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 can alter the viability of human neutrophils via ag

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

4 IVIG is known to regulate the viability of immune cells,

5 IVIG is used to prevent cardiovascular complications rel

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

7 IVIG or albumin control was administered 24 hours before

8 IVIG preparations consisting of pooled IgG are increasin

9 IVIG preparations contain broadly cross-reactive ADCC me

10 IVIG resistance was associated with higher levels of IL-

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

12 IVIG subjects were younger with lower comorbidity indice

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

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

15 IVIG therapy resulted in increased expression of Treg-re

16 IVIG-treated patients with myopathy displayed enhanced e

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

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

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

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

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

22 150 KD patients (126 IVIG responders and 24 IVIG nonresponders) were recruited for this study.

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

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

25 Adjunctive IVIG was administered infrequently in NF with shock and

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

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

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

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

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

31 anges in motor and sensory disturbance after IVIG treatment in patients with EGPA.

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

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

34 mediated by tolerogenic DCs generated after IVIG exposure.

35 score decreased significantly, 1 month after IVIG.

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

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

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

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

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

41 f new functions of monoclonal antibodies and IVIG.

42 ngineering of intact monoclonal antibody and IVIG.

43 Corticosteroid and IVIG treatment was completely stopped.

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

45 or sepsis were susceptible to both IgA- and IVIG-mediated death.

46 bodies against SAgs in many human plasma and IVIG samples and demonstrate that in a major portion of

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

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

49 Both PLEX and IVIG had high response rates.

50 ion these antibody titers are suboptimal and IVIG therapy only incrementally elevates the anti-SAg ti

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 vity, compared with samples collected before IVIG therapy.

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

55 disturbance scores at disease onset, before IVIG, 1 week and 1 month after the end of IVIG.

56 demonstrated a negative correlation between IVIG dose and toxin-triggered T-cell proliferation (r =

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

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

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

60 Activation of basophils by IVIG led to enhanced expression of CD69 and secretion of

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

62 t changes in blood clearance were induced by IVIG.

63 a pathway of promoting the T(H)2 response by IVIG through direct interaction of IgG with human basoph

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

65 ive (D+/R-) HCT patients (33 control, 28 CMV IVIG) was tested using a PC-entry nAb assay and quantita

66 This study provides initial support that CMV IVIG prophylaxis moderately enhances PC-entry nAB activi

67 offs of >=1000 and >=10 000 IU/mL in the CMV IVIG arm.

68 ore antibody among patients newly commencing IVIG.

69 Different commercial IVIG preparations similarly induced cytokine-dependent d

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

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

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

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

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

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

76 The effect of IVIG and F(ab')(2) and Fc IVIG fragments was examined based on expression of vario

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

78 Plasma samples collected following IVIG infusion therapy demonstrated a higher anti-HEV IgG

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

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

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

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

83 Basophil phenotypes were also analyzed from IVIG-treated patients with myopathy.

84 uch as depletion of anti-IgE reactivity from IVIG, blocking antibodies, or inhibitors, were used to i

85 er disease was biphasic and required further IVIG for non-hepatic symptoms.

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

87 One 25-g IVIG dose was sufficient to yield plasma-neutralizing ac

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

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

90 MIS-C included intravenous immune globulin (IVIG) (71%), corticosteroids (61%), and anakinra (18%).

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

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

93 oronary artery aneurysms, some children have IVIG-resistant Kawasaki disease and are at increased ris

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

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

96 Human IVIG preparations contain BKV neutralizing antibodies.

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

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

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

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

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

102 ere treated with intravenous immunoglobulin (IVIG) and 10 who achieved remission by conventional trea

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

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

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

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

107 obial agents and intravenous immunoglobulin (IVIG) as well as hyperbaric oxygen therapy, none have be

108 8 responding to intravenous immunoglobulin (IVIG) did not have corresponding increases in A-IPF, but

109 ic normal IgG or intravenous immunoglobulin (IVIG) exerts anti-inflammatory effects through several m

110 dministration of intravenous immunoglobulin (IVIG) from patients with group A Streptococcus necrotizi

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

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

113 uate efficacy of intravenous immunoglobulin (IVIG) in reducing seizure frequency.

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

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

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

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

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

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

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

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

122 led trial of CMV intravenous immunoglobulin (IVIG) prophylaxis.

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

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

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

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

127 before and after intravenous immunoglobulin (IVIG) therapy, 5 recently treated patients with persiste

128 Although intravenous immunoglobulin (IVIG) treatment reduces the risk of development of coron

129 seline and after intravenous immunoglobulin (IVIG) treatment, and 23 matched control subjects.

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

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

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

133 e KD, and in the intravenous immunoglobulin (IVIG)-resistant group compared to in the IVIG-sensitive

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

135 ed resistance to intravenous immunoglobulin (IVIG).

136 dministration of intravenous immunoglobulin (IVIG).

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

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

139 ctivity of human intravenous immunoglobulin (IVIG).

140 ally with P4 and intravenous immunoglobulin (IVIG).

141 nts treated with intravenous immunoglobulin (IVIG).

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

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

144 terferon-gamma, intravenous immunoglobulins (IVIG), mepolizumab, methotrexate (MTX), omalizumab, upad

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

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

147 rologous influenza strains may be present in IVIG preparations.

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

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

150 ranscripts in the blood of patients with KD, IVIG-resistant KD, or CAA.

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

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

153 ur of the 6 patients entering the open-label IVIG arm reported >=50% reduction in seizure frequency.

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

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

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

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

158 Mechanistically, IVIG induced IL-4 in human basophils by interacting with

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

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

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

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

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

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

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

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

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

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

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

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

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

172 The effect of IVIG and F(ab')(2) and Fc IVIG fragments was examined ba

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

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

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

176 We sought to investigate the effect of IVIG on human basophil functions.

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

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

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

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

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

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

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

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

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

186 re IVIG, 1 week and 1 month after the end of IVIG.

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

188 pathway is implicated in these functions of IVIG and were mediated by F(ab')(2) fragments.

189 Fifteen patients received infusions of IVIG.

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

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

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

193 Superiority of IVIG to placebo reached statistical significance for the

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

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

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

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

198 were treated with anti-IL-6R antibody and/or IVIG, which led to rapid disease resolution.

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

204 Post-IVIG PANDAS sera and IgG-depleted baseline sera did not

205 Post-IVIG serum had reduced IgG binding to CINs, and this red

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

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

208 Patients were randomized to receive IVIG (0.5g/kg day 1, 1g/kg day 2, 0.6g/kg weeks 3 and 5)

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

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

211 nonresponders in the placebo group received IVIG.

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

213 15 HS patients received IVIG (2 g/kg x2 doses)/rituximab (375 mg/m x1) for desen

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

215 133 patients with HPV-B19 PRCA who received IVIG (our 10 patients and 123 from the literature), 63 h

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

217 ficantly lower in EGPA patients who received IVIG than in those who did not receive it.

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

219 In patients who received IVIG, the total motor disturbance score increased signif

220 In patients who received IVIG, we evaluated motor and sensory disturbance scores

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

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

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

224 Two LGI1-IgG-seropositive patients receiving IVIG, but none receiving placebo, were seizure-free at t

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

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

227 nt including plasmapheresis, pulse steroids, IVIG, and rituximab (P = ns).

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

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

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

231 We conclude that IVIG treatment represents a promising therapeutic approa

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

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

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

235 We report that IVIG directly induces activation of IL-3-primed human ba

236 se models of autoimmune disease suggest that IVIG induces IL-4 in basophils by enhancing IL-33 in SIG

237 The IVIG yielded increased DSA clearance compared with histo

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

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

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

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

242 Six of 8 patients in the IVIG group were responders, compared to 2 of 9 in the pl

243 eropositive subgroup, 6 of 8 patients in the IVIG group were responders, compared to zero of 6 in the

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

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

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

247 in (IVIG)-resistant group compared to in the IVIG-sensitive group.

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

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

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

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

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

253 on contributing cross-reactive antibodies to IVIG.

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

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

256 In contrast to IVIG, IgA did not promote cell death of quiescent neutro

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

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

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

260 3 and 4 versus group 1) and the response to IVIG (Fisher's exact P value 4.518x10(-)(03) and 8.224x1

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

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

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

264 rovide a prediction of the responsiveness to IVIG.

265 evidence for the value of adding steroids to IVIG.

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

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

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

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

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

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

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

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

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

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

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

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

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

279 ceived kidney transplantation after DES with IVIG + rituximab +/- PLEX (plasma exchange) +/- tocilizu

280 Desensitization with IVIG + rituximab combined with alemtuzumab induction giv

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

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

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

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

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

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

287 to empirically treat affected patients with IVIG and corticosteroids.

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

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

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

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

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

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

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

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

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

297 may be enhanced by concurrent treatment with IVIG.

298 tively, with or without prior treatment with IVIG.

299 In patients treated without IVIG, we evaluated these scores at disease onset and at

300 remission by conventional treatment without IVIG.