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1 weeks of drug (90% vs. 26%), to be severely thrombocytopenic (84% vs. 60%), and to have normal renal
3 pletion of neutrophils prevented bleeding in thrombocytopenic and GPVI(-/-) mice during IC-mediated d
4 trophil cytotoxic activities were reduced in thrombocytopenic and GPVI(-/-) mice during IC-mediated i
5 syndrome or acute myeloid leukaemia who are thrombocytopenic and unable to receive disease-modifying
6 loma; however, many of these patients become thrombocytopenic, and it is not clear how the proteasome
8 indicate that for severe thrombocytopenia or thrombocytopenic bleeding in the third trimester, intrav
9 normal platelet numbers at E12.5 but became thrombocytopenic by E15.5, suggesting that c-myb is requ
11 s of wound healing, adult mice were rendered thrombocytopenic by intraperitoneal administration of a
12 platelet counts in adult mice that were made thrombocytopenic by tamoxifen-induced suppression of pro
14 e HIT), defined as a transient prothrombotic thrombocytopenic disorder without proximate heparin expo
15 gnosis remains one of exclusion, after other thrombocytopenic disorders are ruled out based on histor
16 une thrombocytopenia, or patients with other thrombocytopenic disorders, the authors concluded that,
21 may result in a liver xenograft with reduced thrombocytopenic effects, which could be used as a bridg
22 site primary endpoint of clinically relevant thrombocytopenic events (CRTE) during weeks 5-12, define
24 was the incidence of clinically significant thrombocytopenic events, defined by grade 3 or 4 thrombo
26 lets occurs in about 18% of immunosuppressed thrombocytopenic hematology/oncology patients and repres
27 eding remains a significant problem for many thrombocytopenic hematology/oncology patients in spite o
28 with a thrombin inhibitor became moderately thrombocytopenic in response to anti-CD40L ICs and had p
30 lets from the bloodstream can be followed in thrombocytopenic individuals, no model exists for quanti
33 eks after transfer, the ITP SCID mice became thrombocytopenic (< 200 x 10(9) platelets/L) and had inc
34 d the Matrigel model, in four animal models: thrombocytopenic, Lyst(bg) (platelet storage pool defici
35 morrhage), inflammation, and injury, whereas thrombocytopenic Mac-1-deficient mice remained resistant
37 that plasma FXIII-A levels were unchanged in thrombocytopenic mice (Bcl-x(Plt20/Plt20) and Mpl(-/-)),
52 thelial growth factor (Vegf) were studied in thrombocytopenic mice, Tph1(-) (/) (-) mice, and through
64 -beta1 was lower in mice rendered profoundly thrombocytopenic or mice with selectively low levels of
65 rease was even more pronounced in profoundly thrombocytopenic patients (31.6 +/- 10.6 units preop ver
68 Antiplatelet GPIIIa49-66 Ab of HIV-related thrombocytopenic patients induces thrombocytopenia and p
69 h allows analysis of platelet aggregation in thrombocytopenic patients or infants, and facilitates st
70 This phenomenon is also observed in immune-thrombocytopenic patients when tested for UVB tolerance.
71 eltrombopag might be a treatment option for thrombocytopenic patients with AML or MDS who are inelig
73 atelet use, and adverse clinical outcomes in thrombocytopenic patients with hematological malignant n
80 y was hereditary spherocytosis (111), immune thrombocytopenic purpura (36), sickle cell disease (SCD)
81 dying 20 patients with congenital thrombotic thrombocytopenic purpura (cTTP) who cannot cleave VWF mu
82 Most current treatments for chronic immune thrombocytopenic purpura (ITP) act by decreasing platele
83 ction in North American patients with immune thrombocytopenic purpura (ITP) and the effect of H pylor
84 ine if megakaryocytes are targeted by immune thrombocytopenic purpura (ITP) autoantibodies, as are pl
85 treatment for adult patients with idiopathic thrombocytopenic purpura (ITP) for more than 50 years.
95 FcgammaR-dependent cytopenias such as immune thrombocytopenic purpura (ITP) or autoimmune hemolytic a
97 somes as a new treatment strategy for immune thrombocytopenic purpura (ITP) through the use of a mous
98 of immune-related diseases, including immune thrombocytopenic purpura (ITP), autoimmune neuropathies,
99 ites in 23 countries with chronic idiopathic thrombocytopenic purpura (ITP), platelet counts less tha
100 s, the authors concluded that, in idiopathic thrombocytopenic purpura (ITP), production of platelets
107 ts, hypertension (n = 2) and immune-mediated thrombocytopenic purpura (n = 1), were possibly related
109 ich includes two major disorders: thrombotic thrombocytopenic purpura (TTP) and hemolytic uremic synd
111 Recovery from acute episodes of thrombotic thrombocytopenic purpura (TTP) appears complete except f
112 leading to idiopathic, autoimmune thrombotic thrombocytopenic purpura (TTP) by identifying naturally
129 (APS), atypical presentations of thrombotic thrombocytopenic purpura (TTP) or heparin-induced thromb
130 factor (VWF)-cleaving protease implicated in thrombocytopenic purpura (TTP) pathogenesis was identifi
131 c ADAMTS13 activity in congenital thrombotic thrombocytopenic purpura (TTP) patients is constrained b
133 Although both aHUS and acquired thrombotic thrombocytopenic purpura (TTP) remain clinical diagnoses
135 f plasma ADAMTS13 activity causes thrombotic thrombocytopenic purpura (TTP), a life-threatening syndr
136 key factor in the pathogenesis of thrombotic thrombocytopenic purpura (TTP), a life-threatening throm
137 n effective empiric treatment for thrombotic thrombocytopenic purpura (TTP), but how therapy affects
138 may precipitate acute episodes of thrombotic thrombocytopenic purpura (TTP), but pregnancy outcomes i
139 d to a life-threatening disorder, thrombotic thrombocytopenic purpura (TTP), characterized by platele
140 t advances have demonstrated that thrombotic thrombocytopenic purpura (TTP), characterized by widespr
141 ted with platelet transfusions in thrombotic thrombocytopenic purpura (TTP), heparin-induced thromboc
142 aHUS from other TMAs, especially thrombotic thrombocytopenic purpura (TTP), is difficult due to over
143 immune thrombocytopenia (ITP) and thrombotic thrombocytopenic purpura (TTP), respectively, illuminate
144 molytic-uremic syndrome (HUS) and thrombotic thrombocytopenic purpura (TTP), the histories and presen
166 le in pathogenesis of the disease thrombotic thrombocytopenic purpura (TTP); however, experimental ev
167 TTP cases from the United Kingdom Thrombotic Thrombocytopenic Purpura (UK TTP) Registry with clinical
169 on the status of current research in immune thrombocytopenic purpura and a preview of agents in deve
171 microangiopathy (TMA), including thrombotic thrombocytopenic purpura and hemolytic-uremic syndrome,
172 us to understand pathogenesis of thrombotic thrombocytopenic purpura and other arterial thromboses a
173 ld be an antithrombotic agent for thrombotic thrombocytopenic purpura and other thrombotic conditions
174 f any treatment for patients with idiopathic thrombocytopenic purpura and persistent severe thrombocy
175 ascular occlusion associated with thrombotic thrombocytopenic purpura and sepsis was revealed by the
176 munoglobulin G from patients with thrombotic thrombocytopenic purpura and sequence alignment of the A
177 ceptable for patients with refractory immune thrombocytopenic purpura and severe thrombocytopenia wit
178 ions including arthritis, cancer, thrombotic thrombocytopenic purpura and the Ehlers-Danlos type VIIC
179 alikes and their distinction from thrombotic thrombocytopenic purpura and the hemolytic uremic syndro
181 gnosis between inherited and acquired immune thrombocytopenic purpura as well as clinical practice on
182 pathy and a possible diagnosis of thrombotic thrombocytopenic purpura between Jan 8, 2004, and Dec 6,
183 Deaths have been reported for 2.9% of immune thrombocytopenic purpura cases treated with rituximab, b
184 tient suffers from a rare form of idiopathic thrombocytopenic purpura caused by a GPVI-specific autoa
185 Patients suffering from acquired thrombotic thrombocytopenic purpura develop autoantibodies directed
187 s for the diagnosis and management of immune thrombocytopenic purpura focused entirely on primary dis
188 re more than 16 years of age, had idiopathic thrombocytopenic purpura for more than 3 months, had a p
190 the pathophysiology of idiopathic thrombotic thrombocytopenic purpura have provided the rationale for
191 unding the diagnosis and treatment of immune thrombocytopenic purpura in children continue to evolve.
192 evision of the present guidelines for immune thrombocytopenic purpura in pregnancy based on evidence-
193 Hematology and British guidelines on immune thrombocytopenic purpura incidence, prevalence, and natu
194 Treatment of chronic refractory idiopathic thrombocytopenic purpura is a dilemma because many patie
199 ed by thrombotic microangiopathy, thrombotic thrombocytopenic purpura is distinguished by a severe de
200 ing protease activity in acquired thrombotic thrombocytopenic purpura is due to an autoantibody inhib
203 about the incidence and prevalence of immune thrombocytopenic purpura is limited, with nearly all dat
204 l investigation of novel therapies in immune thrombocytopenic purpura is undergoing a revolution that
206 of the pathological mechanisms of thrombotic thrombocytopenic purpura not only provide a rationale fo
209 es to be indicated for idiopathic thrombotic thrombocytopenic purpura regardless of ADAMTS13 levels,
210 f delivery of a pregnant patient with immune thrombocytopenic purpura should be determined based on m
211 receiving alemtuzumab developed late immune thrombocytopenic purpura that remitted with standard the
213 itors, and the risk of relapse of thrombotic thrombocytopenic purpura will be important to further va
216 d a molecular distinction between thrombotic thrombocytopenic purpura, a disease characterized by a l
217 uman endothelial cells and causes thrombotic thrombocytopenic purpura, a disease with similarities to
218 insights into the pathophysiology of immune thrombocytopenic purpura, a disorder in which autoantibo
220 0% of patients diagnosed with primary immune thrombocytopenic purpura, and are not associated with di
221 rlying Helicobacter pylori-associated immune thrombocytopenic purpura, and Ghevaert et al. describe a
222 orders, such as rheumatoid arthritis, immune thrombocytopenic purpura, autoimmune hemolytic anemia, s
223 be the most important therapy in thrombotic thrombocytopenic purpura, but clinical data for adjuncti
224 ypical hemolytic uremic syndrome, thrombotic thrombocytopenic purpura, C3GN, and dense deposit diseas
225 hritis, systemic lupus erythematosus, immune thrombocytopenic purpura, chronic cold agglutinin diseas
226 and the pathogenesis of clinical thrombotic thrombocytopenic purpura, especially in relation to ADAM
227 S13 deficiency is associated with thrombotic thrombocytopenic purpura, in which life-threatening epis
228 ia, antiphospholipid syndrome and thrombotic thrombocytopenic purpura, include immunosuppression and
229 n patients with acute episodes of thrombotic thrombocytopenic purpura, independent of ADAMTS13 activi
230 eral systemic diseases, including thrombotic thrombocytopenic purpura, manifest much of their patholo
231 management decisions in suspected thrombotic thrombocytopenic purpura, new evidence supporting the ef
232 sseminated intravascular coagulation, immune thrombocytopenic purpura, or splenic sequestration did n
233 urring in patients with inherited thrombotic thrombocytopenic purpura, resulted in a significant redu
234 associated with diseases such as thrombotic thrombocytopenic purpura, sepsis, and diabetes among oth
238 ease platelet counts in patients with immune thrombocytopenic purpura, without significant adverse ef
239 itial management of patients with thrombotic thrombocytopenic purpura-hemolytic uremic syndrome (TTP-
240 cy, making their distinction from thrombotic thrombocytopenic purpura-hemolytic uremic syndrome diffi
241 ment the reports of occurrence of thrombotic thrombocytopenic purpura-hemolytic uremic syndrome durin
243 greatest risk for development of thrombotic thrombocytopenic purpura-hemolytic uremic syndrome is ne
245 women with congenital or familial thrombotic thrombocytopenic purpura-hemolytic uremic syndrome who w
246 crease the risk for occurrence of thrombotic thrombocytopenic purpura-hemolytic uremic syndrome.
286 ma exchange in some patients with thrombotic thrombocytopenic purpura; conversely such deficiency is
287 ish aHUS from other TMAs, such as thrombotic thrombocytopenic purpura; however, novel bioassays are b
288 ausea, grade 3 infection, grade 3 thrombotic thrombocytopenic purpurea, grade 2 nausea, grade 2 gener
294 tected in sKitL-deficient Mmp9-/- as well as thrombocytopenic Thpo-/- and TPO receptor-deficient (Mpl
297 IL-11, did not induce platelet production in thrombocytopenic, TPO-deficient (Thpo(-/-)) or TPO recep
298 ocytopenic VWD type 2B mice, suggesting that thrombocytopenic VWD type 2B mice were elevated two- to
299 VWF was exclusively detected on platelets of thrombocytopenic VWD type 2B mice, suggesting that throm
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