ライフサイエンスコーパス: hemolytic anemia

1 er affecting 15% of patients with autoimmune hemolytic anemia.

2 in anemic iron-overload disorders caused by hemolytic anemia.

3 n 3 to 5 wk from complications of autoimmune hemolytic anemia.

4 of severe thrombocytopenia and schistocytic hemolytic anemia.

5 results in a mild to moderate nonspherocytic hemolytic anemia.

6 ase center with congestive heart failure and hemolytic anemia.

7 ve in managing symptoms of heart failure and hemolytic anemia.

8 apable of causing immune thrombocytopenia or hemolytic anemia.

9 o impaired ankyrin expression and congenital hemolytic anemia.

10 All cause severe hemolytic anemia.

11 or mutations associated with membrane-linked hemolytic anemia.

12 ten present with common clinical findings of hemolytic anemia.

13 is, membrane biogenesis, and spectrin-linked hemolytic anemia.

14 d a delayed recovery from chemically induced hemolytic anemia.

15 r mutations in patients with spectrin-linked hemolytic anemia.

16 background, they rapidly die from autoimmune hemolytic anemia.

17 4.2 content of the erythrocyte membrane and hemolytic anemia.

18 it reversed their skin photosensitivity and hemolytic anemia.

19 antibodies and the development of autoimmune hemolytic anemia.

20 in red blood cells results in nonspherocytic hemolytic anemia.

21 be exploited to prevent and treat autoimmune hemolytic anemia.

22 ozymes, especially cancer and nonspherocytic hemolytic anemia.

23 although it was efficient in rescuing their hemolytic anemia.

24 y an impaired response to chemically induced hemolytic anemia.

25 y to complement-mediated lysis, resulting in hemolytic anemia.

26 upffer cells in a murine model of autoimmune hemolytic anemia.

27 hrombocytopenia and possibly neutropenia and hemolytic anemia.

28 struction, causing transfusion reactions and hemolytic anemia.

29 nti-C1s antibody sutimlimab would ameliorate hemolytic anemia.

30 have at least one SLE-affected patient with hemolytic anemia.

31 double-knockout mouse developed spontaneous hemolytic anemia.

32 n patients with severe refractory autoimmune hemolytic anemia.

33 o had at least one SLE-affected patient with hemolytic anemia.

34 eir accelerated removal from circulation and hemolytic anemia.

35 res of thrombocytopenia and microangiopathic hemolytic anemia.

36 esent a potential pathway for the control of hemolytic anemia.

37 by fava beans or other agents) or life-long hemolytic anemia.

38 patient program recapitulated the control of hemolytic anemia.

39 by mutations in PKLR and leads to congenital hemolytic anemia.

40 rocytosis (HX) and/or undiagnosed congenital hemolytic anemia.

41 utations present with chronic nonspherocytic hemolytic anemia.

42 anemia is the most common form of autoimmune hemolytic anemia.

43 by poor pharmacokinetics and toxicity due to hemolytic anemia.

44 athway that causes congenital nonspherocytic hemolytic anemia.

45 erythrocyte Abs and is a model of autoimmune hemolytic anemia.

46 presented with severe, transfusion-dependent hemolytic anemia.

47 d commitment under stress conditions such as hemolytic anemia.

48 7(E11)Val --> Met) that were associated with hemolytic anemia.

49 ing AS treatment is an original mechanism of hemolytic anemia.

50 a disorder associated with acute or chronic hemolytic anemia.

51 ase and other chronic hereditary or acquired hemolytic anemias.

52 red cell membrane skeleton underlie multiple hemolytic anemias.

53 tant driver of human disease, including many hemolytic anemias.

54 ve hemophagocytic syndrome (44%), autoimmune hemolytic anemia (33%), and lymphoma (22%) were the comm

55 In children with other congenital hemolytic anemias, a partial splenectomy appears to cont

56 cantly impaired erythropoietic recovery from hemolytic anemia, acute blood loss and myeloablation.

57 ting the TPI protein and clinically features hemolytic anemia, adult-onset neurological impairment, d

58 toimmune disease characterized by autoimmune hemolytic anemia (AHA) and inflammatory bowel disease.

59 Autoimmune hemolytic anemia (AHA) is a common complication in chron

60 s, and signaling kinetics, during autoimmune hemolytic anemia (AIHA) and bone marrow failure.

61 vered ex vivo from a patient with autoimmune hemolytic anemia (AIHA) and characterize their phenotype

62 ively investigated in 308 primary autoimmune hemolytic anemia (AIHA) cases and correlated with serolo

63 complement in the pathogenesis of autoimmune hemolytic anemia (AIHA) has been controversial and may d

64 eous autoimmune diseases, such as autoimmune hemolytic anemia (AIHA) in New Zealand Black (NZB) mice,

65 Autoimmune hemolytic anemia (AIHA) is a disease in which autoantibo

66 rom the deletion of IL-2 in which autoimmune hemolytic anemia (AIHA) is a prominent feature.

67 Autoimmune hemolytic anemia (AIHA) is an uncommon entity that prese

68 Autoimmune hemolytic anemia (AIHA) is the result of increased destr

69 ically imposed severe spontaneous autoimmune hemolytic anemia (AIHA) that is very similar to the corr

70 In autoimmune hemolytic anemia (AIHA), circulating red blood cells (RB

71 erapy in 23 patients with primary autoimmune hemolytic anemia (AIHA).

72 The development of warm-antibody autoimmune hemolytic anemia (also known as warm autoimmune hemolyti

73 mune thrombocytopenia followed by autoimmune hemolytic anemia and 1 Evans syndrome with rheumatoid ar

74 l pathways that can lead to microangiopathic hemolytic anemia and a procoagulant state with or withou

75 While hemolytic anemia and an altered cytokine environment hav

76 totoxicity in in vitro models for autoimmune hemolytic anemia and antibody-mediated rejection of orga

77 ll lymphoproliferation results in autoimmune hemolytic anemia and cold-induced circulatory symptoms.

78 associated with protection from RBV-induced hemolytic anemia and decrease the need for RBV dose redu

79 RHAU deletion in hematopoietic system caused hemolytic anemia and differentiation defect at the proer

80 It is characterized by chronic hemolytic anemia and endothelial dysfunction, resulting

81 ited blood disorder characterized by chronic hemolytic anemia and episodic vaso-occlusive pain crises

82 ations in the aldolase genes in humans cause hemolytic anemia and hereditary fructose intolerance.

83 Hemolytic anemia and hypergammoglobulinemia occurred in

84 Hemolytic anemia and IFN-mediated bone marrow suppressio

85 Abs (mAbs) such as rituximab and Ab-induced hemolytic anemia and immune thrombocytopenia.

86 aracterized by the combination of autoimmune hemolytic anemia and immune thrombocytopenia.

87 limited due to the use of ribavirin causing hemolytic anemia and interferon causing cytopenias.

88 ajor clinical manifestations: severe chronic hemolytic anemia and iterative vaso-occlusive crises.

89 tified laboratory markers of the severity of hemolytic anemia and its associated clinical events as c

90 , and thrombosis, are related to the chronic hemolytic anemia and its current management and can occu

91 h sickle cell disease, which features severe hemolytic anemia and leads to scavenging of nitric oxide

92 The ratio of the presence of both hemolytic anemia and neurologic disorder was approximate

93 in sickle cell disease have centered around hemolytic anemia and nitric oxide metabolism.

94 iron and fat in the viscera in children with hemolytic anemia and obesity, respectively.

95 titute irradiated recipients and correct the hemolytic anemia and organ pathology that characterize t

96 The most common serious adverse events, hemolytic anemia and pharyngitis, each occurred in 2 pat

97 of mCd59b (mCd59b-/-) results in spontaneous hemolytic anemia and progressive loss of male fertility.

98 hocytes) in their circulation, indicative of hemolytic anemia and resembling the human disorder chore

99 substantial improvement of sickle-associated hemolytic anemia and reticulocytosis, key pathophysiolog

100 ion in blood cells, which is responsible for hemolytic anemia and skin photosensitivity.

101 The association between degrees of hemolytic anemia and socioeconomic/demographic, clinical

102 ty in Nrf2(-/-) mice raised a possibility of hemolytic anemia and splenic extramedullary hematopoiesi

103 ency protect against ribavirin (RBV)-induced hemolytic anemia and the need for RBV dose reduction in

104 ce was reflected in reduced pancreatitis and hemolytic anemia and this was associated with distinct c

105 gical hallmark of anti-GBM-GN, combined with hemolytic anemia and thrombocytopenia.

106 been reported in the settings of autoimmune hemolytic anemia and transfusion of crossmatch-incompati

107 merization and downstream adverse effects of hemolytic anemia and vaso-occlusion.

108 cell anemia is a unique disease dominated by hemolytic anemia and vaso-occlusive events.

109 evels of erythrocyte glutathione, leading to hemolytic anemia and, in some cases, impaired neurologic

110 posed as a candidate gene in some Heinz body hemolytic anemias and as a modifier gene in the beta-tha

111 human AE1 cause several types of hereditary hemolytic anemias and/or distal renal tubular acidosis.

112 th this, prdx1-/- mice develop age-dependent hemolytic anemias and/or malignancies.

113 rogenase and NADP (in relation to favism and hemolytic anemia), and the Glu487-->Lys mutation (presen

114 produce HUS with thrombotic microangiopathy, hemolytic anemia, and acute kidney injury.

115 sorder of thrombocytopenia, microangiopathic hemolytic anemia, and acute renal failure.

116 imilarly to those with idiopathic autoimmune hemolytic anemia, and additional therapy for the underly

117 ll spectrum HUS, including thrombocytopenia, hemolytic anemia, and AKI with glomerular thrombotic mic

118 ytopenia, discoid rash, neurologic disorder, hemolytic anemia, and co-occurring neurologic disorder p

119 toimmune lymphocytic thyroiditis, autoimmune hemolytic anemia, and colitis.

120 SCD) results in vascular occlusions, chronic hemolytic anemia, and cumulative organ damage.

121 minase or bilirubin elevations, neutropenia, hemolytic anemia, and depression.

122 ing preexisting TTP signs; thrombocytopenia, hemolytic anemia, and organ damage could not be reversed

123 ontrast, produced fewer reticulocytes during hemolytic anemia, and pA2gata1-DYRK3 progenitors were co

124 nal failure, thrombocytopenia, microvascular hemolytic anemia, and plasma levels of von Willebrand fa

125 layed elevated oxidative stress, symptoms of hemolytic anemia, and premature death.

126 ar thrombosis coupled with thrombocytopenia, hemolytic anemia, and red blood cell fragmentation.

127 l of HUS that includes the thrombocytopenia, hemolytic anemia, and renal failure that define the huma

128 purified Stx-1 results in thrombocytopenia, hemolytic anemia, and renal thrombotic microangiopathy.

129 ion and RBC sickling include vaso-occlusion, hemolytic anemia, and stroke.

130 ection-site erythema and pyrexia, autoimmune hemolytic anemia, and suspected lack of vaccine efficacy

131 at emerge on erythrocytes lead to autoimmune hemolytic anemia, and the causative auto-IgM cross-react

132 hrombosis, which result in thrombocytopenia, hemolytic anemia, and tissue ischemia.

133 ure to PCB-153, leading to oxidative stress, hemolytic anemia, and tumor development in a mouse model

134 ematocrit, sickle cell disease, thalassemia, hemolytic anemias, and malaria, with both arterial and v

135 in the liver also occurs in mouse models of hemolytic anemia, anemia of inflammation, and sickle cel

136 rythrocyte autoantibodies, erythroblastosis, hemolytic anemia, anti-DNA autoantibodies, kidney diseas

137 is, neuropsychiatric involvement, autoimmune hemolytic anemia, anti-double-stranded DNA, and antiphos

138 e, sickling, increased oxidative stress, and hemolytic anemia are accompanied by vasodilation, compen

139 posterior leukoencephalopathy and autoimmune hemolytic anemia are newly reported clinical association

140 Vasculitides and autoimmune hemolytic anemia are the two most common autoimmune mani

141 ze tetramer formation and lead to hereditary hemolytic anemias are located at the N-terminal region o

142 ress model results in enhanced recovery from hemolytic anemia as well as enhanced splenic stress eryt

143 c disorder diagnosed by thrombocytopenia and hemolytic anemia, associated with a deficiency in von Wi

144 a gene mutated in Mendelian non-spherocytic hemolytic anemia, associated with HGB and HCT (SKAT p <

145 ; this risk was largely determined by occult hemolytic anemia-associated pulmonary hypertension.

146 Sixty-five (10%) patients developed hemolytic anemia at some time during the disease course,

147 phlebotomy-induced acute anemia and chronic hemolytic anemia because of 4.1R deficiency, the ratio o

148 with clinically significant immune-mediated hemolytic anemia because the antibody does not block APC

149 re clonal blood disorder that manifests with hemolytic anemia, bone marrow failure, and thrombosis.

150 o multiple vital organ systems and a chronic hemolytic anemia, both contributing to progressive organ

151 hereditary spherocytosis (HS) and autoimmune hemolytic anemia, but also with RBC senescence.

152 Acute hemolytic anemia can be managed effectively provided it

153 Ribavirin-induced hemolytic anemia can prompt dose reductions and lower su

154 Transfusion, in the setting of autoimmune hemolytic anemia, can be a complicated and potentially d

155 ies to treat not only chronic nonspherocytic hemolytic anemia caused by severe G6PD variants, but als

156 ofound thrombocytopenia and microangiopathic hemolytic anemia characterize thrombotic microangiopathy

157 ytosis (OHSt) is a rare dominantly inherited hemolytic anemia characterized by a profuse membrane lea

158 erlot (mot) and chablis (cha) exhibit severe hemolytic anemia characterized by abnormal cell morpholo

159 t reconstituted animals display a persistent hemolytic anemia characterized by increased oxidative da

160 is (HX, MIM 194380) is an autosomal dominant hemolytic anemia characterized by primary erythrocyte de

161 is (HX; MIM 194380) is an autosomal-dominant hemolytic anemia characterized by primary erythrocyte de

162 octurnal hemoglobinuria (PNH) is an acquired hemolytic anemia characterized by the increased sensitiv

163 ong descriptive diagnoses such as autoimmune hemolytic anemia, chronic immune thrombocytopenia, Evans

164 immune thrombocytopenia and warm autoimmune hemolytic anemia, circulating immunoglobulin G (IgG)-ops

165 zymopathies, known as chronic nonspherocytic hemolytic anemia (CNSHA).

166 ice, but which are predisposed to autoimmune hemolytic anemia, develop auto-antibodies to their red b

167 One patient with an autoimmune hemolytic anemia developed PML after treatment with cort

168 editary pyropoikilocytosis (HPP) is a severe hemolytic anemia due to abnormalities of the red blood c

169 of Nrf2 causes regenerative immune-mediated hemolytic anemia due to increased sequestration of damag

170 n to protect against ribavirin (RBV)-induced hemolytic anemia during early stages of treatment.

171 women with previous history of preeclampsia, hemolytic anemia, elevated liver enzymes and low platele

172 vere genetic blood disorder characterized by hemolytic anemia, episodic vaso-occlusion, and progressi

173 e proband developed a transfusion-dependent, hemolytic anemia following birth.

174 hould correct ineffective erythropoiesis and hemolytic anemia following the delivery of only 1 to 2 v

175 lmonary hypertension associated with chronic hemolytic anemia has been moved from Group 1 PAH to Grou

176 encies of EMS proteins in humans lead to the hemolytic anemia Hereditary Spherocytosis (HS) which inc

177 During hemolytic anemia, however, erythropoiesis was markedly d

178 In response to hemolytic anemia, however, reticulocyte production incre

179 mune complications manifesting as autoimmune hemolytic anemia, immune-mediated thrombocytopenia, and

180 eferred second-line therapy of warm antibody hemolytic anemia in adults, although no prospective stud

181 ve, nontoxic strategy for the improvement of hemolytic anemia in beta-thalassemic patients.

182 Drug-induced acute hemolytic anemia in G6PD A- subjects can be life-threate

183 Unfortunately, both drugs cause hemolytic anemia in G6PD-deficient humans.

184 mbosis is a life-threatening complication of hemolytic anemia in humans.

185 The etiology of severe hemolytic anemia in most patients with recessive heredit

186 capacity sensitizes erythrocytes and causes hemolytic anemia in Nrf2(-/-) mice, suggesting a pivotal

187 in the inosine triphosphate (ITPA) gene and hemolytic anemia in patients infected with hepatitis C v

188 is the primary molecular event that leads to hemolytic anemia in sickle cell disease (SCD).

189 a, and co-occurring neurologic disorder plus hemolytic anemia in SLE was observed in 159 affected sib

190 with immune thrombocytopenia and autoimmune hemolytic anemia in the setting of acute infections.

191 We hypothesized that hemolytic anemia in those SLE-affected patients would id

192 none with serious infection), and autoimmune hemolytic anemia in two (resolved with a steroid course

193 cold agglutinin disease (CAD), an autoimmune hemolytic anemia in which autoantibodies (cold agglutini

194 n linked to a recessive syndrome of dRTA and hemolytic anemia in which hypofunction can be discerned

195 n disease is a difficult-to-treat autoimmune hemolytic anemia in which immunoglobulin M antibodies bi

196 11 human pedigrees with dominantly inherited hemolytic anemias in both the hereditary stomatocytosis

197 ng numerous clinical settings such as severe hemolytic anemia, infection, tissue injury, or blood tra

198 Thyrotoxicosis, celiac disease, acquired hemolytic anemia, interstitial cystitis, and Sjogren's s

199 Hemolytic anemia is a forme fruste of systemic lupus ery

200 Ribavirin-associated hemolytic anemia is a potential problem in a patient pop

201 r therapeutic apheresis in diseases in which hemolytic anemia is a prominent feature.

202 Hemolytic anemia is an early disease manifestation and i

203 complement in the development of autoimmune hemolytic anemia is discussed.

204 Warm antibody hemolytic anemia is the most common form of autoimmune h

205 omy for symptomatic children with congenital hemolytic anemias is restricted by concern of postsplene

206 The phenotype of severe nonspherocytic hemolytic anemia, jaundice, hepatosplenomegaly, and mark

207 Drug-induced acute hemolytic anemia led to the discovery of G6PD deficiency

208 f red blood cells in human subjects, causing hemolytic anemia linked to impaired nicotinamide adenine

209 anthomas, premature coronary artery disease, hemolytic anemia, macrothrombocytopenia, and bleeding.

210 zed by thrombocytopenia and microangiopathic hemolytic anemia (MAHA) without an obvious cause, and ma

211 Patients with secondary autoimmune hemolytic anemia may be treated similarly to those with

212 therapies used for warm antibody autoimmune hemolytic anemia may be tried with less likelihood of re

213 blood cell (RBC) cytoskeleton provide severe hemolytic anemia models in which to study multiorgan thr

214 Mechanistic studies in a hemolytic anemia mouse model demonstrated that loss of i

215 in bone marrow and spleen and is lethal in a hemolytic anemia mouse model.

216 thrombocytopenic purpura (ITP) or autoimmune hemolytic anemia, mouse models were used to evaluate eff

217 involves many interactions, the most common hemolytic anemia mutations that disrupt erythrocyte morp

218 actory thrombocytopenia (n = 13), autoimmune hemolytic anemia (n = 15), and vasculitis (n = 6).

219 ADs target hematopoietic (autoimmune hemolytic anemia, n = 20; Evans syndrome, n = 9; autoimm

220 ated with thrombocytopenia, microangiopathic hemolytic anemia, neurologic symptoms, and renal insuffi

221 component of the management of warm antibody hemolytic anemia not only after relapse but as soon as t

222 Notably, an equally severe hemolytic anemia occurs despite minimally decreased memb

223 ending on whether the patient has autoimmune hemolytic anemia of warm antibody type, cold agglutinin

224 The impact of hemolytic anemia on damage accrual and mortality was exa

225 ial diagnosis of unexplained posttransfusion hemolytic anemia or fever, regardless of the season or U

226 a or in urine, is a sign of diseases such as hemolytic anemia or urinary tract infections.

227 sodes of immune thrombocytopenia, autoimmune hemolytic anemia, or neutropenia, in addition to splenom

228 lness characterized by bacteremia and severe hemolytic anemia (Oroya fever), followed by benign, chro

229 Sickle cell disease is characterized by hemolytic anemia, pain, and progressive organ damage.

230 matomyositis, systemic sclerosis, autoimmune hemolytic anemia, pernicious anemia, and ankylosing spon

231 structural changes in cdb3 that lead to the hemolytic anemia phenotype, site-directed spin labeling

232 rious origins, resulting in microangiopathic hemolytic anemia, platelet consumption, fibrin depositio

233 f hemolytic anemia plus thrombocytopenia and hemolytic anemia plus neurologic disorder appeared to be

234 hese clinical features, paired expression of hemolytic anemia plus thrombocytopenia and hemolytic ane

235 ages both in vitro and in vivo under chronic hemolytic anemia, providing evidence for the role of HRI

236 Hemolytic anemia recurred when drug levels were cleared

237 motif of ATP11C, responsible for congenital hemolytic anemia, reduces ATP11C expression, increases r

238 asma exchange in the treatment of autoimmune hemolytic anemia remains uncertain.

239 Finally, we chemically induce hypoxemia via hemolytic anemia resulting in HIF stabilization within c

240 ets, which account for the thrombocytopenia, hemolytic anemia, schistocytes, and tissue injury that c

241 aroxysmal cold hemoglobinuria, or autoimmune hemolytic anemia secondary to an underlying disorder.

242 angiopathy characterized by microangiopathic hemolytic anemia, severe thrombocytopenia, and organ isc

243 Initial therapy for warm antibody autoimmune hemolytic anemia should be corticosteroids, such as pred

244 usion management of patients with autoimmune hemolytic anemia, specifically focusing on published art

245 eased longevity for patients with congenital hemolytic anemias (such as sickle cell disease and thala

246 on human erythrocytes is associated with the hemolytic anemia syndrome paroxysmal nocturnal hemoglobi

247 immune thrombocytopenic purpura, autoimmune hemolytic anemia, systemic lupus erythematosus, and mult

248 Sickle cell disease (SCD), a congenital hemolytic anemia that exacts terrible global morbidity a

249 d a potential early biomarker for autoimmune hemolytic anemia that is based on different levels of er

250 genus babesia, is characterized by nonimmune hemolytic anemia that resolves with antimicrobial treatm

251 tic link between the induction of autoimmune hemolytic anemia, the reduction in naive T cells, and po

252 ly combine skin photosensitivity and chronic hemolytic anemia, the severity of which is related to po

253 Originally isolated from a cat with hemolytic anemia, this strain induces severe hemolytic a

254 SpHUS) is defined by the occurrence of acute hemolytic anemia, thrombocytopenia and acute kidney inju

255 remic syndrome is a disease characterized by hemolytic anemia, thrombocytopenia and acute renal failu

256 sel thrombosis resulting in microangiopathic hemolytic anemia, thrombocytopenia and renal failure.

257 surface level that leads to microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney fai

258 Microangiopathic hemolytic anemia, thrombocytopenia, and acute kidney inj

259 a microangiopathic disease characterized by hemolytic anemia, thrombocytopenia, and acute renal fail

260 emic syndrome is a triad of microangiopathic hemolytic anemia, thrombocytopenia, and acute renal fail

261 drome, including thrombotic microangiopathy, hemolytic anemia, thrombocytopenia, and acute renal fail

262 condition characterized by microangiopathic hemolytic anemia, thrombocytopenia, and ARF.

263 hy that is characterized by microangiopathic hemolytic anemia, thrombocytopenia, and renal failure.

264 yndrome (HUS) is a triad of microangiopathic hemolytic anemia, thrombocytopenia, and renal impairment

265 which produces Shiga toxins (Stx) that cause hemolytic anemia, thrombocytopenia, and renal injury.

266 mic lupus erythematosus, Sjogren's syndrome, hemolytic anemia, thrombocytopenia, hypothyroidism, infl

267 common name for adults with microangiopathic hemolytic anemia, thrombocytopenia, with or without neur

268 marrow failure disorder that manifests with hemolytic anemia, thrombosis, and peripheral blood cytop

269 n, now in clinical trials in warm autoimmune hemolytic anemia to lower IgG antibodies and IgG contain

270 eficiency is associated with either episodic hemolytic anemia (triggered by fava beans or other agent

271 -phosphate dehydrogenase, exhibit non-immune hemolytic anemia upon exposure to aspirin and various an

272 Treatment of autoimmune hemolytic anemias varies depending on whether the patien

273 with sickle cell disease (SCD) is caused by hemolytic anemia, vaso-occlusion, and progressive multio

274 olytic anemia (also known as warm autoimmune hemolytic anemia [WAHA]) in patients with babesiosis has

275 ; the response was better in warm autoimmune hemolytic anemia (WAIHA; overall response, 100% at all t

276 The schistocytic hemolytic anemia was also halted and partially reversed

277 Hemolytic anemia was associated with damage accrual afte

278 Hemolytic anemia was defined as anemia with reticulocyto

279 ables known to affect this outcome; however, hemolytic anemia was not associated with mortality.

280 Hemolytic anemia was stimulated by phenylhydrazine injec

281 Using a murine model of autoimmune hemolytic anemia, we defined the contribution of galacto

282 g patients with severe refractory autoimmune hemolytic anemia, we treated 9 patients with cyclophosph

283 ded TTP onset as severe thrombocytopenia and hemolytic anemia were absent in these animals.

284 les independently associated with degrees of hemolytic anemia were African American ethnicity, thromb

285 order (defined as seizure or psychosis), and hemolytic anemia were observed in 159 SLE-affected sibpa

286 eficiency are at risk for the development of hemolytic anemia when given 8-aminoquinolines (8-AQs), a

287 hemolytic anemia, this strain induces severe hemolytic anemia when inoculated into specific-pathogen-

288 may develop acute and sometimes very severe hemolytic anemia when triggered by ingestion of fava bea

289 dehydration of red blood cells resulting in hemolytic anemia which has been traced to two individual

290 Unlike autoimmune hemolytic anemia, which is characterized by an increased

291 ic NTS infection during malaria is caused by hemolytic anemia, which leads to reduced macrophage micr

292 tients presenting with symptoms and signs of hemolytic anemia with a focus on RBC membrane disorders.

293 xpressing 100% human Hb S, display a chronic hemolytic anemia with compensatory marrow and extramedul

294 alpha-Adducin-null mice display compensated hemolytic anemia with features characteristic of RBCs in

295 present a strong phenotype characterized by hemolytic anemia with increased reticulocytes, anisopoik

296 sis (DHSt) usually presents as a compensated hemolytic anemia with macrocytosis and abnormally shaped

297 eral blood analysis shows evidence of severe hemolytic anemia with reduced number of erythrocytes/hem

298 The infant displayed severe microangiopathic hemolytic anemia with renal involvement, coagulopathy, a

299 d excreta and had fluorescent erythrodontia, hemolytic anemia with reticulocytosis and extramedullary

300 The association of hemolytic anemia with thrombocytopenia suggests a common

301 e reported sporadically in severe autoimmune hemolytic anemia, with inconsistent results.