ライフサイエンスコーパス: cytopenia

1 referentially who present with high fever or cytopenia.

2 pergammaglobulinemia G and A, and autoimmune cytopenia.

3 6, an inhibitor of Syk function, in treating cytopenia.

4 itivity in patients with drug-induced immune cytopenia.

5 eased blood cell apoptosis, and multilineage cytopenia.

6 ls, and the mice succumb to fatal peripheral cytopenia.

7 HU was stopped because of cytopenia.

8 in 72 (79%) of 91 patients with any baseline cytopenia.

9 disease, myeloid cell expansion, and T cell cytopenia.

10 aboratory evidence of hypocomplementemia and cytopenia.

11 involvement, and 25 patients had hematologic cytopenia.

12 dysplastic neutrophils and multiple lineage cytopenia.

13 with myelofibrosis irrespective of baseline cytopenias.

14 ociated with autoimmune diseases and various cytopenias.

15 ctive hematopoiesis that leads to peripheral cytopenias.

16 marrow blast percentage value, and depth of cytopenias.

17 ith autoimmune disorders and immune-mediated cytopenias.

18 sis, congestive heart failure, and prolonged cytopenias.

19 n the development of inflammation-associated cytopenias.

20 s) and is associated with lineage-restricted cytopenias.

21 pmentally compromised and are prone to blood cytopenias.

22 patosplenomegaly, and recurring multilineage cytopenias.

23 rash, elevated transaminases/bilirubin, and cytopenias.

24 at results in fever, hepatosplenomegaly, and cytopenias.

25 ymphadenopathy, splenomegaly, and autoimmune cytopenias.

26 defined by presence of at least 2 autoimmune cytopenias.

27 most common were hematologic toxicities with cytopenias.

28 terium, results in multiple peripheral blood cytopenias.

29 ted with lenalidomide experience significant cytopenias.

30 rse but sometimes manifests with significant cytopenias.

31 ctive hematopoiesis that leads to peripheral cytopenias.

32 cells often associated with immune-mediated cytopenias.

33 ed to hematopoietic malignancies and various cytopenias.

34 vents, corticosteroid-related morbidity, and cytopenias.

35 onditioning regimen who developed autoimmune cytopenias.

36 of cytotoxic T cells (CTLs) associated with cytopenias.

37 re splenectomy did not predict a response in cytopenias.

38 red immunodeficiency syndrome (AIDS)-related cytopenias.

39 iphospholipid autoantibodies, and autoimmune cytopenias.

40 ines, with associated unexplained persistent cytopenias.

41 ction, even in patients with severe baseline cytopenias.

42 dren with refractory multilineage autoimmune cytopenias.

43 and maintained remission of immune-mediated cytopenias.

44 Both patients had prolonged cytopenias.

45 spectively, mostly in those with preexisting cytopenias.

46 utoimmunity, including autoantibody-mediated cytopenias.

47 encountered in 144 patients with unexplained cytopenias.

48 cooperate to contribute to lupus-associated cytopenias.

49 ion of children with refractory multilineage cytopenias.

50 tic anemia, thrombosis, and peripheral blood cytopenias.

51 sing hemolytic anemia and interferon causing cytopenias.

52 ith AEL, 32% had a history of MDS or chronic cytopenia, 32% had therapy-related disease, and 35% had

53 response, 5% complete response with residual cytopenia, 7% nodular partial response, and 43% partial

54 pond at all, and 22 showed an improvement in cytopenias (76%).

55 ies from chemotherapy were mild and included cytopenias (89%), fever and neutropenia (28%), infection

56 of potential risk factors, including initial cytopenia, advanced bone metastatic disease, previous ch

57 Cytopenia after high-dose chemotherapy and autologous st

58 Despite these peripheral cytopenias, all patients had macrophages and plasma cell

59 Cytopenias also occurred in all subjects and were dose-r

60 FA-G patients had more severe cytopenia and a higher incidence of leukemia.

61 o immunosuppression, with persistent, severe cytopenia and a profound deficit in hematopoietic stem c

62 ey were evidenced by the correction of blood cytopenia and a rapid decrease in serum IL-6 and TNF-alp

63 (1.1%) developed BM failure characterized by cytopenia and BM aplasia.

64 l expansion persists, and both CD4(+) T-cell cytopenia and CD8(+) T-cell expansion are associated wit

65 c and non-apoptotic death in contributing to cytopenia and immune suppression.

66 Prolonged cytopenia and pulmonary toxicity each occurred in three

67 mmunity and immune dysregulation may lead to cytopenia and represent key features of many primary imm

68 disorders that result in varying degrees of cytopenia and risk of transformation into acute leukemia

69 C) transplantation results in severe myeloid cytopenia and susceptibility to infections in the lag pe

70 tory disorder is prominently associated with cytopenias and a unique combination of clinical signs an

71 e therapies for myelofibrosis can exacerbate cytopenias and are not indicated for patients with sever

72 similarly indolent diseases characterized by cytopenias and autoimmune conditions as opposed to aggre

73 erstanding of the pathogenesis of autoimmune cytopenias and B-cell lymphomas.

74 ukemia (LGL) is often associated with immune cytopenias and can cooccur in the context of aplastic an

75 identification of germline predisposition to cytopenias and cancer informs the diagnosis and medical

76 in an acute febrile illness associated with cytopenias and characteristic intracellular organisms wi

77 of STAT1 who had life-threatening autoimmune cytopenias and chronic mucocutaneous candidiasis.

78 ecting the myeloid lineage, characterized by cytopenias and clonal evolution to acute myeloid leukemi

79 d by development of progressive multilineage cytopenias and cytological dysplasia.

80 /GFP-expressing cells showed post-transplant cytopenias and decreased numbers of total and gene-modif

81 Mice lacking Brca1 in the BM have baseline cytopenias and develop spontaneous bone marrow failure o

82 f Asxl1 results in progressive, multilineage cytopenias and dysplasia in the context of increased num

83 hat drive clonal expansion in the absence of cytopenias and dysplastic hematopoiesis can be considere

84 Peripheral blood cytopenias and dysplastic hematopoietic progenitors char

85 Severity of cytopenias and elevated immunoglobulin levels also predi

86 ed to be weighed against the higher risks of cytopenias and greater costs with the pegylated formulat

87 ls of IFN-gamma is sufficient to cause acute cytopenias and hemophagocytosis.

88 ed at 8.5%, predominantly resulting in blood cytopenias and hypothyroidism.

89 group of disorders characterized by variable cytopenias and ineffective hematopoiesis.

90 e disease that presents with immune-mediated cytopenias and is characterised by clonal expansion of c

91 n indolent course that ultimately results in cytopenias and massive splenomegaly.

92 tion, are also responsible in part for blood cytopenias and other clinical features of HME.

93 Ineffective hematopoiesis with associated cytopenias and potential evolution to acute myeloid leuk

94 T-cell GLL and from 25 control patients with cytopenias and relative or absolute increases in blood l

95 No relationship between the development of cytopenias and response could be established for lower-r

96 ty responded to ATG with durable reversal of cytopenias and restoration of transfusion independence,

97 However, prolonged cytopenias and severe infections were more common in the

98 virus (HCV) infection frequently experience cytopenias and weight loss.

99 ing at a "lower risk" MDS level, have severe cytopenias and/or poor prognostic factors, found using n

100 tation caused myeloid cell expansion, T cell cytopenia, and dysregulation of immune cell signaling.

101 erapy consisted of thrombocytopenia, granulo-cytopenia, and esophagitis.

102 syndrome, severe aplastic anemia/refractory cytopenia, and others.

103 All patients had cytopenias, and 12.0% presented >/=5% BM blast cells.

104 , impaired differentiation, peripheral-blood cytopenias, and a risk of progression to acute myeloid l

105 phology, the development of peripheral blood cytopenias, and a tendency to evolve into acute myeloid

106 lymphoma, marrow regenerative states, immune cytopenias, and acquired immunodeficiency syndrome.

107 -onset lymphadenopathy, splenomegaly, immune cytopenias, and an increased risk for B cell lymphomas.

108 lymphadenopathy, splenomegaly, multilineage cytopenias, and an increased risk of B-cell lymphoma.

109 epatosplenomegaly, coagulopathy, hematologic cytopenias, and evidence of hemophagocytosis in the bone

110 iagnosis for transplant patients with fever, cytopenias, and hepatitis, especially if exposure to tic

111 -R with poor-risk genetic features, profound cytopenias, and high transfusion burden are candidates f

112 ular coagulation, hepatobiliary dysfunction, cytopenias, and hyperferritinemia.

113 ory failure, human herpes virus 6 infection, cytopenias, and no circulating T cells.

114 al indications included lymphoma, autoimmune cytopenias, and other autoimmune diseases.

115 w-up, and management of ALPS, its associated cytopenias, and other complications resulting from infil

116 ineffective hematopoiesis, peripheral blood cytopenias, and potential for malignant transformation.

117 d by cerebellar ataxia, variable hematologic cytopenias, and predisposition to marrow failure and mye

118 oiesis, aberrant differentiation, peripheral cytopenias, and risk of progression to acute myeloid leu

119 ll removal are, in part, responsible for the cytopenias, and that up-regulation of the "don't eat me"

120 Administered activity and initial cytopenia are the only factors contributing to myelosupp

121 -002) to determine whether treatment-related cytopenias are correlated with lenalidomide response.

122 nical trial Finally, because other causes of cytopenias are more treatable, the diagnosis of myelodys

123 Patients with autoimmune multilineage cytopenias are often refractory to standard therapies re

124 s facilitating acute inflammation-associated cytopenias are unknown.

125 tologic diseases characterized by refractory cytopenias as a result of ineffective hematopoiesis.

126 lt from myelodysplastic syndromes are due to cytopenia associated with bone marrow failure.

127 leukemic cell infiltration and BPDCN-induced cytopenia associated with increased survival after LXR a

128 cyclosporine (CSA) can be used to treat the cytopenia associated with myelodysplastic syndrome (MDS)

129 as been implicated in the pathophysiology of cytopenias associated with myelodysplastic syndromes (MD

130 orders to bone marrow failure and peripheral cytopenias, associated or not with hemophagocytic syndro

131 n and is manifested as persistence of severe cytopenias at 6 months after IST.

132 ion, all three patients exhibited refractory cytopenias before developing overt leukemia.

133 features of MDS, including peripheral blood cytopenias, bone marrow dysplasia, and apoptosis, and tr

134 ay the phenotypic features of MDS, including cytopenias, bone marrow dysplasia, and transformation to

135 tive neoplasm characterised by splenomegaly, cytopenias, bone marrow fibrosis, and debilitating sympt

136 Cytopenias can be observed in all three myeloid lineages

137 This is the first reported example of immune cytopenia caused by sensitivity to a glucuronide conjuga

138 ce of hydroxyurea in two patients because of cytopenias caused by the latter agent.

139 The results in other multilineage autoimmune cytopenia cohorts were encouraging, and sirolimus should

140 se manifestations (eg, massive splenomegaly, cytopenias, constitutional symptoms, and transformation

141 Myelofibrosis (MF) is characterized by cytopenias, constitutional symptoms, splenomegaly, and m

142 These findings shed light on Fc-independent cytopenias, designating desialylation as a potential dia

143 The clinical features of cytopenia, developmental defects, and tumor predispositi

144 ents often present with chronic multilineage cytopenias due to autoimmune peripheral destruction and/

145 rience hematopoietic stem cell attrition and cytopenia during childhood, which along with intrinsic c

146 Most patients experienced cytopenia during treatment, but no mortality was noted.

147 All patients developed one or more grade 3/4 cytopenias during therapy, and more than 90% had a febri

148 features of MDS, including peripheral blood cytopenias, dysplasia, and transformation to AML.

149 elodysplastic syndromes (MDS) are defined by cytopenias, dysplastic morphology of blood and marrow ce

150 Furthermore, autoimmune cytopenia, eczema, and intermittent diarrhea suggested i

151 phadenopathy, hepatosplenomegaly, autoimmune cytopenias, elevated numbers of double-negative T (DNT)

152 d poor graft function with persistent severe cytopenias even after repeated transplants with differen

153 respect to occurrence of grade 3 or greater cytopenias, fatigue, and infections.

154 o expanded hematopoietic cells to ameliorate cytopenia following transplantation of hematopoietic ste

155 myelofibrosis, including those with baseline cytopenias for whom options are particularly limited.

156 asm (MPN), MDS/MPN, or otherwise unexplained cytopenia (for >6 mo).

157 percentage of BM myeloblasts, and number of cytopenias; for survival, in addition to the above, vari

158 Sixteen of 21 patients with baseline cytopenias had sustained hematologic improvement.

159 iocyte Society diagnostic guidelines: fever, cytopenia, hemophagocytosis, hyperferritinemia, and elev

160 that mutant mice lacking AEP develop fever, cytopenia, hepatosplenomegaly, and hemophagocytosis, whi

161 e recently recapitulated hepatosplenomegaly, cytopenia, hypercytokinemia, and the bone-formation defe

162 ommon toxicities included diarrhea, fatigue, cytopenias, hypertension, and nausea.

163 ysfunction, coagulopathy, liver dysfunction, cytopenias, hypertriglyceridemia, hyperferritinemia, hem

164 He developed hyperferritinemia, cytopenias, hypofibrinogenemia, and a cytokine profile d

165 l, candidacy for autologous transplantation, cytopenias, IgM-related complications, hyperviscosity, a

166 tations in the tumor suppressor SAMD9L cause cytopenia, immunodeficiency, variable neurological prese

167 l remission in 10%, partial remission due to cytopenia in 7%, and partial remission due to residual d

168 e ablation of PTPN11/Shp2 resulted in severe cytopenia in BM, spleen, and peripheral blood in mice.

169 ssociated with a decline in the frequency of cytopenia in patients with human immunodeficiency virus

170 yelodysplastic syndrome (MDS) contributes to cytopenia in some patients and can be reversed by treatm

171 patients with quinine-induced immune thrombo-cytopenia in their reactions at various concentrations o

172 r cyclophosphamide as first therapy improves cytopenias in 50% of patients, but long-term use of thes

173 profile that distinguishes MDS from non-MDS cytopenias in a learning sample set.

174 d hypergammaglobulinemia and immune-mediated cytopenias in all patients, as well as urticarial rash,

175 matopoietic failure in autoimmune-associated cytopenias in LGL leukemia.

176 to be a promising drug regimen for treating cytopenias in patients with MMM.

177 noses, and advances in treatment options for cytopenias in PID is provided to facilitate multidiscipl

178 uppressive therapy is effective in improving cytopenias in selected patients.

179 ation mycobacterial disease in subject 1 and cytopenias in subject 2 resolved.

180 Cytopenias in these patients can be the result of spleni

181 ion studies to correct neutropenia and other cytopenias in WHIM syndrome.

182 The pathophysiology of cytopenias includes cytokine effects and direct antigen-

183 iated with deafness, lymphedema, mononuclear cytopenias, infection, myelodysplasia (MDS), and acute m

184 frequently associated with graft failure and cytopenias involving all hematopoietic lineages, but thr

185 itative reductions in naive CD8+ T cells and cytopenias involving nonlymphoid hemopoietic lineages.

186 Autoimmune cytopenia is a frequent manifestation of primary immunod

187 Especially when cytopenia is the initial symptom of a PID, the order and

188 dependently from myeloblast characteristics, cytopenias, karyotype, and comorbidities.

189 r if the prior treatment resulted in grade 4 cytopenias lasting longer than 7 days.

190 lodysplastic syndromes (MDS) have refractory cytopenias leading to transfusion requirements and infec

191 The main clinical manifestations include cytopenias, liver dysfunction, coagulopathy resembling d

192 Cytopenias, LKS loss, and mobilization are all caused by

193 g should be used cautiously because profound cytopenias may occur initially.

194 In contrast, after an initial period of mild cytopenia, mice reconstituted with the P140K mutant (0.8

195 with most having lymphadenopathy, autoimmune cytopenias, multiorgan autoimmunity (lung, gastrointesti

196 s are premalignant diseases characterized by cytopenias, myeloid dysplasia, immune dysregulation with

197 depth study of disorders including inherited cytopenias, myeloproliferative disorders, and erythromeg

198 reduction in spleen size with improvement in cytopenias (n = 1).

199 edian number of treatment cycles was 4, with cytopenias (n = 10) and fatigue (n = 3) the most common

200 alone with the most common toxicities being cytopenias (n = 10), nausea/vomiting (n = 9), and asthen

201 In patients with acquired AA with persistent cytopenias (n = 40), there was significant correlation b

202 rocedure was well tolerated with anticipated cytopenias, neutropenic fever, and disease-related fever

203 Cytopenias occur frequently in systemic lupus erythemato

204 Grade 3-4 cytopenias occurred in 37% of the 2-CdA -treated patient

205 ts (63%) in association with the presence of cytopenias, occurrence of autoimmune diseases, and splen

206 Lenalidomide-induced cytopenias occurring early in treatment may serve as a s

207 are not fulfilled, a condition termed clonal cytopenia of undetermined significance.

208 erred to as unexplained anemia or idiopathic cytopenia of unknown significance.

209 as a single agent, is effective in improving cytopenias of some MDS patients, especially those who pr

210 Cytopenias of uncertain etiology are commonly observed i

211 were diagnosed with MDS, 15% with idiopathic cytopenias of undetermined significance (ICUS) and some

212 Cytopenias often accompany infection with HIV.

213 he morbidity and mortality caused by chronic cytopenias, often without disease progression to acute m

214 reduction, symptom stabilization, and tumor cytopenia on repeat (68)Ga-DOTA-TATE positron emission t

215 ble only to patients with moderate to severe cytopenia or splenomegaly.

216 T-LGL leukemia, defined by accompanying cytopenias or autoimmune phenomena (or both), had the be

217 mutations among individuals with idiopathic cytopenias or clonal hematopoiesis of undetermined signi

218 ely penetrant, while 2 developed subclinical cytopenias or elevated Flt3L.

219 ents suffer from the consequences of chronic cytopenias or progression to acute myelogenous leukemia.

220 bjective response (improvement in peripheral cytopenias or spleen size).

221 system and clinical manifestations including cytopenias, organomegaly and bone disease.

222 al manifestations of ALPS include autoimmune cytopenias, organomegaly, and lymphadenopathy.

223 at contributed to hematotoxicity was initial cytopenia (P < 0.001).

224 (diarrhea, anorexia, and nausea), skin rash, cytopenias, pleural effusions, and fatigue.

225 uding lupus nephritis, and antibody-mediated cytopenias, possibly in combination with other immunosup

226 We studied 2 families with cytopenia, predisposition to MDS with chromosome 7 aberr

227 This model exhibits a prolonged period of cytopenias prior to transformation to leukemia and is th

228 ic syndrome (MDS) and one or more refractory cytopenias received treatment with amifostine in a Phase

229 atopoiesis characterized by peripheral-blood cytopenias, reduced marrow cellularity, lower frequency

230 rapeutic intervention is aimed at preventing cytopenia-related morbidity and preserving quality of li

231 w cytogenetics, marrow blast percentage, and cytopenias remained the basis of the new system.

232 Five of 19 patients developed cytopenias requiring treatment interruption and/or dose

233 atients, the first episode of either type of cytopenia resolved spontaneously.

234 complete response (CR) or CR with incomplete cytopenia response (20% vs 5%) favored 2000 mg obinutuzu

235 roliferative disorder of CTL associated with cytopenias resulting from an immune and cytokine attack

236 nd cytogenetics in patients who present with cytopenia(s) can identify patients for whom GATA2 sequen

237 e also treated 12 patients with multilineage cytopenias secondary to common variable immunodeficiency

238 One example is the development of multiple cytopenias secondary to cytolytic or cytotoxic antibodie

239 ivatives of primary medications cause immune cytopenia seem warranted.

240 r without dissemination signs (skin lesions, cytopenia) should alert for travel-acquired fungal infec

241 apy in 5% of patients, most often because of cytopenia, skin disorders, or gastrointestinal reactions

242 on within the lung, hypercytokinemia, T cell cytopenia, skin ulcerations, and premature death.

243 myeloproliferative neoplasm associated with cytopenias, splenomegaly, poor quality of life, and shor

244 's anemia (an) mutant shows peripheral blood cytopenias, spontaneous aneuploidy and a predisposition

245 of Syk would be useful in FcgammaR-dependent cytopenias such as immune thrombocytopenic purpura (ITP)

246 was temporally associated with viral-induced cytopenias, suggesting an immune-mediated clearance of t

247 n about abrogating its function to treat the cytopenias that accompany this disease.

248 lanation for the induction of the idiopathic cytopenias that are typical of individuals infected with

249 The hematopoietic cytopenias that characterize AP syndrome and the selecti

250 with clinical variables, including specific cytopenias, the proportion of blasts, and overall surviv

251 ation [41%], and nausea [38%]) and grade 3/4 cytopenias (thrombocytopenia [29%] and anemia [15%]).

252 characterized by multistage progression from cytopenias to acute myeloid leukemia (AML).

253 s with percentage of BM blasts and number of cytopenias to generate a prognostic model.

254 he susceptibility of humans with mononuclear cytopenias to mycobacterial infections and highlight the

255 ong-term single-agent therapy for refractory cytopenias using rapamycin in 30 patients and show remar

256 The risk of autoimmune cytopenia was at least 120 times higher than in the gene

257 Severe cytopenia was observed in all patients; leukopenia (with

258 Recovery from cytopenias was slower after CPX-351 (median days to abso

259 Post-HSCT hematological autoimmunity (cytopenias) was reported in 4 patients, acute graft-vers

260 ality (TRM), primarily due to infections and cytopenias, was significantly higher for 13 patients rec

261 Episodes of severe cytopenia were also frequent and were attributable to th

262 Patients with any degree of cytopenia were eligible.

263 High fever and cytopenia were less common in Lyme-HGA coinfection than

264 Cytopenias were assessed during the first 8 weeks of the

265 Cytopenias were common and could be managed by dose modi

266 Cytopenias were common, including grade 3 to 4 neutropen

267 Cytopenias were infrequent and modest.

268 Cytopenias were more frequent and severe with dasatinib.

269 Prior to therapy, grade 3/4 cytopenias were observed in 86% of patients.

270 Multilineage peripheral blood cytopenias were observed in adult mice lacking both isof

271 Cytopenias were rare; only one patient experienced anemi

272 Cytopenias were the most common grade 3/4 events, with t

273 Six children with single-lineage autoimmune cytopenias were treated and only 2 responded.

274 netic and molecular markers, and reversal of cytopenias) were not uniformly improved, a survival adva

275 In patients with no known history of cytopenias who are treated intensively at diagnosis, the

276 ry anemia with RS (RARS), 43 with refractory cytopenia with multilineage dysplasia (RCMD)-RS, 11 with

277 so in other MDS subtypes, such as refractory cytopenia with multilineage dysplasia and ring siderobla

278 Four patients had refractory cytopenia with multilineage dysplasia and ringed siderob

279 n = 1; refractory anemia, n = 1; refractory cytopenia with multilineage dysplasia, n = 1) had no UPD

280 es are manageable, mostly consisting of mild cytopenias with no significant neuropathy.

281 Patients often also exhibit autoimmune cytopenias with symptoms of abnormal T cell function, in

282 also led to more effective treatment of the cytopenias without significant complications.