ライフサイエンスコーパス: AL amyloidosis

1 A) or monoclonal immunoglobulin light chain (AL amyloidosis).

2 1.70 after MM, 1.85 after WM and 2.31 after AL amyloidosis.

3 important independent prognostic factors in AL amyloidosis.

4 n is emerging as a novel standard of care in AL amyloidosis.

5 has become a cornerstone in the treatment of AL amyloidosis.

6 light chains before clinical presentation of AL amyloidosis.

7 esent a novel clinicopathological pattern of AL amyloidosis.

8 onses and promising long-term OS in relapsed AL amyloidosis.

9 forty-three-year-old male patient with kappa AL amyloidosis.

10 will help develop risk-adapted therapies for AL amyloidosis.

11 S were significant predictors of survival in AL amyloidosis.

12 mide, cyclophosphamide, and dexamethasone in AL amyloidosis.

13 atumumab-CyBorD vs CyBorD in newly diagnosed AL amyloidosis.

14 udy has demonstrated a survival advantage in AL amyloidosis.

15 ntribute to the site selectivity observed in AL amyloidosis.

16 volvement were assessed in 191 patients with AL amyloidosis.

17 the diagnosis and treatment of patients with AL amyloidosis.

18 for patients with other dominant features of AL amyloidosis.

19 contribution of autoimmunity in this type of AL amyloidosis.

20 at lenalidomide can be effective in treating AL amyloidosis.

21 ion with dexamethasone, for the treatment of AL amyloidosis.

22 thogenesis of the neuropathy associated with AL amyloidosis.

23 c, mild cardiac, and severe cardiac involved AL amyloidosis.

24 in a substantial proportion of patients with AL amyloidosis.

25 of a patient diagnosed with kappa 1 (kappa1) AL amyloidosis.

26 otential involvement of this modification in AL amyloidosis.

27 from the spleens or livers of patients with AL amyloidosis.

28 ciation of monoclonal lambda 6 proteins with AL amyloidosis.

29 and therefore, we evaluated its efficacy for AL amyloidosis.

30 he genesis of heart failure in patients with AL amyloidosis.

31 chains (sFLCs) drive disease progression in AL amyloidosis.

32 be a new standard for response assessment in AL amyloidosis.

33 for patients with relapsed and/or refractory AL amyloidosis.

34 dney biopsy confirmed the diagnosis of kappa AL amyloidosis.

35 ing system and be predictive for survival in AL amyloidosis.

36 ability to appropriately stage patients with AL amyloidosis.

37 at referral centers, is mandatory to confirm AL amyloidosis.

38 responding, heavily pretreated patients with AL amyloidosis.

39 LC dimer could be a useful strategy to treat AL amyloidosis.

40 are limited data on endothelial function in AL amyloidosis.

41 ntigens in 111 newly diagnosed patients with AL amyloidosis.

42 .60 after MGUS, 1.76 after WM and 2.18 after AL amyloidosis.

43 usively from uptake in patients with cardiac AL amyloidosis.

44 uld be considered a new standard of care for AL amyloidosis.

45 e is reshaping the approach to patients with AL amyloidosis.

46 ed with improved biomarker response rates in AL amyloidosis.

47 potential new therapy for the management of AL amyloidosis.

48 ruitment, and cytotoxicity that may occur in AL amyloidosis.

49 humanized 2B6 MoAb in patients with systemic AL-amyloidosis.

50 risk of mortality than matched patients with AL-amyloidosis.

51 e needed to clarify its role in light chain (AL) amyloidosis.

52 ry systemic amyloid light chain amyloidosis (AL) amyloidosis.

53 onsidered a standard of care in light-chain (AL) amyloidosis.

54 rst results in systemic amyloid light-chain (AL) amyloidosis.

55 ise in the treatment of amyloid light-chain (AL) amyloidosis.

56 ohort of patients with systemic light-chain (AL) amyloidosis.

57 of patients with immunoglobulin light chain (AL) amyloidosis.

58 d be complicated by light chain amyloidosis (AL) amyloidosis.

59 ients with multiple myeloma and light chain (AL) amyloidosis.

60 rminant of survival in systemic light-chain (AL) amyloidosis.

61 myeloma (MM) and immunoglobulin light-chain (AL) amyloidosis.

62 tory drugs are active agents in light-chain (AL) amyloidosis.

63 apsed/refractory immunoglobulin light chain (AL) amyloidosis.

64 or relapsed/refractory systemic light-chain (AL) amyloidosis.

65 c parameter in systemic amyloid light chain (AL) amyloidosis.

66 determines prognosis in amyloid light-chain (AL) amyloidosis.

67 LS was more depressed in both ATTRwt and AL amyloidosis (-11+/-3% and -12+/-4%, respectively, P=0

68 a significant effect on overall survival in AL amyloidosis (16.2 months vs. 1.4 months; p = 0.003).

69 Among 701 patients with AL amyloidosis, 394 (56%) were eligible for high-dose me

70 age range, 24-88 years) and 67 patients with AL amyloidosis (43 men, 24 women; median age, 65 years;

71 Sixty patients with systemic AL amyloidosis (65% men, median age 65 years) underwent

72 IGKV1-8 was overrepresented compared with (p)AL amyloidosis (75% vs 11.1%, P = .0033).

73 In amyloid light chain (AL) amyloidosis, a small B-cell clone, most commonly a p

74 rapy for patients with systemic light-chain (AL-) amyloidosis, a protein deposition and monoclonal pl

75 At least some patients with AL amyloidosis achieve complete remission of their plasm

76 Fifty patients with cardiac light-chain (AL) amyloidosis acted as disease comparators.

77 Immunoglobulin light-chain (AL) amyloidosis affects multiple systemic organs.

78 of birtamimab in patients with Mayo stage IV AL amyloidosis (AFFIRM-AL; NCT04973137) is currently enr

79 ) in patients with persistent or progressive AL amyloidosis after >= 1 prior therapy.

80 d to adult patients with relapsed/refractory AL amyloidosis after 1 or more prior lines of therapy (i

81 AL amyloidosis age-adjusted annual incidence was 5.73 pe

82 rs or more after the histologic diagnosis of AL amyloidosis; all received alkylating-agent therapy.

83 In immunoglobulin light chain (AL) amyloidosis, amyloid fibril deposits derived from im

84 0 with non-ATTR cardiac amyloidosis [34 with AL amyloidosis and 16 with nonamyloid heart failure with

85 Both AL amyloidosis and 2 of 10 TTR-noPN subjects were Congo

86 0.54) than in ATTRm (-15+/-4%, P<0.01 versus AL amyloidosis and ATTRwt).

87 disproportionately expanded in patients with AL amyloidosis and characterized by increased expression

88 Patients with AL amyloidosis and congestive heart failure have a very

89 Seven patients with AL amyloidosis and controls were studied.

90 y ASCT is feasible in selected patients with AL amyloidosis and heart failure, and that such a strate

91 ve had a favorable effect in 3 patients with AL amyloidosis and heart failure.

92 iac involvement predicts outcome in systemic AL amyloidosis and influences therapeutic options.

93 6 transgenic model replicates the process of AL amyloidosis and is useful for testing the antifibril

94 is an effective combination for treatment of AL amyloidosis and leads to durable hematologic response

95 is well tolerated in patients with relapsed AL amyloidosis and leads to rapid and deep hematologic r

96 s feasible in selected patients with cardiac AL amyloidosis and may confer substantial survival benef

97 d as an independent predictor of survival in AL amyloidosis and offered incremental information beyon

98 ne its diagnostic potential in patients with AL amyloidosis and other systemic amyloidoses.

99 /expansion study of NEOD001 in patients with AL amyloidosis and persistent organ dysfunction (NCT0170

100 owed by SCT was performed in 5 patients with AL amyloidosis and predominant cardiomyopathy.

101 ed plasma cells from a patient (Wil) who had AL amyloidosis and renal amyloid deposits; the second wa

102 esponses are rare but possible in stage IIIb AL amyloidosis and translate to longer survival.

103 proves risk stratification for patients with AL amyloidosis and will help develop risk-adapted therap

104 e, to our knowledge, the association between AL-amyloidosis and AION was not previously described.

105 markedly better than observed with systemic AL amyloidosis, and outcomes with renal replacement ther

106 ously reported nontransplantation regimen in AL amyloidosis, and risk adaptation allows its use in po

107 t observed in patients with cardiac involved AL amyloidosis, and they suggest that amyloid LC protein

108 ment predicts poor prognosis in light chain (AL) amyloidosis, and the current prognostic classificati

109 Light chain (LC) amyloidosis (AL amyloidosis) appears to be caused by the misfolding,

110 Here we show that the clonal plasma cells in AL amyloidosis are highly primed to undergo apoptosis an

111 eria of hematologic response in light-chain (AL) amyloidosis are based on the measurement of circulat

112 strom macroglobulinemia (WM) and light chain AL amyloidosis, are characterized by clonal expansion of

113 stemic amyloidogenic light chain-associated (AL) amyloidosis, are presumed to be the source of light

114 AL amyloidosis associated with immunoglobulin M (IgM) pa

115 oves the nephrotic syndrome in patients with AL amyloidosis-associated renal disease.

116 Unlike cardiac AL amyloidosis, asymmetrical septal left ventricular hyp

117 MFC is prognostic for AL amyloidosis at diagnosis and at EOT.

118 AL amyloidosis-attributable costs were obtained by subtr

119 Compared with ATTRm and AL amyloidosis, ATTRwt was characterized by greater LV w

120 eria for response to first-line treatment in AL amyloidosis, based on their association with survival

121 dosis can be misdiagnosed as Ig light-chain (AL) amyloidosis because family history is an ineffective

122 undetermined significance who are developing AL amyloidosis before they become symptomatic.

123 all Mayo Clinic patients with a diagnosis of AL amyloidosis between January 1, 1966 and March 1, 1987

124 cardiographic studies have been performed in AL amyloidosis but not in TTR amyloidosis and might give

125 ation (ASCT) has become a common therapy for AL amyloidosis, but there is an exceedingly high treatme

126 of patients with immunoglobulin light-chain (AL) amyloidosis, but little is known on progression or r

127 ffective treatment for systemic light-chain (AL) amyloidosis, but many patients are ineligible becaus

128 Patients were diagnosed with AL amyloidosis by tissue biopsy and categorized by perfo

129 Treatment of selected patients with AL amyloidosis by using high-dose melphalan and stem-cel

130 ont-line therapy with a DEX-based regimen in AL amyloidosis can lead to durable reversal of AL amyloi

131 t of the underlying plasma cell dyscrasia in AL amyloidosis can lead to the amelioration of amyloid-r

132 oidosis, which accounts for 6% to 10% of all AL amyloidosis cases, is a rare and poorly studied clini

133 x, and area of residence to patients without AL amyloidosis (comparators) randomly selected from the

134 or 65 patients (aged 65 years or older) with AL amyloidosis compared with outcomes for 280 younger pa

135 Care of patients with AL amyloidosis currently is limited by the lack of objec

136 h no therapies are approved for light chain (AL) amyloidosis, cyclophosphamide, bortezomib, and dexam

137 ickness but lesser mortality than those with AL amyloidosis, despite very similar degrees of LS impai

138 of patients with immunoglobulin light chain (AL) amyloidosis die within 6 months of diagnosis and 25%

139 Of 368 consecutive patients with systemic AL amyloidosis evaluated at Boston Medical Center, 32 pa

140 upport is feasible therapy for patients with AL amyloidosis, even when there is clinical evidence of

141 ed normal range, precedes the development of AL amyloidosis for many years.

142 All patients with confirmed, newly diagnosed AL amyloidosis from 01-Jan-2016 until 31-Dec-2019 were e

143 ) was derived from a cohort of patients with AL amyloidosis from the UK National Amyloidosis Centre.

144 ment outcomes of 346 patients with stage III AL amyloidosis from the United Kingdom, Italy, Germany,

145 with immunoglobulin light chain amyloidosis (AL amyloidosis) generally present with advanced organ dy

146 ntification of this atypical presentation of AL amyloidosis has important implications for early dete

147 Survival in AL amyloidosis has improved markedly as novel chemothera

148 development of less intensive treatments for AL amyloidosis has made less certain the role of autolog

149 The management of light chain (AL) amyloidosis has improved in recent years thanks to a

150 but its efficacy and safety in light-chain (AL) amyloidosis has not been formally studied.

151 flow cytometry (MFC) in amyloid light-chain (AL) amyloidosis has not been widely adopted and, consequ

152 Primary systemic (amyloid light-chain [AL]) amyloidosis has a variety of cutaneous manifestatio

153 Patients with IgM AL amyloidosis have a significant IgM paraprotein (media

154 Previous reports of PXE-like plaques in AL amyloidosis have been reported as part of a very rare

155 Overall, outcomes among patients with AL amyloidosis have improved with earlier diagnosis, hig

156 een percent of newly diagnosed patients with AL amyloidosis have low dFLC and had a better outcome.

157 No published series of patients with AL amyloidosis have reported survival of more than 10 ye

158 a monoclonal component in patients with non-AL amyloidosis, highlighting the risk of misdiagnosis an

159 used in multiple myeloma can be effective in AL amyloidosis; however, patients with this disease ofte

160 led behind the progress made in the field of AL amyloidosis in diagnosis, prognosis, and hematologic

161 Prognostic and response criteria for AL amyloidosis in general have not been validated in thi

162 including active AL amyloidosis (n = 30) or AL amyloidosis in hematologic remission for more than 1

163 Use of BDex+AA in the treatment of AL amyloidosis in patients presenting with symptomatic h

164 are discussed, with particular reference to AL amyloidosis in the heart.

165 o have high sensitivity in imaging of AA and AL amyloidosis in visceral organs.

166 ivariate analysis, predictors of survival in AL amyloidosis included sex, Karnofsky index, New York H

167 tudy included 40 subjects with biopsy-proven AL amyloidosis including active AL amyloidosis (n = 30)

168 ated CTD (CTDa) in 75 patients with advanced AL amyloidosis, including 44 patients with clonal relaps

169 e associated with prognosis in patients with AL amyloidosis, independently of other features of the d

170 Therapeutic decision-making for AL amyloidosis involves choosing between high-dose chemo

171 AL amyloidosis is a disorder characterized by expansion

172 IgM AL amyloidosis is a distinct clinical entity.

173 AL amyloidosis is a fatal disease resulting from tissue

174 AL amyloidosis is a life-threatening disease caused by d

175 AL amyloidosis is a rare condition characterized by the

176 AL amyloidosis is an insidious and potentially fatal con

177 The incidence of AL amyloidosis is approximately 12 cases per million per

178 nsive cardiac amyloid deposition in systemic AL amyloidosis is associated with a grave prognosis.

179 AL amyloidosis is associated with a high incidence of ca

180 The morbidity and lethality of AL amyloidosis is caused by the deposition of lg light c

181 Survival of patients with AL amyloidosis is no more than 1 to 2 years from the tim

182 Although cardiac death in patients with AL amyloidosis is usually associated with extensive myoc

183 Immunoglobulin light chain-derived (AL) amyloidosis is a debilitating disease without known

184 Primary (AL) amyloidosis is a plasma cell dyscrasia characterized

185 Amyloid light chain (AL) amyloidosis is a protein misfolding disease where im

186 Immunoglobulin light-chain (AL) amyloidosis is a rare, incurable plasma cell disorde

187 Amyloid light-chain (AL) amyloidosis is a rare, typically fatal disease chara

188 Light chain (AL) amyloidosis is an incurable human disease characteri

189 Light chain (AL) amyloidosis is caused by a usually small plasma cell

190 Light chain (AL) amyloidosis is caused by the accumulation of misfold

191 Systemic light chain (AL) amyloidosis is caused by the clonal production of an

192 Systemic antibody light chains (AL) amyloidosis is characterized by deposition of amyloi

193 Primary light-chain-associated (AL) amyloidosis is characterized by the deposition in ti

194 Light chain (AL) amyloidosis is characterized by the misfolding of im

195 Light chain (or AL) amyloidosis is characterized by the pathological dep

196 Amyloid-deposited light chain (AL) amyloidosis is correlated with the overproduction of

197 The median survival in primary systemic (AL) amyloidosis is less than 18 months.

198 Light chain (or AL) amyloidosis is the most common form of systemic amyl

199 Systemic light chain (AL) amyloidosis is the most common of these conditions,

200 osis of any involved organ, and light-chain (AL) amyloidosis is the most serious form of the disease.

201 Light chain, or AL, amyloidosis is a pathological condition arising from

202 Immunoglobulin light chain amyloidosis (AL amyloidosis) is caused by misfolded light chains that

203 In amyloid light-chain (AL) amyloidosis, kappa cases were more difficult to diag

204 A woman in her 50s with a history of AL amyloidosis manifesting as macroglossia and bilateral

205 It is known that light-chain (AL) amyloidosis may rarely affect the temporal arteries,

206 The present case shows that AL-amyloidosis may present with AION, high ESR, and temp

207 Since the amyloid fibril deposits in AL amyloidosis most often consist of the N-terminal frag

208 Thirty-four patients with AL amyloidosis, most with prior therapies, were enrolled

209 iopsy-proven AL amyloidosis including active AL amyloidosis (n = 30) or AL amyloidosis in hematologic

210 phritis with MIg deposits (PGNMID) (n = 13), AL amyloidosis (n = 5), light chain deposition disease (

211 nephritis with MIg deposits (PGNMID) (n=13), AL amyloidosis (n=5), light chain deposition disease (n=

212 We analyzed 172 patients with CA (AL amyloidosis, n=80; ATTRm, n=36; ATTRwt, n=56) by stan

213 e earliest and had the worst graft survival, AL amyloidosis occurred the latest and had the best graf

214 e earliest and had the worst graft survival, AL amyloidosis occurred the latest and had the best graf

215 y (AION) showing histopathologic evidence of AL-amyloidosis of the temporal arteries.

216 current five-year survival rate for systemic AL amyloidosis or multiple myeloma is ~51%, indicating t

217 mains in the form of either amyloid fibrils (AL-amyloidosis) or amorphous deposits, light-chain depos

218 lation in the forearm skin was attenuated in AL amyloidosis patients (p = 0.007).

219 s and their associated variable domains from AL amyloidosis patients and non-patients.

220 Early in the disease, AL amyloidosis patients present with impaired endothelia

221 ment, and outcome among 1551 newly diagnosed AL amyloidosis patients seen in our institution from 200

222 Intrigued by the unique response rates of AL amyloidosis patients to the first-in-class proteasome

223 Full-length LC dimers derived from AL amyloidosis patients unfold more rapidly than other f

224 A total of 1976 AL amyloidosis patients were identified.

225 Thus, treatment of AL amyloidosis patients with HDM/SCT produces measurable

226 Treatment of AL amyloidosis patients with high-dose melphalan chemoth

227 f the full-length LC dimers, even those from AL amyloidosis patients, are amyloidogenic.

228 unction in the cutaneous microcirculation of AL amyloidosis patients.

229 Finally, clonal AL amyloidosis plasma cells were identified based on the

230 patients with systemic amyloid light-chain (AL) amyloidosis, presumably due to adsorption of factor

231 aracterized the internalization of AL-09, an AL amyloidosis protein into mouse cardiomyocytes.

232 and its modulation in patients with systemic AL-amyloidosis receiving high-dose melphalan.

233 amyloidosis can lead to durable reversal of AL amyloidosis-related organ dysfunction and prolonged s

234 ions were observed in 24% and improvement in AL amyloidosis-related organ dysfunction occurred in 45%

235 ch domain and the role of endoproteolysis in AL amyloidosis remain unclear.

236 patients with cardiac stage III light chain (AL) amyloidosis remain poorly studied.

237 Light-chain (AL) amyloidosis remains incurable despite recent therape

238 prognosis and response to therapy in cardiac AL amyloidosis, respectively.

239 show a survival advantage for patients with AL amyloidosis responding to salvage treatment with poma

240 trate that infusion of LC from patients with AL amyloidosis result in diastolic dysfunction similar t

241 Systemic AL amyloidosis results from the aggregation of an amyloi

242 A 64 year-old woman with AL-amyloidosis secondary to a monoclonal gammopathy of u

243 nostic value independent of age, Mayo Clinic AL amyloidosis stage, prior autologous stem-cell transpl

244 n additional mechanism for LV dysfunction in AL amyloidosis, such as previously demonstrated light-ch

245 Five percent of patients with AL amyloidosis survived for 10 years or more.

246 To characterize symptoms and signs of AL amyloidosis that may bring patients to the attention

247 essment of renal response and progression in AL amyloidosis that should be used in clinical practice

248 10 to 2015 and included patients with kidney AL amyloidosis that was evaluable for kidney response an

249 ctive regimen producing durable responses in AL amyloidosis; the deep clonal responses may overcome p

250 ng patients with immunoglobulin light chain (AL) amyloidosis, there is little consensus on when reins

251 hoc analysis of patients with Mayo stage IV AL amyloidosis, those at the highest risk of early morta

252 tructures, and bones can bring patients with AL amyloidosis to the attention of rheumatologists.

253 month 9, 74% of patients with Mayo stage IV AL amyloidosis treated with birtamimab and 49% of those

254 tudies have suggested that, in patients with AL amyloidosis treated with high-dose melphalan and auto

255 80 patients with immunoglobulin light chain (AL) amyloidosis treated with high-dose melphalan and ste

256 utive patients newly diagnosed with systemic AL amyloidosis underwent echocardiography, cardiac bioma

257 tic mutation carriers, and 119 patients with AL amyloidosis, underwent LGE cardiovascular magnetic re

258 pulmonary kappa light chain amyloidosis ((p)AL amyloidosis) used as controls.

259 the various organs of subjects with systemic AL amyloidosis using (18)F-florbetapir PET/CT.

260 ystem for patients with amyloid light-chain (AL) amyloidosis using a test set of 461 patients from Pa

261 Patient survival in AL amyloidosis was 8.9 years among those who had achieve

262 ent staging and response criteria in non-IgM AL amyloidosis was applied to this series to assess its

263 AL amyloidosis was defined by >= 2 ICD-10-CM codes or po

264 daratumumab monotherapy for the treatment of AL amyloidosis was designed to determine the safety, tol

265 pa1 LC purified from urine of a patient with AL amyloidosis was incubated in the presence or absence

266 ajor advances in immunoglobulin light chain (AL) amyloidosis, we evaluated the trends in presentation

267 Ninety-seven biopsy-proven patients with AL amyloidosis were divided into 3 groups.

268 996 and 2003, 93 patients with biopsy-proven AL amyloidosis were enrolled in a prospective US nationa

269 Twenty-two patients with previously treated AL amyloidosis were enrolled.

270 six consecutive patients with biopsy-proven AL amyloidosis were investigated in this prospective obs

271 functional class >/=II heart failure due to AL amyloidosis were retrospectively studied.

272 the 21 years of the study, 841 patients with AL amyloidosis were seen.

273 amethasone for the treatment of light chain (AL) amyloidosis were to determine the safety, tolerabili

274 -chain variable domain, SMA, associated with AL amyloidosis, were investigated by (15)N relaxation di

275 Immunoglobulin M (IgM)-related light chain (AL) amyloidosis, which accounts for 6% to 10% of all AL

276 This amyloid light-chain (AL) amyloidosis, which is a hereditary type of amyloidos

277 esents a distinctive subset of patients with AL amyloidosis who have a wider variety of underlying cl

278 imited toxicity for patients with pretreated AL amyloidosis who have limited therapeutic options.

279 Patients with AL amyloidosis who have more than 10% BMPCs have a poor

280 d as the preferred therapy for patients with AL amyloidosis who meet functional criteria for autologo

281 Patients with AL amyloidosis who need second-line therapy after respon

282 e present our experience of 43 patients with AL amyloidosis who received cyclophosphamide, bortezomib

283 We studied 173 patients with AL amyloidosis who underwent MFC immunophenotyping of bo

284 de and dexamethasone (PDex) in patients with AL amyloidosis who were previously exposed to bortezomib

285 atients with congestive heart failure due to Al amyloidosis who were seen between 1983 and 1994.

286 Patients with light chain (AL) amyloidosis who present with severe heart failure du

287 tment plasma cells of patients with systemic AL-amyloidosis who then had a complete response to high-

288 as to examine the spectrum of immunoglobulin AL amyloidosis with and without MM, with a goal of defin

289 AL amyloidosis with heart failure is associated with dec

290 AL amyloidosis with IgM paraproteinemia represents a dis

291 rrow plasma cell (BMPC) number to qualify as AL amyloidosis with MM.

292 d should therefore be considered together as AL amyloidosis with MM.

293 tested the associations of MGUS, MM, WM and AL amyloidosis with subsequent eye diseases identified f

294 is consensus that patients with light chain (AL) amyloidosis with hypercalcemia, renal failure, anemi

295 ons characterize immunoglobulin light-chain (AL) amyloidosis with major heart involvement.

296 Current therapy of primary systemic (AL) amyloidosis with oral melphalan and prednisone remai

297 To report an unusual case of light-chain (AL) amyloidosis with progressive bilateral chorioretinal

298 active in patients with relapsed/refractory AL amyloidosis, with a generally manageable safety profi

299 redict for 1-year mortality in patients with AL amyloidosis without CRAB to produce two additional gr

300 Outcome and organ function of stage III AL amyloidosis without very elevated NT-proBNP and low S