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1 ight attenuate the severity of outcomes from vaso-occlusive and hemolytic crises.
2                                   Unheralded vaso-occlusive cardiovascular events (myocardial infarct
3 ous cellular and soluble participants in the vaso-occlusive cascade.
4 emoglobin (HbF) and decreases morbidity from vaso-occlusive complications in patients with sickle cel
5                 Current treatments to reduce vaso-occlusive complications include chronic hydroxyurea
6 mbosis, but also impact on many of the other vaso-occlusive complications of SCD.
7                   To determine whether early vaso-occlusive complications predicted subsequent advers
8 nt and pentoxifyllin therapy in another, the vaso-occlusive complications were eliminated.
9 pproval for shortening the duration of acute vaso-occlusive complications, likely highlighting the co
10   Non-DMT users had the lowest prevalence of vaso-occlusive crises (mean [SD], 0.8 [2.4]), acute ches
11 nconsistent users had a higher prevalence of vaso-occlusive crises (mean [SD], 3.7 [4.7]), splenic co
12 atients at steady state and 6 during painful vaso-occlusive crises (pVOC).
13 ry hemoglobinopathy characterized by painful vaso-occlusive crises (VOC) and chronic hemolysis.
14                                 Treatment of vaso-occlusive crises (VOC) or events in sickle cell dis
15                   A unique feature of SCD is vaso-occlusive crises (VOCs) characterized by episodic,
16 al ischemia during acute sickle cell-related vaso-occlusive crises (VOCs) has been suggested.
17 c disorder causing painful and unpredictable Vaso-occlusive crises (VOCs) through blood vessel blocka
18 ia/reperfusion (H/R) stress, mimicking acute vaso-occlusive crises (VOCs), increased bone turnover, o
19            Six serious AEs (SAEs) included 4 vaso-occlusive crises (VOCs), non-VOC-related shoulder p
20 focus on health care utilization for painful vaso-occlusive crises (VOCs).
21 es of emergency department visits related to vaso-occlusive crises [VOC] and hospitalizations related
22 vels in subjects with severe SCD (at least 3 vaso-occlusive crises [VOCs] per year) were 18.5 +/- 1.2
23 ase, including the frequency and severity of vaso-occlusive crises and acute chest syndrome episodes.
24                                              Vaso-occlusive crises are the main acute complication in
25 tly targeted a reduction in the frequency of vaso-occlusive crises as an endpoint, but increasingly,
26                                              Vaso-occlusive crises at index admission were associated
27 ch as cold exposure are known to precipitate vaso-occlusive crises by still unclear mechanisms.
28 om from inpatient hospitalization for severe vaso-occlusive crises for at least 12 consecutive months
29 nce interval [CI], 83 to 100) were free from vaso-occlusive crises for at least 12 consecutive months
30  to 100) were free from hospitalizations for vaso-occlusive crises for at least 12 consecutive months
31 he primary end point was freedom from severe vaso-occlusive crises for at least 12 consecutive months
32            Treatment with exa-cel eliminated vaso-occlusive crises in 97% of patients with sickle cel
33 ocirculation and is characterized by painful vaso-occlusive crises in deep tissues.
34 cell disease who had had at least two severe vaso-occlusive crises in each of the 2 years before scre
35 ism for the increased occurrence of clinical vaso-occlusive crises in individuals with sickle cell di
36      The SUSTAIN study showed a reduction of vaso-occlusive crises in patients treated with 5 mg/kg c
37 nhibitor ticagrelor vs placebo in preventing vaso-occlusive crises in pediatric patients with sickle
38 d or stress, which have been associated with vaso-occlusive crises in SCD.
39 e blood vessel wall, thereby contributing to vaso-occlusive crises in sickle cell disease.
40 hydroxyurea use to decrease the frequency of vaso-occlusive crises is completely defined only in 2 te
41  primary endpoint was the annualised rate of vaso-occlusive crises leading to a health-care visit ove
42       Ratios of adjusted annualised rates of vaso-occlusive crises leading to health-care visits were
43 alysis showed an adjusted annualised rate of vaso-occlusive crises of 2.49 (95% CI 1.90-3.26) in the
44  crises, number of ACS events, and number of vaso-occlusive crises requiring hospitalization or emerg
45 42, linking hemolysis- and infection-induced vaso-occlusive crises to TLR4 signaling.
46 t was not met: estimated yearly incidence of vaso-occlusive crises was 2.74 in the ticagrelor group a
47               In conclusion, no reduction of vaso-occlusive crises was seen with ticagrelor vs placeb
48        The primary end point was the rate of vaso-occlusive crises, a composite of painful crises and
49 e complications of SCD such as acute anemia, vaso-occlusive crises, and acute chest syndrome; and/or
50 line to week 72, the annualised incidence of vaso-occlusive crises, and patient functioning, as asses
51 ciated with milder disease phenotypes, fewer Vaso-occlusive crises, and reduced organ damage.
52 outcomes included the incidences of malaria, vaso-occlusive crises, and serious adverse events.
53 term reductions in the occurrence of painful vaso-occlusive crises, but the long-term safety and effi
54 od disorder that is characterized by painful vaso-occlusive crises, for which there are few treatment
55 mability and blood rheology in precipitating vaso-occlusive crises.
56 ckle cell anemia is characterized by painful vaso-occlusive crises.
57 ased total hemoglobin and HbF, and no severe vaso-occlusive crises.
58 evere chronic hemolytic anemia and iterative vaso-occlusive crises.
59 cterized by basal inflammation and recurrent vaso-occlusive crises.
60 cute presentations of osteomyelitis (OM) and vaso-occlusive crisis (VOC) bone infarction in children
61                                      Painful vaso-occlusive crisis (VOC) is the most common complicat
62                                              Vaso-occlusive crisis (VOC) is the primary cause of morb
63  a phase 3, randomized, controlled trial for vaso-occlusive crisis (VOC) requiring hospitalization (R
64 Severe ACS often develops in the course of a vaso-occlusive crisis (VOC), but currently there are no
65                           HTRs induced acute vaso-occlusive crisis (VOC), resulting in shortened surv
66  SCD were evaluated at baseline (n = 36), in vaso-occlusive crisis (VOC; n = 12), and during ACS (n =
67 et of hydroxyurea (HU) treatment or during a vaso-occlusive crisis and at steady-state.
68 ry and secondary endpoints-rates of clinical vaso-occlusive crisis and hemolytic events, blood transf
69 ther, in men, and likely all patients during vaso-occlusive crisis and the acute chest syndrome, nitr
70 y (AKI), a risk factor for CKD, often during vaso-occlusive crisis associated with acute intravascula
71 gated the protective effect of IVIG on acute vaso-occlusive crisis caused by neutrophil recruitment a
72 t enrolment, and who had between one and ten vaso-occlusive crisis events in the previous 12 months w
73                                  The rate of vaso-occlusive crisis events per person-year was 2.30 in
74 mportance in the development of the hallmark vaso-occlusive crisis in sickle cell disease (SCD).
75 or dysregulation to the development of acute vaso-occlusive crisis in sickle cell disease have been i
76                       The pathophysiology of vaso-occlusive crisis in sickle cell disease involves in
77 r the treatment or prevention of pain due to vaso-occlusive crisis in sickle cell disease nor reassur
78 nt disease-modifying therapy for alleviating vaso-occlusive crisis in sickle cell disease.
79 lium and inflammation play a central role in vaso-occlusive crisis in sickle cell disease.
80 , or who had been admitted to hospital for a vaso-occlusive crisis in the previous 14 days were exclu
81                                  Pain due to vaso-occlusive crisis is the major cause of hospital use
82  with varied patterns of health-care use and vaso-occlusive crisis management as well as the commerci
83 LA2 (steady state mean = 10.0 +/- 8.4 ng/mL; vaso-occlusive crisis mean = 23.7 +/- 40.5 ng/mL; ACS me
84 n patients with ACS but not in patients with vaso-occlusive crisis or non-SCD patients with pneumonia
85 ng the incidence of ACS adjusted for that of vaso-occlusive crisis over time.
86                                  Features of vaso-occlusive crisis pathophysiology such as red cell a
87 escents with sickle cell anemia, the rate of vaso-occlusive crisis was not significantly lower among
88        The primary end point was the rate of vaso-occlusive crisis, a composite of painful crisis or
89 ing 20 admissions for ACS, 10 admissions for vaso-occlusive crisis, and during 12 clinic visits when
90 or; monthly incidence of hospitalization for vaso-occlusive crisis, asthma crisis, and acute pyelonep
91 and may be a measurable laboratory marker of vaso-occlusive crisis.
92 symptomatic sickle cell disease nor in acute vaso-occlusive crisis.
93  of hospitalization in children with SCD and vaso-occlusive crisis.
94 tudy period, the most common being grade 2-3 vaso-occlusive crisis.
95 ickle cell disease (SCD) is characterized by vaso-occlusive crisis.
96 well as a link with acute chest syndrome and vaso-occlusive crisis.
97 suggest that INO may be beneficial for acute vaso-occlusive crisis.
98  whether heterozygosity of Nf1 would lead to vaso-occlusive disease in genetically engineered mice in
99 spholipid syndrome is a rare cause of ocular vaso-occlusive disease, but is associated with significa
100 lopathy, which mirrors features of human NF1 vaso-occlusive disease, identifies a potential therapeut
101 tress in the sickle mouse precipitates acute vaso-occlusive disease.
102 ically less than 3 days to attenuate rebound vaso-occlusive disease.
103  hereby participating in the pathogenesis of vaso-occlusive diseases.
104 thy, retinopathy of prematurity, and retinal vaso-occlusive diseases.
105 ivated VSMCs is a potential strategy against vaso-occlusive disorders such as in-stent restenosis, ve
106  CD98hc is a potential therapeutic target in vaso-occlusive disorders.
107 arbon emulsion (PFE) was tested for its anti-vaso-occlusive effects in the ex vivo mesocecum vasculat
108                                              Vaso-occlusive episode (VOE) is a common and critical co
109 rotective effect of ADAMTS13 but exacerbated vaso-occlusive episode in mice with SCA.
110  (VWF)-cleaving protease ADAMTS13 alleviated vaso-occlusive episode in mice with SCA.
111 th fixed-dose hydroxyurea indicate decreased vaso-occlusive episodes (0.60; 95% CI 0.52-0.70; p<0.000
112 CD patients experience erythrocyte sickling, vaso-occlusive episodes (VOE), and progressive organ dam
113                                              Vaso-occlusive episodes (VOEs) are a major concern in pa
114                                  Here, using vaso-occlusive episodes (VOEs) of sickle cell disease as
115               SCD patients suffer from acute vaso-occlusive episodes (VOEs), chronic organ damage, an
116                                              Vaso-occlusive episodes are the primary cause of emergen
117 r 188 reported shortened duration of painful vaso-occlusive episodes in SCD, particularly in children
118 proaches to both prevention and treatment of vaso-occlusive episodes in SCD.
119 tive agents are available to prevent painful vaso-occlusive episodes of sickle cell disease (SCD), th
120 e moderate to severe pain typical of painful vaso-occlusive episodes requiring hospitalization were i
121 d to be the initiating event in the periodic vaso-occlusive episodes that characterize sickle cell di
122 th a broad range of complications, including vaso-occlusive episodes, acute chest syndrome (ACS), pai
123    Hydroxyurea (HU) therapy results in fewer vaso-occlusive episodes, and we postulated that HU-relat
124 l apoptosis, and inflammation occur owing to vaso-occlusive episodes, hypoxia, and ischemic injury.
125 al of hydroxyurea to reduce the frequency of vaso-occlusive episodes, sickle cell disease (SCD) has c
126    This is a key factor in the initiation of vaso-occlusive episodes, the hallmark of SCD.
127 population of neutrophils that can stimulate vaso-occlusive episodes.
128 me to last dose of parenteral opioids during vaso-occlusive episodes.
129  do not support the use of poloxamer 188 for vaso-occlusive episodes.
130 and (in the patient with SCD) elimination of vaso-occlusive episodes.
131 d hypoxia could lead to an increased risk of vaso-occlusive episodes.
132 ease-modifying therapies for ongoing painful vaso-occlusive episodes; treatment remains supportive.
133           Clinical manifestations resemble a vaso-occlusive event and include edema, intraretinal hem
134 with SCD during acute pain associated with a vaso-occlusive event increases the calcium responses to
135 tations of tumor cells migrating away from a vaso-occlusive event.
136 c/anoxic focus, often triggered by a central vaso-occlusive event.
137 reatment reduced the median rate of clinical vaso-occlusive events (0 compared with 1.0 per year, P <
138 her key safety outcomes, sickle cell related vaso-occlusive events (16.7 [n=11] vs 21.9% [n=14]; diff
139 16D) expression and >80% reduction in severe vaso-occlusive events (secondary endpoints).
140 ed in this analysis was the number of severe vaso-occlusive events after LentiGlobin infusion among p
141        We hypothesized that sickling-induced vaso-occlusive events and attendant oxidative stress wil
142 e been shown in preclinical models to reduce vaso-occlusive events and improve cardiovascular functio
143  with studies showing a reduced incidence of vaso-occlusive events and reduced mortality.
144 nd Akti XII has immediate benefits for acute vaso-occlusive events and survival in SCD mice exceeding
145 of sustained haemolytic anaemia and episodic vaso-occlusive events drive the development of end-organ
146 on of venous thrombosis in vivo and inhibits vaso-occlusive events in a human sickle cell disease equ
147 M, we show that hematopoietic DREAM promotes vaso-occlusive events in microvessels following TNF-a ch
148 M, we show that hematopoietic DREAM promotes vaso-occlusive events in microvessels following TNF-alph
149 c cell-cell adhesion and aggregation mediate vaso-occlusive events in patients with sickle cell disea
150 r whether it has immediate benefits in acute vaso-occlusive events in SCD patients.
151 roved clinical efficacy for preventing acute vaso-occlusive events in severely affected adults.
152 erion that required a minimum of four severe vaso-occlusive events in the 24 months before enrollment
153 n infusion among patients with at least four vaso-occlusive events in the 24 months before enrollment
154 duce endothelial injury and facilitate acute vaso-occlusive events in transgenic SAD mice.
155 termine the contribution of LW activation to vaso-occlusive events in vivo, we investigated whether i
156                                              Vaso-occlusive events promote ischemia/reperfusion patho
157           This interaction may contribute to vaso-occlusive events that are an important cause of mor
158 concentration, reduce hemolysis, and prevent vaso-occlusive events that cause additional increases in
159 on and thus contribute to the association of vaso-occlusive events with physiologic stress.
160 d be evaluated, all had resolution of severe vaso-occlusive events, as compared with a median of 3.5
161     Hydroxyurea use reduced the incidence of vaso-occlusive events, infections, malaria, transfusions
162  cell free hemoglobin that in turn initiates vaso-occlusive events, we conclude that cleavage of PTP1
163 l disease (SCD) is characterized by repeated vaso-occlusive events, which result in substantial morbi
164 ocytes to endothelium and may play a role in vaso-occlusive events.
165  hemolysis and complete resolution of severe vaso-occlusive events.
166 tin-independent mechanism promotes remaining vaso-occlusive events.
167 s characterized by the painful recurrence of vaso-occlusive events.
168                                There were no vaso-occlusive events.
169 anylate cyclase, causes similar increases in vaso-occlusive events.
170 olysis, improving blood flow, and preventing vaso-occlusive events.
171 e possible role played by such aggregates in vaso-occlusive events.
172  in inflammation, blood flow impairment, and vaso-occlusive events.
173 ue disease dominated by hemolytic anemia and vaso-occlusive events.
174 served in SCD and increases the incidence of vaso-occlusive events.
175 l was related to HbF levels and frequency of vaso-occlusive events.
176  for children and adolescents with recurrent vaso-occlusive events; recent evidence documents sustain
177 ences blood rheology and plays a key role in vaso-occlusive manifestations of sickle cell disease.
178 mon serious adverse event in both groups was vaso-occlusive pain (11 events in five [8%] patients wit
179 sed with hydroxyurea use, including rates of vaso-occlusive pain (98.3 vs. 44.6 events per 100 patien
180 mia (SCA) admitted to the hospital for acute vaso-occlusive pain (VOC).
181 95% confidence interval [CI], 0.34 to 0.54), vaso-occlusive pain crises (incidence rate ratio, 0.43;
182 dentified to support the occurrence of acute vaso-occlusive pain crises in individuals with SCT.
183 ial Doppler velocity >200 cm/s (n = 2), >/=3 vaso-occlusive pain crises per year (n = 12), or >/=2 ac
184 zed by chronic hemolytic anemia and episodic vaso-occlusive pain crises.
185 ncompassing 185 children hospitalized with a vaso-occlusive pain crisis and a reference group of 65 c
186 patients with sickle cell disease (SCD) with vaso-occlusive pain crisis.
187 3; 95% confidence interval [CI], 0.06-0.91), vaso-occlusive pain episodes (11 studies, 1219 participa
188                                              Vaso-occlusive pain episodes (VOE) cause severe pain in
189 onicities are often used during treatment of vaso-occlusive pain episodes (VOE), the major cause of m
190 comes acutely deficient in SCD patients with vaso-occlusive pain episodes (VOE).
191      The MSH analysis suggests that rates of vaso-occlusive pain episodes in these patients were unre
192 ted to initiate or contribute to sickle cell vaso-occlusive pain episodes.
193 nd is associated with increased incidence of vaso-occlusive pain events, acute chest syndrome episode
194                                       Acute, vaso-occlusive pain is the most characteristic complicat
195  malaria infection, non-malarial infections, vaso-occlusive pain, and acute chest syndrome.
196 nd keywords related to "sickle cell trait," "vaso-occlusive pain," and "death," yielding 18 of 1474 c
197    A composite SCA-related clinical outcome (vaso-occlusive painful crisis, dactylitis, acute chest s
198 SCD), which often occurs in the setting of a vaso-occlusive painful crisis.
199 globin, is characterized by inflammatory and vaso-occlusive pathologies.
200 ransduction in SS RBCs may contribute to the vaso-occlusive pathology observed in sickle cell disease
201  combination of antiangiogenic treatment and vaso-occlusive PDT.
202 erize, thereby reducing the frequency of the vaso-occlusive phenomena associated with the disease.
203 ypothesis that the ability of HU to ease the vaso-occlusive phenomena may, in part, be attributed to
204  integral part of the pathophysiology of the vaso-occlusive phenomenon in sickle cell anemia.
205  The results suggest that PMNs contribute to vaso-occlusive processes and endothelial cell injury in
206 r aggregate formation drive the inflammatory vaso-occlusive processes associated with sickle cell ane
207 rea (HU) acute administration in diminishing vaso-occlusive processes in sickle cell disease (SCD) mi
208 potentially visually devastating necrotizing vaso-occlusive retinitis affecting both healthy and immu
209 S) are important in governing whether or not vaso-occlusive sickle cell crises will occur.
210 re no data to support the diagnosis of acute vaso-occlusive sickle cell crisis as a cause of death in
211 function of the formation and persistence of vaso-occlusive thrombi that limit tumor blood supply.

 
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