ライフサイエンスコーパス: anemia

1 R9 agonism, including worse splenomegaly and anemia.

2 rmaceutical mainly used for the treatment of anemia.

3 improves hemoglobin levels in patients with anemia.

4 ions to prevent complications of sickle cell anemia.

5 cription factor and causes dyserythropoietic anemia.

6 ted with diseases such as cancer and Fanconi anemia.

7 and dynamics of CH in older individuals with anemia.

8 topenia, and 14 (52%) versus eight (35%) for anemia.

9 mong extremely-low-birth-weight infants with anemia.

10 ars of age who had been admitted with severe anemia.

11 ty of decision-making in management of renal anemia.

12 lication affecting children with sickle cell anemia.

13 t with common clinical findings of hemolytic anemia.

14 including malignancy, in individuals with no anemia.

15 nd predispose to osteopenia, sarcopenia, and anemia.

16 in antagonists in treating cancer-associated anemia.

17 antiretroviral regimen, body mass index, and anemia.

18 macrophages and symptoms of iron deficiency anemia.

19 umeni and Bloom syndrome, as well as Fanconi anemia.

20 used to investigate factors associated with anemia.

21 rdiovascular events in patients with CKD and anemia.

22 , retinal AVMs to avert retinal bleeding and anemia.

23 tal delay, cataracts, growth impairment, and anemia.

24 ed their skin photosensitivity and hemolytic anemia.

25 heal disease, acute respiratory illness, and anemia.

26 f 44 months, irrespective of the presence of anemia.

27 or to cure refractory autoimmune haemolytic anemia.

28 largest and appeared to have some effect on anemia.

29 rocytes (or red blood cells, RBCs) and cause anemia.

30 resent with chronic nonspherocytic hemolytic anemia.

31 decreased hemoglobin expression, and caused anemia.

32 lelic, result in a severe subtype of Fanconi anemia.

33 into cerebrovascular disease in sickle cell anemia.

34 t causes congenital nonspherocytic hemolytic anemia.

35 vention and intervention for arsenic-related anemias.

36 offers a new strategy for overcoming chronic anemias.

37 potential therapeutic tool for iron loading anemias.

38 (48%), G3-G4 thrombocytopenia (10%), and G3 anemia (10%).

39 ommonly neutropenia (51%), infections (24%), anemia (12%), and febrile neutropenia (10%).

40 in > 10% of patients were neutropenia (22%), anemia (13%), thrombocytopenia (13%), and electrocardiog

41 revalence of 16% (95% CI 5-29%), followed by anemia 15% (95% CI 3-31%), and nausea or vomiting 14% (9

42 Prevalence of anemia (15%), and iron (15% based on body iron), seleniu

43 de >= 3 treatment-emergent adverse event was anemia (25.2%; 29 of 115 patients).

44 utropenia (79%), thrombocytopenia (76%), and anemia (43%).

45 more frequently detected in individuals with anemia (46.6%) compared with control individuals (39.1%;

46 ommon treatment-emergent adverse events were anemia (64.8%), thrombocytopenia (62.0%), hypokalemia (4

47 a (14%), pneumonia (11%), hypertension (7%), anemia (7%), and diarrhea (5%).

48 Acquired aplastic anemia (AA) and paroxysmal nocturnal hemoglobinuria (PNH

49 Idiopathic aplastic anemia (AA) has 2 key characteristics: an autoimmune res

50 l individuals at least 60 years old who have anemia according to World Health Organization criteria (

51 naling kinetics, during autoimmune hemolytic anemia (AIHA) and bone marrow failure.

52 ents, with 2 of them presenting with grade 2 anemia already at baseline.

53 In this severe congenital anemia, alterations secondary to the primary hemoglobin

54 We estimated the prevalence of anemia among school children and investigated factors as

55 These data indicate that anemia among school children in Kuwait is of mild public

56 eceived standard in-hospital care for severe anemia and a 3-day course of artemether-lumefantrine at

57 tients there is a strong correlation between anemia and anti-PS antibodies.

58 in in vitro models for autoimmune hemolytic anemia and antibody-mediated rejection of organ transpla

59 ase, increases risk of infection, and causes anemia and bone disease, among other complications that

60 female patient with a history of symptomatic anemia and cotton wool appearance in retina during ophth

61 t 5 common scenarios of patients with HF and anemia and describe our personal approach on how we migh

62 child feeding (IYCF)-SQ-LNS intervention on anemia and growth in children aged 6-18 mo in the Democr

63 less, p53(KQ/-) mice died prematurely due to anemia and hematopoiesis failure.

64 loss, life-threatening autoimmune haemolytic anemia and hemophagocytosis.

65 epatocyte-targeted Ncoa4 knockdown exhibited anemia and hypoferremia similar to control mice with int

66 ors to test the hypotheses that treatment of anemia and ID in HF would improve symptoms and long-term

67 ron products used to treat cancer-associated anemia and illustrate how we use commonly available labo

68 ) such as rituximab and Ab-induced hemolytic anemia and immune thrombocytopenia.

69 associated with a reduction in prevalence of anemia and improvement in mean hemoglobin.

70 signaling pathway, reduces the incidence of anemia and improves hemoglobin levels in patients with a

71 mbosis, are related to the chronic hemolytic anemia and its current management and can occur at any a

72 in a cohort of 283 patients with sickle cell anemia and known pediatric cerebrovascular outcomes.

73 Patients with anemia and lower-risk myelodysplastic syndromes in whom

74 ups that were more or less likely to develop anemia and lymphopenia.

75 Anemia and nausea were the main toxic effects in patient

76 nemia (CDA) type IV, characterized by severe anemia and non-erythroid-cell-related symptoms.

77 echanism by which arsenic exposure may cause anemia and provide critical insights into potential prev

78 omising therapeutic agent for improvement of anemia and provide the basis for a clinical trial using

79 as erythroid maturation agents to alleviate anemia and related comorbidities in MDSs and other condi

80 nt in about 10% of children with sickle cell anemia and represent a genetic risk factor that is poten

81 Eight patients (40%) had grade 3 anemia and required a transfusion, three patients had gr

82 nduced damage to erythrocytes contributes to anemia and splenic retention of damaged cells in infecte

83 of human IL-10 (hIL-10) has been limited by anemia and thrombocytopenia following systemic injection

84 Grade >= 3 anemia and thrombocytopenia were observed in 34% and 14%

85 ophages, increased IL-1beta and IL-6 levels, anemia and thrombocytopenia.

86 MDS are characterized by anemia and transfusion requirements.

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

88 ents that exploit or target TMPRSS6 to treat anemias and iron-related diseases.

89 re convulsions, 1057/2340 (45.2%) had severe anemia, and 441/2239 (19.7%) had severe respiratory dist

90 prevalence, maternal sepsis, higher risk of anemia, and higher risk of all fractures among people li

91 ison with postoperative status, hypotension, anemia, and hypoxia.

92 ia, lower placenta and embryo weight, embryo anemia, and increased embryo mortality.

93 cells, predisposing patients to hemorrhage, anemia, and infections.

94 causing increased risk of immune compromise, anemia, and malignancy.

95 al infection during late pregnancy, maternal anemia, and maternal psychiatric history.

96 ated oxidative stress, symptoms of hemolytic anemia, and premature death.

97 d CD47(-/-) mice exhibited hemophagocytosis, anemia, and splenomegaly.

98 C sickling include vaso-occlusion, hemolytic anemia, and stroke.

99 immune functions with chronic inflammation, anemia, and susceptibility to Salmonella infection.

100 -153, leading to oxidative stress, hemolytic anemia, and tumor development in a mouse model.

101 rypsin (aOR: 4.82; 95% CI: 1.01, 25.29), and anemia (aOR: 3.63; 95% CI: 1.62, 8.58) were positively a

102 LDLR (Ldlr(-/-), SCD(bmt) mice) had similar anemia as Ldlr(+/+), SCD(bmt) mice despite higher serum

103 tion are a standard of care for treatment of anemias associated with chronic inflammation, including

104 temic autoimmune disease and die from severe anemia between 18 and 80 days of age.

105 ent diseases due to folate inadequacy (e.g., anemia, birth defects, and cancer).

106 Additional pathways, such as the Fanconi anemia-BRCA pathway, became perturbed only after long-te

107 BRCA1, BRCA2, or other genes in the Fanconi anemia/BRCA pathway, and these tumors have been shown to

108 Inflammation and Nutritional Determinants of Anemia (BRINDA) project were analyzed.

109 Inflammation and Nutritional Determinants of Anemia (BRINDA)] using measured concentrations of inflam

110 Low agonist doses did not cause maternal anemia but still adversely affected the embryo, causing

111 attributed to inadequate carrying capacity (anemia) but may also relate to inefficient gas exchange

112 enables rapid correction of iron-deficiency anemia, but certain formulations induce fibroblast growt

113 homeostasis and erythropoiesis, resulting in anemia, but whether inhibition of IL-1beta can reverse t

114 n describe our approach to cancer-associated anemia by identifying the contributing causes before sel

115 o difference in rates of diarrhea, fever, or anemia by treatment arm at baseline and at all phases of

116 Acute hemolytic anemia can be managed effectively provided it is promptl

117 Here, we present 3 cases that illustrate how anemia can be perioperatively managed in patients underg

118 rge period, as persistence and recurrence of anemia can further undermine patient's outcomes.

119 Among those with baseline anemia, canakinumab increased mean hemoglobin levels by

120 order related to cohesinopathies and Fanconi anemia, caused by bi-allelic mutations in DDX11.

121 of a murine iron-refractory iron-deficiency anemia-causing mutant (Mt2I286F) in the complement prote

122 The Congenital Dyserythropoietic Anemia (CDA) Registry was established with the goal to f

123 mutation causes congenital dyserythropoietic anemia (CDA) type IV, characterized by severe anemia and

124 Congenital dyserythropoietic anemias (CDAs) are a heterogeneous group of inherited an

125 iduals, other mutations were enriched in the anemia cohort, including TP53 and SF3B1.

126 ns (DNMT3A, TET2, ASXL1) in individuals with anemia compared with control individuals, other mutation

127 acts on DNA-bound, monoubiquitinated Fanconi anemia complementation group D2 (FANCD2) protein in the

128 DBA is characterized by anemia, congenital anomalies, and cancer predisposition.

129 The congenital sideroblastic anemias (CSAs) can be caused by primary defects in mitoc

130 Diamond Blackfan Anemia (DBA) is a congenital bone marrow failure syndrom

131 Diamond-Blackfan anemia (DBA) was the first ribosomopathy described and i

132 al protein (RP) genes drive Diamond-Blackfan anemia (DBA), a bone marrow failure syndrome that can al

133 eroids for the treatment of Diamond Blackfan anemia (DBA), the mechanisms through which glucocorticoi

134 Grade >= 3 anemia, dehydration, diarrhea, and fatigue were greater

135 stablish whether Samd14-Enh deletion reduces anemia-dependent c-Kit signaling by lowering SAMD14 leve

136 ysis, we observed that both cAMP and Fanconi anemia DNA damage repair pathways were affected by SCNAs

137 of SMAD2/3 signaling pathways in MDSs causes anemia due to impaired erythroid maturation.

138 s reveal a role for IL-33 in pathogenesis of anemia during inflammatory disease and define a new targ

139 ary fatty acid that attenuates inflammation, anemia, dyslipidemia, and fibrosis in vivo, potentially

140 pair proteins including those of the Fanconi anemia (FA) and the homologous recombination (HR) pathwa

141 Children with Fanconi anemia (FA) are a paradigm for extreme SCC susceptibilit

142 eplication fork stabilization by the Fanconi anemia (FA) DNA repair pathway.

143 uble-stranded break (DSB) repair and Fanconi anemia (FA) factors active in the S/G2 phase as potent i

144 Fanconi anemia (FA) is a chromosome instability syndrome of chil

145 Fanconi anemia (FA) is the most common genetic cause of bone mar

146 We find that the Fanconi Anemia (FA) pathway is required for dsDonor HDR and that

147 The Fanconi anemia (FA) pathway is the principal mechanism for ICL r

148 Bone marrow failure (BMF) in Fanconi anemia (FA) patients results from dysfunctional hematopo

149 paired DNA crosslink repair leads to Fanconi anemia (FA), characterized by a unique manifestation of

150 ying progressive BM failure (BMF) in Fanconi anemia (FA), the most frequent inherited BMF disorder in

151 s in their corresponding genes cause Fanconi anemia (FA).

152 ect the severity of BRCA1-associated Fanconi anemia (FA).

153 d its corporation with the canonical Fanconi anemia (FA)/BRCA pathway remain unclear.

154 lted in increased bleeding, bodyweight loss, anemia, fibrin deposition, and loss of colon epithelial

155 The current clinical method for detecting anemia focuses on measuring the concentration of hemoglo

156 ploring therapies to counteract the aplastic anemia for the treatment of FA patients.

157 ica eating disorder (sand and sponge) due to anemia from 5 years and 10 months of age and developed e

158 Monoubiquitination of Fanconi anemia group D2 protein (FANCD2) by the multisubunit ubi

159 the global burden of iron deficiency-related anemia have focused on classical breeding and transgenic

160 Mph1, the budding yeast ortholog of Fanconi anemia helicase FANCM, prevents precocious DSB strand ex

161 bocytopenia (platelet count <=50 x 10(9)/L), anemia (hemoglobin <=10 g/dL), and bleeding (WHO grade >

162 Primary outcome was incident anemia (hemoglobin level <130 g/L in men or <120 g/L in

163 aged 18 years and older with iron-deficiency anemia (hemoglobin level <=11 g/dL; serum ferritin level

164 Laboratory investigations showed mild anemia (hemoglobin level, 10 g/dL; normal range, 12-15 g

165 ytes is an important contributor to malarial anemia; however, the mechanisms underlying this patholog

166 Frailty was associated with anemia, hypoalbuminemia, low creatinine, and the use of

167 rs used for the diagnosis of iron-deficiency anemia (IDA) in patients with CKD have limitations, lead

168 ult in hematopoietic malignancies, including anemia, immune deficiency, leukemia, and lymphoma.

169 His GI symptoms and anemia improved on a multiple-food-elimination diet.

170 comprised transient hematotoxicity, such as anemia in 22% of patients, leukopenia in 13%, lymphocyto

171 ound that 8 of these antibodies could induce anemia in antigen-positive mice.

172 ldren who have been hospitalized with severe anemia in areas of Africa in which malaria is endemic ha

173 to single treatments in ameliorating IE and anemia in beta-thalassemia and could provide guidance to

174 upon iron chelation with full correction of anemia in CEP mice treated at the highest dose of deferi

175 better iron absorption, and amelioration of anemia in chronic kidney disease (CKD).

176 ors (HIs) are effective for the treatment of anemia in chronic kidney disease patients and may also b

177 hropoietin production is the major driver of anemia in CKD, iron deficiency stands out among the mech

178 Iron deficiency plays a significant role in anemia in CKD.

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

180 NTOS was not designed to assess the cause of anemia in individual trial participants.

181 cantly reduced gastrointestinal bleeding and anemia in inducible ALK1-deficient adult mice.

182 However, testosterone worsens anemia in iron-deficient mice because of ineffective ery

183 erfere with erythropoiesis and contribute to anemia in malaria patients.

184 centration and ferritin were associated with anemia in multivariable analysis.

185 Luspatercept reduced the severity of anemia in patients with lower-risk myelodysplastic syndr

186 ose levels correlate with the development of anemia in patients.

187 iciency of PCSK9 is associated with worsened anemia in SCD mice due to increased hemolysis.

188 Further reduction in anemia in school girls should focus on correcting iron d

189 Among children with sickle cell anemia in sub-Saharan Africa, hydroxyurea with dose esca

190 y, and efficacy in children with sickle cell anemia in sub-Saharan Africa, with studies showing a red

191 rtial nephrectomy induced cardiomyopathy and anemia in the mice, introducing oxidant stress and an al

192 ne thrombocytopenia and autoimmune hemolytic anemia in the setting of acute infections.

193 p and 27 of 150 [18%] in the control group), anemia (in 46 [30%] and 42 [28%], respectively), and cyt

194 Anemia incidence increased with rising baseline levels o

195 llutant models, including diabetes mellitus, anemia, intestinal infection, liver diseases, gastrointe

196 -difference analyses to calculate changes in anemia, iron and vitamin A deficiencies, stunting, wasti

197 endent beta-thalassemia (TDT) mainly chronic anemia, iron overload and iron chelator toxicity.

198 Anemia is a common finding in the perioperative setting

199 Anemia is a complication that affects a majority of indi

200 Anemia is a frequent complication of kidney disease.

201 Anemia is a hematological disorder that adversely affect

202 Anemia is a major and currently poorly understood clinic

203 Severe anemia is a major cause of death by malaria.

204 Sickle cell anemia is a unique disease dominated by hemolytic anemia

205 Anemia is a very common comorbidity in patients with hea

206 We conclude that inducing anemia is not a sufficient condition for amelioration of

207 Cancer-related anemia is present in more than 60% of newly diagnosed ca

208 Malaria-induced anemia is related to autoimmune antibodies against the m

209 congenita, pulmonary fibrosis, and aplastic anemia, is characterized by severely short telomeres, of

210 Anemia, leukocytosis, and abnormal liver enzyme tests we

211 agonist caused maternal iron restriction and anemia, lower placenta and embryo weight, embryo anemia,

212 Surveillance systems for anemia may consider using a cut-off point that is specif

213 omarkers, including declining hemoglobin and anemia, may be targeted to delay the effects of aging in

214 rrow and spleen and is lethal in a hemolytic anemia mouse model.

215 led A*T-to-G*C base editing of a sickle cell anemia mutation using a previously inaccessible CACC PAM

216 cerebral malaria, n = 253 or severe malarial anemia, n = 211) or community children (n = 206) were fo

217 Blood tests showed mild anemia, neutrophilic leukocytosis and elevated inflammat

218 a probable association with older age, sex, anemia, obesity, low hemoglobin, gastroduodenal ulcers,

219 g, weight loss, melena, hematemesis and deep anemia occur, especially in the second trimester, and en

220 Anemia occurred on >=1 day in 90% of patients; on 78% of

221 eed to define novel strategies to ameliorate anemia of chronic disease (ACD).

222 rient deficiency (P = .84), individuals with anemia of chronic inflammation and unexplained anemia re

223 e reversible on-switches in gene therapy for anemia of chronic kidney disease(6), we demonstrated reg

224 ociated with chronic inflammation, including anemia of chronic kidney disease.

225 poiesis-stimulating agents (ESAs) because of anemia of inflammation.

226 investigate the relationship between CH and anemia of the elderly, we explored the landscape and dyn

227 history of a 6-month hypochromic microcytic anemia of unknown cause.

228 nfluence the development and exacerbation of anemia, one major contributing factor is the impairment

229 t their hallmark symptoms of deficiency like anemia or birth defects.

230 Comorbidities such as anemia or hypertension and physiological factors related

231 of red blood cells (RBCs; e.g., sickle cell anemia or malaria), the mechanical properties and thus s

232 re obscure gastrointestinal bleeding (occult/anemia or overt/active, OGIB) of 46% (246/536) and defin

233 ine, is a sign of diseases such as hemolytic anemia or urinary tract infections.

234 Preoperative anemia (OR 2.08; 95% CI 1.27-3.40; P = 0.004) and more t

235 There was no evidence of hemorrhage, anemia, or AVMs in major organs to explain the reduced a

236 in diseases such as malaria and sickle cell anemia, or following blood transfusions.

237 tological disorder causing painful episodes, anemia, organ damage, stroke, and even deaths.

238 Thoracic Surgeons score of >=8 (p < 0.0001), anemia (p = 0.02), chronic kidney disease (p = 0.003), a

239 e cell disease is characterized by hemolytic anemia, pain, and progressive organ damage.

240 ion group D2 (FANCD2) protein in the Fanconi anemia pathway of the DNA damage response.

241 cluding single-strand DNA repair and Fanconi anemia pathways, suggesting that DNA repair after dual t

242 .8; P < 0.01) adjusted relative reduction in anemia prevalence and a mean +0.26-g/dL (95% CI: 0.04, 0

243 o had recently received treatment for severe anemia prevented more deaths or readmissions for any rea

244 Timely detection of anemia prior to high-blood loss surgeries can allow clin

245 Inflammation and Nutritional Determinants of Anemia project.

246 rom 16 families of the International Fanconi Anemia Registry.

247 g use of targeted therapies to treat cancer, anemia remains a common complication of cancer therapy.

248 ood pressure ranging from 140 to 190 mm Hg), anemia requiring blood transfusions, thrombocytopenia, a

249 , ranging from fetal hydrops and symptomatic anemia requiring lifelong transfusions to fully compensa

250 with Darbepoetin alfa on iron metabolism and anemia resolution in 2 different, well-established, and

251 emia of chronic inflammation and unexplained anemia revealed a higher prevalence of CH (P = .035 and

252 has recently re-emerged as a cause of severe anemia (SA) in African children.

253 Severe aplastic anemia (SAA) is a rare disorder characterized by hypopla

254 ed with diastolic dysfunction in sickle cell anemia (SCA).

255 lusive processes associated with sickle cell anemia (SCA).

256 and a loss of blood cells similar to Fanconi anemia.See related article by Park et al., p.

257 processes in conditions such as sickle cell anemia, sepsis, transfusion reactions, medical-device as

258 as well as for potential novel modifiers of anemia severity.

259 Treatment of anemia should be guided by the etiology and may include

260 Finally, screening for and management of anemia should continue in the postoperative and postdisc

261 g, weight loss, melena, hematemesis and deep anemia should suggest malignancy.

262 ), and ribosome biogenesis (Diamond-Blackfan anemia, Shwachman-Diamond syndrome).

263 bral malaria (CM; n = 79) or severe malarial anemia (SMA; n = 77).

264 cterized by ineffective erythropoiesis (IE), anemia, splenomegaly, and systemic iron overload.

265 centration in the circulation of sickle cell anemia (SS) patients.

266 jectories or extramedullary hematopoiesis in anemias such as SCD.

267 cesses, including DNA damage repair (Fanconi anemia), telomere maintenance (dyskeratosis congenita),

268 The course of anemia tends to track the decline in kidney function, wi

269 t any dosage had significantly less incident anemia than those who received placebo (hazard ratio, 0.

270 CDAs) are a heterogeneous group of inherited anemias that affect the normal differentiation-prolifera

271 nistration of Tmprss6-ASO alone improved the anemia, the combination of Tmprss6-ASO + EPO or Tmprss6-

272 skin photosensitivity and chronic hemolytic anemia, the severity of which is related to porphyrin ov

273 ients with cancer receiving no or suboptimal anemia therapy.

274 lated adverse events in NCT02042989 included anemia, thrombocytopenia, fatigue, nausea, vomiting, and

275 ion was notable for profound iron deficiency anemia, thrombocytosis, and hyperhomocysteinemia.

276 still adversely affected the embryo, causing anemia, tissue iron deficiency (including in the brain),

277 rpinnings of numerous diseases, ranging from anemia to cancer.

278 clinical trials in warm autoimmune hemolytic anemia to lower IgG antibodies and IgG containing ICs ma

279 below the bulk Hb concentration that defines anemia varies not only from donor to donor but also in t

280 s (MLV), the S2 protein of equine infectious anemia virus (EIAV), and the Nef protein of human immuno

281 The prevalence of mild, moderate and severe anemia was 5.94%, 1.91% and 0.21%, respectively.

282 The prevalence of anemia was 8.06% (95% CI: 6.69-9.60%), which was signifi

283 Anemia was more prevalent in treatment regimens containi

284 mice compared to Pcsk9(+/+), SCD(bmt) mice, anemia was more severe in Pcsk9(-/-), SCD(bmt) mice.

285 After TAT, grade 3 anemia was observed in 3 of the 14 patients, with 2 of t

286 Anemia was seen in 27 patients; no patients had grade IV

287 Anemia was the main adverse event.

288 Moderate or severe anemia was the most common major criterion (33.2%); age

289 olving 756 adults with stage-3 to -5 CKD and anemia, we evaluated incidence of red blood cell transfu

290 Data on risk factors for anemia were collected from parents and adolescents.

291 Thrombocytopenia and anemia were common, but product availability was substan

292 benefits of IL-1beta inhibition on incident anemia were observed among participants with the most ro

293 op acute and sometimes very severe hemolytic anemia when triggered by ingestion of fava beans, by any

294 Anemia, which is associated with increased mortality in

295 rtant comorbidity of chronic inflammation is anemia, which may be related to dysregulated activity of

296 ls included liver dysfunction and microcytic anemia, while one had fatal cardiomyopathy with lactic a

297 of 3.7 years, participants without baseline anemia who received canakinumab at any dosage had signif

298 ized trials of patients with iron-deficiency anemia who were intolerant of or unresponsive to oral ir

299 th upper GIS endoscopy performed due to deep anemia, who underwent simultaneous cesarean section and

300 senting with symptoms and signs of hemolytic anemia with a focus on RBC membrane disorders.