specifically to white IVIG nonresponders (P=0.007).

274 creases in A-IPF, but 2 with IVIG and 1 with IVIG anti-D did.

275 corresponding increases in A-IPF, but 2 with IVIG and 1 with IVIG anti-D did.

276 unosuppressive activity of IgG, such as with IVIG, may be related to the activity of regulatory T cel

277 ositive patients (n = 20) were compared with IVIG-untreated, PCR-positive patients (n = 17).

278 Desensitization with IVIG + rituximab combined with alemtuzumab induction giv

279 l transplantation after desensitization with IVIG and rituximab and to identify patients at risk for

280 Desensitization with IVIG and rituximab is associated with a higher incidence

281 Desensitization with IVIG and rituximab is associated with a higher incidence

282 nsitized patients after desensitization with IVIG and rituximab was analyzed.

283 nsitized patients after desensitization with IVIG and rituximab was analyzed.

284 sted that pretransplant desensitization with IVIG and rituximab was not successful in highly sensitiz

285 We conclude that desensitization with IVIG+rituximab is clinically and cost-effective, with bo

286 highly sensitized patients desensitized with IVIG+rituximab+/-plasma exchange were enrolled and rando

287 rdiomyopathy/endocardial fibroelastosis with IVIG and corticosteroids potentially improves the outcom

288 to empirically treat affected patients with IVIG and corticosteroids.

289 one responded, 5 of 10 patients treated with IVIG alone responded, and 9 of 10 patients who received

290 untered in our institutions and treated with IVIG and corticosteroids from 1998 to 2009.

291 hout graft dysfunction that are treated with IVIG and Rituximab have similarly good early survival as

292 reviewed all HPV-B19 PRCA cases treated with IVIG between January 2000 and December 2005 in the Assis

293 all cases of HPV-B19 PRCA cases treated with IVIG in the literature.

294 spiratory failure may be better treated with IVIG.

295 the top of the DD waitlist were treated with IVIG/R.

296 Two weeks after commencing treatment with IVIG (2 g/kg), the median serum albumin level decreased

297 s determined before and after treatment with IVIG and related to clinical outcome: muscle weakness (m

298 develop hypoalbuminemia after treatment with IVIG, which is related to a more severe clinical course

299 may be enhanced by concurrent treatment with IVIG.

300 tively, with or without prior treatment with IVIG.