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1 asound findings in patients with sickle cell anaemia.
2 indices in the diagnosis of iron deficiency anaemia.
3 ating stroke risk in adults with sickle cell anaemia.
4 nd ineffective correction of iron-deficiency anaemia.
5 scular impairment in adults with sickle cell anaemia.
6 ication for haemoglobin less than 100 g/L or anaemia.
7 e the other two patients had weight loss and anaemia.
8 rd blood transfusion in children with severe anaemia.
9 ed donor transplantation for severe aplastic anaemia.
10 erited bone marrow failure syndrome, Fanconi anaemia.
11 leviates anaemia in a mouse model of chronic anaemia.
12 lower than 80 g/L or if they had symptoms of anaemia.
13 (-/-) mice from PHZ-induced acute haemolytic anaemia.
14 ed donor transplantation for severe aplastic anaemia.
15 nd iron-deficiency rather than megaloblastic anaemia.
16 1 patients assigned to six cycles had severe anaemia.
17 needed for chronic leg ulcers in sickle cell anaemia.
18 tic stem cell pool confers profound aplastic anaemia.
19 s Disease, Neurofibromatosis and Sickle Cell Anaemia.
20 the phenotypes seen in patients with Fanconi anaemia.
21 dren and achieve global targets for reducing anaemia.
22 y abnormalities in patients with sickle cell anaemia.
23 cers of autoantibodies that promote malarial anaemia.
24 , but with increased risk of severe malarial anaemia.
25 inability to estimate the cumulative risk of anaemia.
26 of corticosteroids in treating Epo-resistant anaemias.
27 se events that occurred through week 24 were anaemia (10 [5%]), cardiac failure (5 [2%]), pyrexia (4
28 mmon adverse events of grade 3 or worse were anaemia (11 [8%] of 132 patients in the gefitinib group
30 common grade 3 or worse adverse events were anaemia (14 [14%] of 104 in the momelotinib group vs sev
31 lycaemia (17 [22%] of 76 vs two [3%] of 78), anaemia (14 [18%] vs nine [12%]), neutropenia (13 [17%]
32 enia (21 [100%] patients for each toxicity); anaemia (14 [67%] patients); and infection (six [29%] pa
34 up vs 21 [14%] of 150 in the control group), anaemia (14 [9%] vs 26 [17%]), and decreased neutrophil
35 e most common adverse events of grade 1 were anaemia (14 patients) and fatigue (13 patients), and the
36 18 [35%]), pneumonia (15 [29%] vs 19 [37%]), anaemia (15 [29%] vs 12 [23%]), and sepsis (eight [16%]
37 p), thrombocytopenia (21 [11%] vs 32 [16%]), anaemia (15 [8%] vs 20 [10%]) and infusion-related react
38 n both groups were haematological, including anaemia (150 [48%] of 313 patients in the doxorubicin pl
39 rse events were hypophosphataemia (19 [6%]), anaemia (17 [5%]), abdominal pain (13; 4%), and elevated
42 el (15; 5%), and in the nilotinib group were anaemia (18; 6%), elevated lipase level (15; 5%), elevat
43 eutropenia (43 [40%]), infection (21 [20%]), anaemia (19 [18%]), and thrombocytopenia (16 [15%]).
45 rodysaesthesia syndrome (27 [8%] vs 3 [1%]), anaemia (19 [6%] vs 53 [17%]), hyperglycaemia (3 [1%] vs
46 he availability of pre-endoscopy serology in anaemia; 2) the sensitivities and cost effectiveness of
48 ir; and nasopharyngitis (40 [23.5%] of 170), anaemia (23 [13.5%] of 170), and headache in those recei
49 thrombocytopenia (23 [25%] of 93 patients), anaemia (23 [25%] of 93 patients), and sepsis (16 [17%]
50 rol patients: 26 (41%) versus nine (26%) had anaemia, 23 (36%) versus seven (21%) pyrexia, 22 (34%) v
52 f 91 patients), thrombocytopenia (26 [29%]), anaemia (26 [29%]), decreased white blood cell count (17
54 endoscopy coeliac screening with Simtomax in anaemia; 3) whether other anaemia-related pathologies co
55 eight [2%]), fatigue (39 [12%] vs 18 [5%]), anaemia (30 [9%] vs 34 [10%]), and abdominal pain (20 [6
56 common grade 3 or higher adverse events were anaemia (34 [18%] of 184 patients in the rigosertib grou
57 l tolerated; fatigue (42 [40%] patients) and anaemia (35 [33%]) of any grade were the most common adv
58 f 298 patients vs 97 [32%] of 299 patients), anaemia (37 [12%] vs 43 [14%]), and fatigue (30 [10%] vs
59 Common grade 3-4 adverse events included anaemia (37 [38%] of 97 patients) and thrombocytopenia (
60 atment, the most common grade 3 toxicity was anaemia (37 [47%]) and the most common grade 4 toxicity
61 rse events of grade 3 or worse severity were anaemia (38 [19%] of 195 patients in the olaparib group
62 ]), musculoskeletal pain (none vs ten [8%]), anaemia (39 [33%] vs six [5%]), and thrombocytopenia (38
63 acebo group), fatigue (40 [11%] vs 35 [9%]), anaemia (40 [10%] vs 43 [11%]), and colitis (18 [5%] vs
64 y were thrombocytopenia (43 [96%] patients), anaemia (41 [91%]), neutropenia (23 [51%]), diarrhoea (2
66 in grade 3/4 toxicities were haematological: anaemia (45%), thrombocytopenia (45%), and neutropenia (
67 [15%]), stomatitis (59 [13%] vs three [1%]), anaemia (46 [10%] vs six [3%]) and diarrhoea (43 [9%] vs
68 Common treatment-related toxic effects were anaemia (48 patients [48%]), nausea (42 [42%]), fatigue
69 and pneumonia (4 [2%]) with pacritinib, and anaemia (5 [5%]), sepsis (2 [2%]), and dyspnoea (2 [2%])
70 group), leucopenia (106 [38%] vs 82 [29%]), anaemia (53 [19%] vs 17 [6%]), febrile neutropenia (44 [
71 uzumab emtansine 2.4 mg/kg weekly group were anaemia (59 [26%]) and thrombocytopenia (25 [11%]) compa
73 were febrile neutropenia (97 [39%] of 252), anaemia (61 [24%]), thrombocytopenia (33 [13%]), sepsis
75 equent grade 3 or higher adverse events were anaemia (67 [14%] of 463 patients in the carfilzomib gro
76 openia (70 [22%] of 315 vs 61 [20%] of 312), anaemia (68 [22%] vs 49 [16%]), fatigue (23 [7%] vs 18 [
77 requent grade 3 or worse adverse events were anaemia (76 [16%] of 463 patients in the carfilzomib gro
78 febrile neutropenia (103 (46%) vs 30 [13%]), anaemia (78 [35%] vs 10 [5%]), and thrombocytopenia (75
79 uded multicentric lymphadenopathy (128/128), anaemia (79/91), elevated C-reactive protein (65/79), hy
80 [7%] vs 2 [2%]), infections (14 [7%] vs 0), anaemia (8 [4%] vs 1 [1%]), fatigue (7 [3%] vs 1 [1%]),
81 tivity (anaemia: 91% [95% CI 81-96]); severe anaemia 83% (33-98), but at the expense of specificity (
82 se events were diarrhoea (92 [37%] of 252]), anaemia (86 [34%]), fatigue (83 [33%]), elevated asparta
84 the HCS could result in higher sensitivity (anaemia: 91% [95% CI 81-96]); severe anaemia 83% (33-98)
85 ents (aged </=65 years) with severe aplastic anaemia, adequate organ function, and an unrelated adult
88 her all the patients with chronic haemolytic anaemia and alcoholic cirrhosis had black pigment GS.
90 the chronic effects of sustained haemolytic anaemia and episodic vaso-occlusive events drive the dev
91 H2AX knockout mice showed cell-autonomous anaemia and erythroid dysplasia, mimicking dyserythropoi
92 ebo-controlled period: one event of aplastic anaemia and five serious adverse events related to raise
97 , and lymphopenia (all for patient number 2; anaemia and lymphopenia were dose-limiting toxicities);
100 ed to the discontinuation of any study drug--anaemia and neutropenia--were associated with peginterfe
104 litinib; one patient (1%) reported grade 3-4 anaemia and three patients (4%) reported grade 3-4 throm
105 generally well tolerated, with low rates of anaemia and treatment discontinuation in non-cirrhotic p
106 llent diagnostic accuracy in iron deficiency anaemia and was comparable to conventional serology.
107 high concentration of creatine kinase, mild anaemia), and radiological (thickened calvarium) feature
111 uracy of the HCS in primary care to diagnose anaemia, and compared this with clinical assessment.
112 ecommend coeliac serology in iron deficiency anaemia, and duodenal biopsy for those tested positive t
113 tients), increased alanine aminotransferase, anaemia, and fatigue (two [1%] each); for ICC, these inc
115 rious adverse events were: thrombocytopenia, anaemia, and lymphopenia (all for patient number 2; anae
116 h as clinical malaria, maternal and neonatal anaemia, and miscarriage, all of which increase the over
117 sis, and acute management of iron deficiency anaemia, and outstanding research questions for treatmen
118 od flow, degree of vasculopathy, severity of anaemia, and presence of prior infarct; findings were in
119 is to exclude thrombocytosis and sickle cell anaemia, and serum angiotensin-converting enzyme (SACE)
121 ow failure diseases such as Diamond-Blackfan anaemia, are not treatable with erythropoietin (Epo), be
122 han 5 x 10(8) cells per L, and in those with anaemia, as any increase in haemoglobin of 20 g/L or hig
123 el therapeutic approach for the treatment of anaemia associated with lower-risk myelodysplastic syndr
124 R] 3.25 [95% CI 2.99-3.54]); AORs for severe anaemia associated with P. falciparum, P. vivax, and P.
125 ects (29.3% of Asian females) presented with anaemia, associated with decreased RBCs volume (MCV) and
126 intervention was observed for prevalence of anaemia at either 12 or 24 months (adjusted risk ratio [
130 (C=calcium elevation; R=renal impairment; A=anaemia; B=bone involvement) criteria with measurable di
131 a, which occurred in nine (3%) patients, and anaemia, back pain, and pain in extremities, each of whi
132 protocol adherence, separation in degree of anaemia between groups, and non-significant reduction in
133 There was no difference in the prevalence of anaemia between the simeprevir and placebo groups (35 [1
134 ore common in the co-trimoxazole group), and anaemia (both grades equally common in both groups).
135 nductance both increase during chronic fetal anaemia, but the coronary microvascular changes responsi
136 Hydroxyurea treatment reduces haemolysis and anaemia by increasing foetal haemoglobin, which leads to
142 effective erythropoiesis, chronic haemolytic anaemia, compensatory haemopoietic expansion, hypercoagu
144 (three [7%]) in the bone sarcoma group, and anaemia, decreased lymphocyte count, and prolonged activ
145 f high body lead content, is associated with anaemia, developmental and neurological deficits in chil
146 tious diseases, nutritional deficiencies and anaemia, diabetes, and cardiovascular disease in the bla
149 e case of mice with a non-functional Fanconi anaemia DNA repair pathway, led to a complete collapse o
150 nd efficacy of luspatercept in patients with anaemia due to lower-risk myelodysplastic syndromes.
153 %]), decreased neutrophil count (four [2%]), anaemia, dyspnoea, hyponatraemia, increased alanine amin
154 ive), vomiting (12 [38%] of 32 vs zero), and anaemia (eight [25%] of 32 vs one [20%] of five); genera
155 roup compared with in the placebo group were anaemia (eight [4%] of 207 vs five [5%] of 102 patients)
156 The most common serious adverse events were anaemia (eight [4%]), upper gastrointestinal haemorrhage
158 ng treatment: two (17%) patients experienced anaemia, eight (67%) neutropenia, and ten (83%) thromboc
159 Repeated sickling and ongoing haemolytic anaemia, even when subclinical, lead to parenchymal inju
165 of pregnancy, maternal conditions including anaemia, fever during labour, and hypertension accounted
166 se events were neutropenia (18 [40%] of 45), anaemia (five [11%]), and peripheral sensory neuropathy
167 group), hypertension (20 [7%] vs two [2%]), anaemia (five [2%] vs six [5%]), and neutropenia (two [1
168 s in the brentuximab vedotin and AVD group), anaemia (five [20%] vs three [12%]), febrile neutropenia
172 ] of 18 patients), lymphopenia (five [28%]), anaemia (four [22%], and thrombocytopenia in three [17%]
173 (four [25%]), thrombocytopenia (four [25%]), anaemia (four [25%]), fever and infection (four [25%]),
174 al (nine), metabolic (seven), fatigue (six), anaemia (four), pain (four), constitutional (three), and
175 1%], grade 4 11 [10%] in the placebo group), anaemia (grade 3 12 [11%] vs grade 3 16 [15%]), and fati
176 d systemic pathological effects ranging from anaemia, growth stunting, impaired cognition, and decrea
178 , infection (2 [6%]), and one (3%) each with anaemia, haemolysis, fatigue, and a neurological, metabo
181 [3%] vs 14 [5%]; HEC-2: 16 [6%] vs 14 [5%]), anaemia (HEC-1: one [<1%] vs one [<1%]; HEC-2: seven [3%
183 follow-up, 25 (46%) of 58 patients had mild anaemia (ie, not requiring intervention), 22 (45%) had h
184 se events were recorded in 2 of 15 patients (anaemia in 1 patient; pneumonia in 1 patient); all arose
186 toxicities in the 174 treated patients were anaemia in 16 (9%) patients, hyperglycaemia in 18 (10%),
188 lated treatment-emergent adverse events were anaemia in 32 (5%) patients, thrombocytopenia in 15 (2%)
189 ] of 81 patients vs 13 [33%] of 39 patients; anaemia in 32 [40%] vs 11 [28%]; and thrombocytopenia in
191 of which were hypertension, neutropenia, and anaemia in both groups, and mild-to-moderate transient i
192 children 0.5-14 y old (primary outcome) and anaemia in children <5 y old (secondary outcome) were co
193 IEZO1 cause an autosomal dominant haemolytic anaemia in humans called dehydrated hereditary stomatocy
194 cyte age and dose-dependent acute haemolytic anaemia in individuals with glucose-6-phosphate dehydrog
195 tolerated and effective for the treatment of anaemia in lower-risk myelodysplastic syndromes and so c
196 e suggests that low maternal iron status and anaemia in pregnancy may increase the risk of childhood
197 24%) patients (grade 4 in one [2%] patient), anaemia in seven (14%) patients, and thrombocytopenia in
198 rmalities in adult patients with sickle cell anaemia in steady state attending the Haematology clinic
200 patients and included pyrexia in nine (16%), anaemia in three (5%), confusional state in two (4%), de
205 cular flux rate in response to chronic fetal anaemia is consistent with expected reductions in capill
206 clude that the correction of iron deficiency anaemia is in some part due to the treatment of the unde
208 comprise a wide range of diseases including anaemia, malignant blood disorders, and haemorrhagic dis
209 ual changes in microvascular function during anaemia may indicate novel adaptive strategies in the fe
210 on of Postn results in peripheral blood (PB) anaemia, myelomonocytosis and lymphopenia, while the num
211 (P < 0.05) in participants with sickle cell anaemia (n = 27) not receiving monthly blood transfusion
212 e imaging method were applied in sickle cell anaemia (n = 34) and healthy race-matched control (n = 1
213 tenance therapy group were fatigue (n=1) and anaemia (n=1) and in the local consolidative therapy gro
214 ative therapy group were oesophagitis (n=2), anaemia (n=1), pneumothorax (n=1), and abdominal pain (n
215 vents; the most frequent adverse events were anaemia (n=14), weight loss (n=12), and vomiting (n=10).
216 oea (n=11 [5%]) in the pacritinib group, and anaemia (n=16 [15%]), thrombocytopenia (n=12 [11%]), dys
218 eutropenia (n=6), febrile neutropenia (n=1), anaemia (n=2), lymphopenia (n=1), diarrhoea (n=2), hypoa
219 rade 3-4 adverse events through week 24 were anaemia (n=37 [17%]), thrombocytopenia (n=26 [12%]), and
220 children are frequently admitted with severe anaemia needing an urgent blood transfusion, but blood i
221 -week group; 14 [23%] in the 16-week group), anaemia (nine [15%] in the 12-week group; 12 [20%] in th
222 the most common grade 3 or worse events were anaemia (nine [15%] of 62) and decreased neutrophil coun
224 ) in those given pembrolizumab 10 mg/kg; and anaemia (nine [5%]), fatigue (eight [5%]), neutropenia (
226 ocedures exist for children with sickle cell anaemia, no accepted screening procedures exist for asse
227 e frequently associated with iron deficiency anaemia--notably chronic kidney disease, chronic heart f
229 worse treatment-emergent adverse events were anaemia or decreased haemoglobin (45 [22%] patients), an
230 placebo group, the most common of which were anaemia or decreased haemoglobin concentration (70 [19%]
233 elofibrosis (with no exclusions for baseline anaemia or thrombocytopenia) were randomly assigned (2:1
234 th at least one of grade 3 thrombocytopenia, anaemia, or bleeding at grade 3 or worse, with palpable
236 x functions in the activation of the Fanconi anaemia pathway of the DNA damage response, in regulatin
237 DX2 and functions in parallel to the Fanconi anaemia pathway to promote efficient homologous recombin
238 the intra-S-phase checkpoint and the Fanconi anaemia pathway, which promote ICL incision, translesion
239 ient fibroblasts (PD20) derived from Fanconi anaemia patients displayed reduced spontaneous SCE forma
240 se of alternative donor sources for aplastic anaemia patients remains limited and problematic, but no
241 ltrasonography of 50 consecutive sickle cell anaemia patients were compared with those of 50 age- and
244 ique was associated with a reduction in twin anaemia polycythaemia sequence (3% vs 16% for the standa
245 outcome was a composite of incidence of twin anaemia polycythaemia sequence, recurrence of twin-to-tw
247 trations of mean haemoglobin were lowest and anaemia prevalence was highest in south Asia and central
249 licated by observations that iron deficiency anaemia protects against falciparum malaria, and that ir
253 g with Simtomax in anaemia; 3) whether other anaemia-related pathologies could be missed by this targ
258 ve refractory disease, autoimmune haemolytic anaemia requiring treatment, chronic or active infection
259 ll transplantation (HSCT) in severe aplastic anaemia (SAA) have improved steadily over the past decad
262 e pembrolizumab plus chemotherapy group were anaemia (seven [12%] of 59) and decreased neutrophil cou
263 (26 [53%]), thrombocytopenia (eight [16%]), anaemia (seven [14%]), febrile neutropenia (six [12%]),
264 The most common in the olaparib group were anaemia (seven [4%] patients), abdominal pain (three [2%
266 nts) being pyrexia and autoimmune haemolytic anaemia (seven [7%] each), pneumonia (six [6%]), and feb
269 requent grade 3 or worse adverse events were anaemia (six [14%]), decreased lymphocyte count (five [1
270 re neutropenia (eight [44%] of 18 patients), anaemia (six [33%]), thrombocytopenia (five [28%]), incr
272 improvement from baseline in FACT-An score, anaemia subscale score, and the EQ-5D-5L were reported a
273 her than coeliac disease for iron deficiency anaemia, suggesting that biopsy avoidance in Simtomax ne
274 matological adverse events of any grade were anaemia (ten [14%] of 74 in the ruxolitinib group vs two
275 [1%] in the fulvestrant plus placebo group), anaemia (ten [3%] and three [2%]), and leucopenia (95 [2
276 in group five had a serious adverse event of anaemia, thought to be related to ribavirin treatment.
277 four [4%]), febrile neutropenia (four [4%]), anaemia (three [3%]), and neutropenia (three [3%]) in th
278 such events were pneumonia (three [8%]) and anaemia, thrombocytopenia, abdominal pain, anxiety, and
279 ), hypertension in three patients (10%), and anaemia, thrombocytopenia, and diarrhoea in two patients
281 of six predefined factors in the IMDC model (anaemia, thrombocytosis, neutrophilia, Karnofsky perform
284 f SMC and the prevalence of parasitaemia and anaemia, to monitor molecular markers of drug resistance
286 dverse event, with neutropenia (five [56%]), anaemia (two [22%]), and febrile neutropenia (two [22%])
287 The most common adverse events were nausea, anaemia, upper respiratory tract infection, and headache
288 he pooled sensitivity of the HCS to diagnose anaemia was 80% (95% CI 68-88) compared with 52% for cli
289 not noted in those younger than 5 years and anaemia was no more frequent with zidovudine than with t
293 ents were balanced between groups except for anaemia, which occurred more frequently in the combined
295 rolled patients with diagnosis of refractory anaemia with excess blasts (RAEB)-1, RAEB-2, RAEB-t, or
296 -eg, by early identification and reversal of anaemia with haematinics or by reversal of the underlyin
298 Health (Bethesda, MD, USA) with sickle cell anaemia with leg ulcers (with a surface area of 2.5-100
299 white blood cell count <13 000/muL), and had anaemia with or without red blood cell transfusion suppo
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