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1 alarial infections, vaso-occlusive pain, and acute chest syndrome.
2 e-dependent innate immune pathway to prevent acute chest syndrome.
3 ive crisis, a composite of painful crisis or acute chest syndrome.
4 ckle cell disease-related events, especially acute chest syndrome.
5 ies, or with severe or recurrent episodes of acute chest syndrome.
6 ssemia was admitted to the internal ward for acute chest syndrome.
7 equency of acute pain episodes or history of acute chest syndrome.
8 death, stroke, frequent pain, and recurrent acute chest syndrome.
9 ad frequent pain, and 3 (1.8%) had recurrent acute chest syndrome.
10 is area are current and uniquely relevant to acute chest syndrome.
11 rienced further episodes of pain, stroke, or acute chest syndrome.
12 hospitalized with mild to moderately severe acute chest syndrome.
14 aso-occlusive crises (mean [SD], 0.8 [2.4]), acute chest syndrome (109 of 3712 [2.9%]), and inpatient
16 25.0%]), kidney disease (21 of 144 [14.6%]), acute chest syndrome (18 of 144 [12.5%]), and health car
17 patients) included ileus (5), bleeding (4), acute chest syndrome (5), pneumonia (2), portal vein thr
20 ts with sickle cell disease hospitalized for acute chest syndrome (ACS) are at high risk of in situ p
39 e contributing factor for the development of Acute Chest Syndrome (ACS), a major cause of morbidity a
41 vasoactive mediator endothelin (ET-1) in the acute chest syndrome (ACS), we incubated bovine pulmonar
46 Those with H1N1 influenza more often had acute chest syndrome (ACS; 34% vs 13%, P = .01) and requ
47 tted with sickle cell crisis, complicated by acute chest syndrome, acute respiratory distress syndrom
48 e substantially reduces episodes of pain and acute chest syndrome, admissions to hospital, and transf
50 generation of F2 isoprostanes, occurs during acute chest syndrome and may have an important role in t
51 stress may contribute to the pathogenesis of acute chest syndrome and measured F2 isoprostanes, a non
52 usion for prevention of stroke, treatment of acute chest syndrome and perioperative transfusion manag
53 ions of SCD are of particular importance, as acute chest syndrome and pulmonary hypertension have the
56 y repeated episodes of severe acute pain and acute chest syndrome, and by other complications includi
57 ses significantly, decrease the incidence of acute chest syndrome, and decrease the need for blood tr
58 centration and rate of and recent episode of acute chest syndrome, and elevated systolic blood pressu
59 velocity, white blood cell count, history of acute chest syndrome, and hemoglobin levels, demonstrate
60 and recurrent episodes of pain, dactylitis, acute chest syndrome, and hospitalization; even infants
61 splenic sequestration, or priapism) and the acute chest syndrome, and patient-reported outcomes were
62 ion associated with increased rates of pain, acute chest syndrome, and premature death in human sickl
63 bF, lowers rates of pain crisis, episodes of acute chest syndrome, and requirements for blood transfu
65 as acute anemia, vaso-occlusive crises, and acute chest syndrome; and/or from pregnancy-related comp
66 ome, the etiological mechanisms that trigger acute chest syndrome are largely unknown.Objectives: To
67 cute exacerbation of asthma or an episode of acute chest syndrome are two distinct entities that need
68 increase in F2 isoprostanes in patients with acute chest syndrome as compared with normal volunteers.
69 t pulmonary manifestations of SCD, including acute chest syndrome, asthma, and pulmonary hypertension
70 cell disease include airway hyperreactivity, acute chest syndrome, chronic sickle lung disease, pulmo
73 Risk factors for asthma exacerbation and an acute chest syndrome episode are similar, and both can p
74 usive pain crises per year (n = 12), or >/=2 acute chest syndrome episodes (n = 4) in the 2 years pre
75 , children with sickle cell disease who have acute chest syndrome episodes have worse pulmonary funct
79 episodes (0.60; 95% CI 0.52-0.70; p<0.0001), acute chest syndrome events (0.21; 0.13-0.33; p<0.0001),
81 ted crises (defined as crises other than the acute chest syndrome, hepatic sequestration, splenic seq
82 p<0.0001), with some evidence for decreased acute chest syndrome, hospitalisation rates, and transfu
83 t period, but significant benefits for pain, acute chest syndrome, hospitalizations, and transfusions
84 enter study, we analyzed 671 episodes of the acute chest syndrome in 538 patients with sickle cell di
85 eal life support could be helpful for severe acute chest syndrome in adults sickle cell disease, beca
86 corporeal life support experience for severe acute chest syndrome in four referral centers in France.
87 thods: TASC (Therapeutic Anticoagulation for Acute Chest Syndrome in Sickle Cell Disease) is a random
88 roved pulmonary hypertension associated with acute chest syndrome in sickle cell disease, and several
89 have been implicated in the pathogenesis of acute chest syndrome in subjects with sickle cell anemia
90 ammatory state" that predisposes patients to acute chest syndrome in the setting of triggering factor
91 02; 95% CI 1.00-1.003; P = .015), and higher acute chest syndrome incidence rate (HR per event/year 1
92 uired extracorporeal life support for severe acute chest syndrome, including 10 (45%) veno-venous and
93 by hemolytic anemia, acute and chronic pain, acute chest syndrome; increased incidence of stroke, nep
95 Among patients with sickle cell disease, the acute chest syndrome is commonly precipitated by fat emb
99 udy was ICU survival of patients with severe acute chest syndrome managed with extracorporeal life su
100 ious complications and organ damage, such as acute chest syndrome, multiorgan failure, and sudden dea
101 uded a history of stroke (n = 12), recurrent acute chest syndrome (n = 5), and recurrent painful cris
102 10 (91%) of 11 serious adverse events were acute chest syndrome (nine in the no-preoperative-transf
103 atients during vaso-occlusive crisis and the acute chest syndrome, nitric oxide is destroyed by incre
106 ratio, 0.43; 95% CI, 0.34 to 0.56), cases of acute chest syndrome or pneumonia (incidence rate ratio,
107 of hypoperfusion/hypoxia, as observed during acute chest syndromes or acute anemic events (AAE), and
108 oke syndromes) or remote organ injury (e.g., acute chest syndrome) or the systematization of inflamma
111 een patients with sickle cell disease during acute chest syndrome (pre- and postexchange transfusion)
113 (vaso-occlusive painful crisis, dactylitis, acute chest syndrome, splenic sequestration, or blood tr
115 known to occur in the lung and contribute to acute chest syndrome, the etiological mechanisms that tr
118 ute respiratory distress syndrome, including acute chest syndrome, were 56 of 3144 deliveries (1.8%)