ライフサイエンスコーパス: cytopenia

1 th inflammatory complications accompanied by cytopenia.

2 aboratory evidence of hypocomplementemia and cytopenia.

3 involvement, and 25 patients had hematologic cytopenia.

4 dysplastic neutrophils and multiple lineage cytopenia.

5 referentially who present with high fever or cytopenia.

6 pergammaglobulinemia G and A, and autoimmune cytopenia.

7 conditions that mainly result in monolinear cytopenia.

8 6, an inhibitor of Syk function, in treating cytopenia.

9 itivity in patients with drug-induced immune cytopenia.

10 eased blood cell apoptosis, and multilineage cytopenia.

11 ary haemorrhage in a patient with persistent cytopenia.

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

13 gan involvement: liver, spleen, and/or blood cytopenia.

14 ontrolled HIV infection is a risk factor for cytopenia.

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

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

17 spectively, mostly in those with preexisting cytopenias.

18 utoimmunity, including autoantibody-mediated cytopenias.

19 encountered in 144 patients with unexplained cytopenias.

20 cooperate to contribute to lupus-associated cytopenias.

21 ion of children with refractory multilineage cytopenias.

22 tic anemia, thrombosis, and peripheral blood cytopenias.

23 ng to ineffective hematopoiesis and clinical cytopenias.

24 ociated with autoimmune diseases and various cytopenias.

25 ctive hematopoiesis that leads to peripheral cytopenias.

26 marrow blast percentage value, and depth of cytopenias.

27 ith autoimmune disorders and immune-mediated cytopenias.

28 sis, congestive heart failure, and prolonged cytopenias.

29 n the development of inflammation-associated cytopenias.

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

31 pmentally compromised and are prone to blood cytopenias.

32 patosplenomegaly, and recurring multilineage cytopenias.

33 rash, elevated transaminases/bilirubin, and cytopenias.

34 at results in fever, hepatosplenomegaly, and cytopenias.

35 ymphadenopathy, splenomegaly, and autoimmune cytopenias.

36 defined by presence of at least 2 autoimmune cytopenias.

37 e development of infection-driven autoimmune cytopenias.

38 most common were hematologic toxicities with cytopenias.

39 terium, results in multiple peripheral blood cytopenias.

40 ted with lenalidomide experience significant cytopenias.

41 rse but sometimes manifests with significant cytopenias.

42 ctive hematopoiesis that leads to peripheral cytopenias.

43 cells often associated with immune-mediated cytopenias.

44 ed to hematopoietic malignancies and various cytopenias.

45 vents, corticosteroid-related morbidity, and cytopenias.

46 onditioning regimen who developed autoimmune cytopenias.

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

48 disposing to infection-associated autoimmune cytopenias.

49 oalbuminemia (18.6% vs 5.2%, P < 0.001), and cytopenias.

50 most affected, with all subjects developing cytopenias.

51 ermine possible associations between HIV and cytopenias.

52 athy, massive hepatosplenomegaly, and severe cytopenias.

53 with myelofibrosis irrespective of baseline cytopenias.

54 and maintained remission of immune-mediated cytopenias.

55 sing hemolytic anemia and interferon causing cytopenias.

56 ction, even in patients with severe baseline cytopenias.

57 dren with refractory multilineage autoimmune cytopenias.

58 Both patients had prolonged cytopenias.

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

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

61 ude male preponderance, frequent preexisting cytopenia, additional somatic DDX41 mutation, and relati

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

63 oietic cell transplantation (HCT) autoimmune cytopenia (AIC) is a potentially life-threatening compli

64 affected by autoantibody-mediated autoimmune cytopenias (AICs) and lymphadenopathy.

65 are altered in CVID subjects with autoimmune cytopenias (AICs; CVID+AIC) and the causes of these dera

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

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

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

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

70 (1.1%) developed BM failure characterized by cytopenia and BM aplasia.

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

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

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

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

75 HSCT seems to be an effective option to cure cytopenia and severe autoinflammation in PAMI syndrome a

76 of age, half of the Hopx(-/-) mice developed cytopenia and splenomegaly.

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

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

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

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

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

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

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

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

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

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

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

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

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

90 Peripheral blood cytopenias and dysplastic hematopoietic progenitors char

91 Severity of cytopenias and elevated immunoglobulin levels also predi

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

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

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

95 se of common clinical manifestations such as cytopenias and immune dysfunction.

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

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

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

99 The relationship between peripheral blood cytopenias and myeloid neoplasms-such as myelodysplastic

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

101 ons in the SBDS gene) or clinical diagnosis (cytopenias and pancreatic dysfunction) of Shwachman-Diam

102 e noncurative and aimed instead at improving cytopenias and quality of life and delaying disease prog

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

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

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

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

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

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

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

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

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

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

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

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

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

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

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

118 lymphoproliferation, systemic inflammation, cytopenias, and life-threatening multi-organ dysfunction

119 d by lymphadenopathy, systemic inflammation, cytopenias, and life-threatening multiorgan dysfunction.

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

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

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

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

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

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

126 history of childhood-onset antibody defects, cytopenias, and T lymphocytic pneumonitis and colitis, w

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

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

129 Cytopenias are an important clinical problem associated

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

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

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

133 s facilitating acute inflammation-associated cytopenias are unknown.

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

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

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

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

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

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

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

141 ry from irradiation-induced peripheral blood cytopenia, bone marrow damage as well as apoptosis in st

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

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

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

145 mage response, and more severe pretransplant cytopenias, but not with bone marrow blast count, MDS tr

146 Cytopenias can be observed in all three myeloid lineages

147 CH in the setting of peripheral blood cytopenias carries a very high risk of progression to a

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

149 ome develops in late adulthood, with fevers, cytopenias, characteristic vacuoles in myeloid and eryth

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

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

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

153 immunodeficiency associated with autoimmune cytopenia (CVID+AIC) generate few isotype-switched B cel

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

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

156 Cytopenias distinguished MIS-C from KD and the degree of

157 The cytopenias do not appear to be harmful.

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

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

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

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

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

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

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

165 slational in vivo models to predict clinical cytopenia effects.

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

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

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

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

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

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

172 symptoms, hepatic and liver enlargement, and cytopenias; hematophagocytic syndrome can also occur.

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

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

175 teristic features include unremitting fever, cytopenias, hepatosplenomegaly, and elevation of typical

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

177 ophagocytosis, hypercytokinemia, consumptive cytopenias, hyperferritinemia, and other hemophagocytic

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

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

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

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

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

183 Cytopenias improved in all patients within the first wee

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

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

186 in two patients (10%), and grade 4 prolonged cytopenia in six patients (32%).

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

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

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

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

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

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

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

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

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

196 Cytopenias in these patients can be the result of spleni

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

198 mon adverse events of grade 3 or higher were cytopenias (in 94% of the patients) and infections (in 3

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

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

201 Autoimmune cytopenia is a frequent manifestation of primary immunod

202 Cytopenia is rare in people with well-controlled HIV, bu

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

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

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

206 ase syndrome (22%), neurologic events (12%), cytopenias lasting more than 28 days (32%), infections (

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

208 ing to severe symptoms and organ damage (eg, cytopenias, liver dysfunction, portal hypertension, mala

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

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

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

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

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

214 3)Ra treatment because of progression and/or cytopenia (n = 23) showed significantly higher uptake (3

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

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

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

218 Cytopenias occur frequently in systemic lupus erythemato

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

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

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

222 topoiesis of indeterminate potential, clonal cytopenia of undetermined significance, and aplastic ane

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

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

225 Cytopenias of uncertain etiology are commonly observed i

226 of indeterminate potential (CHIP) and clonal cytopenias of undetermined significance (CCUS).

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

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

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

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

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

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

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

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

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

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

237 crease neutrophil counts but does not affect cytopenias other than neutropenia.

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

239 and 4 adverse events (the most common being cytopenia, peripheral neuropathy, and heart failure) wer

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

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

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

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

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

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

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

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

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

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

250 mathematical modeling methods for assessing cytopenia risk rely on indirect measurements of drug eff

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

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

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

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

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

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

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

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

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

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

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

262 The hematopoietic cytopenias that characterize AP syndrome and the selecti

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

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

265 tion mutations cause lung disease and T cell cytopenia through unknown mechanisms.

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

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

268 deficiency (up to 17.6-fold) and autoimmune cytopenias (up to 12-fold).

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

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

271 were well tolerated, and only mild transient cytopenia was noted.

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

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

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

275 Patients with any degree of cytopenia were eligible.

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

277 Cytopenias were assessed during the first 8 weeks of the

278 Cytopenias were common and could be managed by dose modi

279 f combination antiretroviral therapy (cART), cytopenias were common in people with human immunodefici

280 Cytopenias were common, including grade 3 to 4 neutropen

281 Cytopenias were infrequent and modest.

282 level (P = .025) were more important whereas cytopenias were less profound (platelet count, 22 x 103/

283 Cytopenias were more frequent and severe with dasatinib.

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

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

286 Cytopenias were predominant among grade 3/4 events and r

287 Cytopenias were rare; only one patient experienced anemi

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

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

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

291 etic system developed myeloproliferation and cytopenia, which is reversed in Kras(G12D) mice lacking

292 imposable features, including neonatal-onset cytopenia with dyshematopoiesis, autoinflammation, rash,

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

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

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

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

297 nic lymphoid leukemia, n = 1; and refractory cytopenia with multilineage dysplasia, n = 1).

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

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

300 ancy, and 15 (46%) had a personal history of cytopenia years before MDS/AML diagnosis.