ライフサイエンスコーパス: thrombotic

1 on or venous thromboembolism were 7.8 (acute thrombotic), 15.0 (postthrombotic), and 0 (nonthrombotic

2 We included 379 patients: 160 with acute thrombotic, 193 with postthrombotic, and 26 with nonthro

3 te was 80.5% (95% CI, 73.0%-88.0%) for acute thrombotic, 59.2% (95% CI, 50.4%-68.0%) for postthrombot

4 uced cerebral CD4(+) T-cell infiltration and thrombotic activity following experimental stroke result

5 lasma generated TF-bearing NETs that induced thrombotic activity of HAECs.

6 bin and haem, anti-inflammatory agents, anti-thrombotic agents and anti-platelet agents.

7 Compared with patients who were unexposed to thrombotic agents, the rates of hematuria-related compli

8 templates for the development of novel anti-thrombotic agents.

9 coronary intervention (PCI), periprocedural thrombotic and bleeding complications can lead to increa

10 tes concomitant evaluation of the individual thrombotic and bleeding risks related to both clinical a

11 Thrombotic and hemorrhagic complications are prevalent i

12 eutic perspectives in cTTP and in general in thrombotic and inflammatory disorders associated with en

13 rombin plays a critical role in coordinating thrombotic and inflammatory responses and has long been

14 ted coagulopathy, characterised by increased thrombotic and microvascular complications.

15 rse events related to the cardiovascular and thrombotic and musculoskeletal systems.

16 r organs of the patients and causes frequent thrombotic and neurological complications.

17 of ADAMTS13 (an enzyme that cleaves the pro-thrombotic and proinflammatory von Willebrand factor) an

18 ew approach for treating or preventing acute thrombotic and thromboembolic conditions.

19 ellular) that cause anticoagulant-refractory thrombotic antiphospholipid syndrome are now better unde

20 Anticoagulant-refractory thrombotic antiphospholipid syndrome can be broadly defi

21 is the standard anticoagulant treatment for thrombotic antiphospholipid syndrome.

22 how noninferiority to dose-adjusted VKAs for thrombotic APS and, in fact, showed a non-statistically

23 These complications are caused by thrombotic arterial occlusion localized at the site of h

24 dial infarction (MI), recurrent ischemia, or thrombotic bailout at 96 h (4-way endpoint) and the comp

25 performed for all study patients, and plasma thrombotic biomarkers were measured in a nested cohort (

26 showed an improved effect of rivaroxaban on thrombotic burden as compared with standard anticoagulan

27 of 75 patients with repeat imaging had their thrombotic burden resolved, 43 (57%) patients improved,

28 a similarly low recurrence risk and reduced thrombotic burden without increased bleeding, as compare

29 non-valvular AF were recruited and rates of thrombotic/cardiovascular events, major bleeding and mor

30 otype, with an overall rate of 49.2% for all thrombotic, coagulation, platelet count, and function di

31 Radial artery occlusion (RAO) is a thrombotic complication of transradial catheterization t

32 nce interval [CI], 2.9-7.3), and the overall thrombotic complication rate was 9.5% (95% CI, 6.8-12.8)

33 primary outcome was a composite of death and thrombotic complications (nonfatal myocardial infarction

34 s to more stringent diagnostic screening for thrombotic complications and to the early institution of

35 significant promise to reduce the burden of thrombotic complications and ultimately improve the prog

36 osing patients to an increased risk of early thrombotic complications and underscoring the need to de

37 Thrombotic complications are a major cause of morbidity

38 Given thrombotic complications are central determinants of the

39 Importantly, thrombotic complications are markers of severe COVID-19

40 drugs, they could decrease inflammation and thrombotic complications associated with COVID-19.

41 folds (BVS) are associated with an excess of thrombotic complications compared with metallic everolim

42 In particular, thrombotic complications in patients with COVID-19 are c

43 her risk factors for atherosclerosis and its thrombotic complications include hypertension, cigarette

44 et activation and potentially contributes to thrombotic complications occurring in cirrhosis.

45 ibes the rate and severity of hemostatic and thrombotic complications of 400 hospital-admitted COVID-

46 a substantial shift in the mechanisms of the thrombotic complications of atherosclerosis.

47 Studies are needed to further understand the thrombotic complications of COVID-19, together with the

48 provide a therapeutic opportunity to prevent thrombotic complications of HIT, while sparing systemic

49 onstrate that this species can cause serious thrombotic complications of trichinellosis in humans.

50 19) is associated with a significant risk of thrombotic complications ranging from microvascular thro

51 d procalcitonin were higher in patients with thrombotic complications than in those without.

52 r in the future, particularly in view of the thrombotic complications that have been reported when em

53 No thrombotic complications were reported under DOAC until

54 not detect evidence of an increased risk of thrombotic complications with TXA exposure.

55 s placebo, without a higher risk of death or thrombotic complications within 30 days after surgery.

56 atelet hyperactivity, systemic inflammation, thrombotic complications, and coagulopathy.

57 These conditions include thrombotic complications, myocardial dysfunction and arr

58 Because of their increased risk of thrombotic complications, patients with DM commonly achi

59 immunothrombosis, ultimately causing (micro)thrombotic complications, such as deep vein thrombosis,

60 s that contribute to atherosclerosis and its thrombotic complications.

61 rugs, for both the prevention and therapy of thrombotic complications.

62 inding association with either neurologic or thrombotic complications.

63 associated with adverse pregnancy outcomes, thrombotic conditions, and accelerated atherosclerosis i

64 f CLEC-2 KO models, but not their hemostatic/thrombotic defect.

65 Small arterial, venous thrombi, thrombotic depositions on damaged endothelial surface, a

66 apeutic paradigm in APS, which may extend to thrombotic disease in the general population.

67 or challenge given the serious nature of the thrombotic disease observed, which has become refractory

68 tors XIIa and XIa, 2 factors contributing to thrombotic disease while playing a limited role in hemos

69 e roles in infection, sepsis, wound healing, thrombotic disease, and cancer propagation, all of which

70 Although trichinellosis is known to cause thrombotic disease, serious thrombotic events are rare a

71 VID-19) is thought to predispose patients to thrombotic disease.

72 nts with functional connections to a complex thrombotic disease.

73 yndrome (APS), a life-threatening autoimmune thrombotic disease.

74 in its circulating levels may contribute to thrombotic diseases, such as venous thromboembolism (VTE

75 ogy and the pathogenesis of inflammatory and thrombotic diseases.

76 Genetic factors contribute to the risk of thrombotic diseases.

77 rd a therapeutic for patients suffering from thrombotic disorders and a diagnostic tool for monitorin

78 ibility of their therapeutic use in treating thrombotic disorders associated with aberrant expression

79 t activation may contribute to various human thrombotic disorders involving both the micro- and macro

80 morbidity and the mortality associated with thrombotic disorders, defining the mechanisms underlying

81 fened clots are associated with bleeding and thrombotic disorders.

82 tions for the understanding and treatment of thrombotic disorders.

83 erotic properties of PXR ligands, these anti-thrombotic effects may provide additional cardio-protect

84 ular system and linked them to anti- and pro-thrombotic effects of aspirin.

85 e production of thromboxane (Tx)A(2) , a pro-thrombotic eicosanoid.

86 ologic patterns observed in the nonbacterial thrombotic endocarditis group were similar to those obse

87 ia (n = 1/11, 9%; p = 0.03) and nonbacterial thrombotic endocarditis groups (n = 0/7, 0%; p = 0.02).

88 conditions, namely bacteremia, nonbacterial thrombotic endocarditis, and healthy controls.

89 Endothelial cells actively maintain an anti-thrombotic environment; loss of this protective function

90 poxic, ischemic/hypertensive, infectious and thrombotic etiologies were diagnosed, blinded to exposur

91 % of BMS patients (p = 0.95), and a coronary thrombotic event (myocardial infarction and/or stent thr

92 ies were not associated with the hazard of a thrombotic event (P = .4163), but were significantly ass

93 that in addition to their role in the acute thrombotic event at the time of myocardial infarction, p

94 that did or did not experience bleeding or a thrombotic event during follow-up.

95 s, death occurred in 49 patients (14%) and a thrombotic event in 34 (10%).

96 ng thrombus formation and growth following a thrombotic event in normal or pathological conditions.

97 gth of stay, infusion-related reactions, and thrombotic event occurrence during multiple predefined p

98 than clopidogrel were associated with fewer thrombotic event occurrences further solidified the dual

99 id and clopidogrel was associated with lower thrombotic event rates than acetylsalicylic acid monothe

100 first prescription date to the earliest of a thrombotic event, medication discontinuation, death, or

101 g inclusion criteria for the occurrence of a thrombotic event, which were censored at hospital discha

102 was 27.1% for a major bleed and 26.3% for a thrombotic event.

103 splenomegaly or symptoms in the absence of a thrombotic event.

104 l events (15 cohorts; n>2543 fistulas), 0.24 thrombotic events (26 cohorts; n=4232 fistulas), and 0.0

105 ] DDAVP, 0 mEq/L [0-2 mEq/L]; p = 0.089) and thrombotic events ([+] DDAVP, 7.3% vs [-] DDAVP, 1.4%; p

106 Thrombotic events after MPN and before second cancer wer

107 Fibrin both promotes thrombotic events and drives obesity pathophysiology, bu

108 IgA isotype (IgA-aB2GP1) have been linked to thrombotic events and mortality in hemodialysis patients

109 or or prasugrel at 12 months with respect to thrombotic events and resulted in a lower incidence of b

110 Since thrombotic events are frequent in severe COVID-19 and re

111 s known to cause thrombotic disease, serious thrombotic events are rare and have not been previously

112 rker potential of procoagulant platelets for thrombotic events as well as on the possible clinical be

113 Factor Xa inhibitors and aspirin each reduce thrombotic events but have not yet been tested in combin

114 prothrombotic state with a high incidence of thrombotic events during hospitalization; however, data

115 asome complex, is a key determinant of acute thrombotic events during hypoxic conditions.

116 ing the first 3 treatment days and new-onset thrombotic events during the first 7 days.

117 id not significantly affect serum sodium and thrombotic events during the study period.

118 The incidence of major venous-thrombotic events during the study was 1.22 per 100 pers

119 At 90 days, thrombotic events had occurred in 6.3% of the patients i

120 Most arterial thrombotic events have a clear atherosclerotic or cardio

121 en the graft and host vasculatures; however, thrombotic events have been reported upon graft implanta

122 plant surgery, a well-known trigger of acute thrombotic events in aPL carriers.

123 hat complement activation is associated with thrombotic events in APS.

124 n independent and predictive risk factor for thrombotic events in humans.

125 predictive value for the appearance of acute thrombotic events in patients who are going to undergo t

126 antiphospholipid antibodies (aPL Abs) effect thrombotic events in patients with antiphospholipid synd

127 /Q scanning is superior to CTPA in detecting thrombotic events in SCD.

128 integration and graft perfusion and prevent thrombotic events in the grafts.

129 testinal manifestations and can present with thrombotic events in young patients with iron deficiency

130 Neither hemolysis nor thrombotic events increased the risk of mortality.

131 ity worldwide, and is a consequence of acute thrombotic events involving activation of platelets and

132 However, recurrent thrombotic events occur in ~1 in 10 patients in the firs

133 Thrombotic events occurred almost entirely within 6 mont

134 We observed no thrombotic events or development of de-novo antidrug ant

135 Treatments to prevent acute thrombotic events should focus on B2A-CIC-positive patie

136 ith thalassemia exhibit an increased risk of thrombotic events that is augmented after splenectomy.

137 Rates of major bleeding and coronary thrombotic events were no different and were associated

138 count, coagulation tests, heparin dose, and thrombotic events were not.

139 No thrombotic events were observed.

140 of how to provide optimal protection against thrombotic events without excessive increases in bleedin

141 We investigated the efficacy (thrombotic events) and safety (hemorrhagic and other adv

142 -factor Xa, the incidence of hemorrhagic and thrombotic events, and the amount of blood products tran

143 ased risk not only for bleeding but also for thrombotic events, including all-cause mortality.

144 wenty-five (3.8%) patients had a total of 26 thrombotic events, of which 22 occurred in the first 14

145 influenza virus infection to cardiovascular thrombotic events, we develop a dynamic model which inco

146 f coronary artery disease and acute coronary thrombotic events.

147 k between NSAID use and an increased risk of thrombotic events.

148 ciated with a reduction in the occurrence of thrombotic events.

149 dence for a causal role of these proteins in thrombotic events.

150 ma levels on the risk of arterial and venous thrombotic events.

151 f time-of-day-dependent vessel type-specific thrombotic events.

152 presence of B2A-CIC is a predictor of acute thrombotic events.

153 has been associated with occurrence of acute thrombotic events.

154 Hemolysis was predictive of subsequent thrombotic events.

155 have become first-line treatment for venous thrombotic events.

156 ients (KTRs) for prevention and treatment of thrombotic events.

157 come was the proportion of patients with new thrombotic events; the primary safety outcome was major

158 Cirrhosis is associated with hemorrhagic and thrombotic extrahepatic complications.

159 Historically, the thrombotic function of platelets has received significan

160 Platelets mediate vascular occlusion through thrombotic functions but are also recognized to have imm

161 rates for the nonthrombotic and chronic post-thrombotic groups were 96.2% and 79.8%, respectively.

162 evention and treatment of cardiovascular and thrombotic issues associated with novel MM therapies hav

163 ad significant CAD, 35 (64%) of 55 had acute thrombotic lesions, and 46 (84%) of 55 had percutaneous

164 Although neutrophils were abundant in thrombotic lesions, depletion of circulating Ly6G-positi

165 In this review, we will discuss cases with thrombotic manifestations and the tailored management of

166 features, symptoms, and risk factors of rare thrombotic manifestations are heterogeneous and in large

167 eview is focused on the treatment of unusual thrombotic manifestations as reported in the most recent

168 idence to date supports the concept that the thrombotic manifestations of severe COVID-19 are due to

169 pulmonary arterial obstruction by organized thrombotic material stemming from incompletely resolved

170 ovember 2016, 170 patients (127 chronic post-thrombotic, mean age 54 years, 56.4% female) at 22 sites

171 mary hypercoagulable disorders, but also pro-thrombotic medications or substances, vascular and anato

172 ndrome during pregnancy, and implications of thrombotic microangiopathies for subsequent pregnancies

173 enrolled in the French Reference Center for Thrombotic Microangiopathies registry between 2000 and 2

174 60.5%), interstitial hemorrhages (31.6%), or thrombotic microangiopathy (15.8%).

175 the development of T3SS-dependent intestinal thrombotic microangiopathy (iTMA) and ischemic enteritis

176 Transplant-associated thrombotic microangiopathy (TA-TMA) is a common and poor

177 (HSCT) recipients with transplant-associated thrombotic microangiopathy (TA-TMA), and untreated patie

178 emonstration of impaired C regulation in the thrombotic microangiopathy (TMA) atypical hemolytic urem

179 purpura (TTP) is an acute, life-threatening thrombotic microangiopathy (TMA) caused by acquired or c

180 ase reports have described the occurrence of thrombotic microangiopathy (TMA) following IV abuse of e

181 s developed hemolytic uremic syndrome (HUS), thrombotic microangiopathy (TMA), or HUS-like events, ex

182 ic uremic syndrome (aHUS), the prototypes of thrombotic microangiopathy (TMA).

183 receptor) is associated with renal-specific thrombotic microangiopathy (TMA).

184 horiocapillaris degeneration, and glomerular thrombotic microangiopathy (TMA).

185 tion of innate immunity, as characterized by thrombotic microangiopathy (TMA).

186 a clinical picture consistent with an acute thrombotic microangiopathy (TMA).

187 are high-risk periods for different forms of thrombotic microangiopathy (TMA).

188 V-2) and complement components in regions of thrombotic microangiopathy (TMA).

189 -the PLASMIC score-to stratify patients with thrombotic microangiopathy according to their risk of ha

190 cascade, protected homozygous C3KI mice from thrombotic microangiopathy and aHUS.

191 lytic uremic syndrome (aHUS), a rare form of thrombotic microangiopathy caused by complement pathogen

192 Hemolytic uremic syndrome (HUS) is a thrombotic microangiopathy characterized by intravascula

193 purpura (TTP) is a rare and life-threatening thrombotic microangiopathy characterized by microangiopa

194 ring system also more consistently diagnosed thrombotic microangiopathy due to severe ADAMTS13 defici

195 AMR was associated with subclinical thrombotic microangiopathy in 2 patients.

196 nitoring of such pregnancies for episodes of thrombotic microangiopathy is essential but, the best st

197 All patients with transplant-associated thrombotic microangiopathy should be screened for the ca

198 l role in creating the hyperinflammation and thrombotic microangiopathy that appear to contribute to

199 d related to a hyper-inflammatory status and thrombotic microangiopathy that are observed in severe C

200 Endothelial dysfunction links thrombotic microangiopathy to steroid-refractory graft-v

201 5N (C3KI) mice developed spontaneous chronic thrombotic microangiopathy together with hematuria, thro

202 atient demonstrated biological recurrence of thrombotic microangiopathy under treatment.

203 214 patients with thrombotic microangiopathy were included in the derivati

204 in patients with either C3 glomerulopathy or thrombotic microangiopathy).

205 thies, HELLP syndrome, transplant-associated thrombotic microangiopathy, antiphospholipid antibody sy

206 In addition, two patients had findings of thrombotic microangiopathy, one had pauci-immune crescen

207 ne response that fuels hyperinflammation and thrombotic microangiopathy, thereby increasing coronavir

208 Among the syndromes characterised by thrombotic microangiopathy, thrombotic thrombocytopenic

209 endothelial growth factor (VEGF) results in thrombotic microangiopathy, we addressed the possibility

210 typical hemolytic uremic syndrome, a form of thrombotic microangiopathy.

211 luminal deposits, which are classic signs of thrombotic microangiopathy.

212 essing the diagnostic challenge presented by thrombotic microangiopathy.

213 rted quality of life, and increased risk for thrombotic microangiopathy.

214 and increasing attention is directed towards thrombotic microembolism as the underlying cause of hypo

215 and local activation of tissue factor in the thrombotic milieu.

216 ation of coagulation, potentially leading to thrombotic obstruction of small and midsize vessels, the

217 ng cause of synthetic graft failure includes thrombotic occlusion and intimal hyperplasia at the site

218 -catalyzed oxidative reaction for preventing thrombotic occlusion and neointimal formation of synthet

219 A complete thrombotic occlusion developing from an atherosclerotic

220 One patient had thrombotic occlusion of the centrifugal pump, and one ha

221 In vivo, reperfusion of carotid artery thrombotic occlusion was also enhanced.

222 l defense mechanism against lasting arterial thrombotic occlusion.

223 fective platelet plug formation, and delayed thrombotic occlusion.

224 autoreactive-mediated complications such as thrombotic or neurologic events.

225 sma VWF levels in a manner representative of thrombotic or pro-inflammatory conditions such as arteri

226 No thrombotic or thromboembolic events, systemic allergic r

227 rbor variants associated with rare bleeding, thrombotic, or platelet disorders (BTPDs).

228 RBC transfusion mediates inflammatory and/or thrombotic outcomes.

229 taining the integrity of the vasculature and thrombotic pathways linked to this, given they surprisin

230 , range 10 to 260 mm (mean 125.3 mm for post-thrombotic patients and 70.2 mm for nonthrombotic patien

231 ated in thalassemia, which may contribute to thrombotic phenomena in these patients.

232 osition of patients with COVID-19 to develop thrombotic phenomena.

233 he Coagulation System, could account for the thrombotic phenotype in CBS(-/-) patients and the absenc

234 additional triggers also results in a venous thrombotic phenotype in mice, most notably with vessel o

235 and CLEC-2 stimulation and enhanced platelet thrombotic phenotype on collagen matrix under shear stre

236 lled complement activation and a more severe thrombotic phenotype.

237 basis underlying these disparately different thrombotic phenotypes, we analyzed plasma proteomes of C

238 a therapeutic option for patients with acute thrombotic, postthrombotic, and nonthrombotic obstructio

239 ny cardiovascular complications, including a thrombotic propensity.

240 distinguish acute recurrent DVT from chronic thrombotic remains.

241 reatment of uncontrolled tissue-damaging and thrombotic responses in COVID-19.

242 e (UPR) with downstream inflammatory and pro-thrombotic responses.

243 C5 antibody might be helpful for C5-mediated thrombotic retinal diseases.

244 residual serum TXB2 associated with elevated thrombotic risk (<99.0% inhibition or TXB2 >3.1 ng/ml) w

245 mellitus (DM) are characterized by enhanced thrombotic risk attributed to multiple mechanisms includ

246 nt of platelet hyperreactivity and increases thrombotic risk during aging.

247 f heparanase or the JAK-2 pathway may reduce thrombotic risk in thalassemia.

248 studies have consistently demonstrated that thrombotic risk is significantly reduced in individuals

249 vating capacity of FVL carriers modifies the thrombotic risk of this common prothrombotic mutation.

250 sociated with both lower efficacy and higher thrombotic risk over time.

251 wledge about risk of bleeding and short-term thrombotic risk resides in many specialties, further com

252 nt, including general strategies to minimise thrombotic risk, intensification of anticoagulation, add

253 activates the immune response and increases thrombotic risk, negating any protective effects in seps

254 In keeping with their reduced thrombotic risk, plasma VWF levels are ~25% lower in hea

255 different subtypes vary with regard to their thrombotic risk.

256 o account for confounders of transfusion and thrombotic risk.

257 ed by abnormal megakaryopoiesis and enhanced thrombotic risk.

258 of target lesion revascularization, without thrombotic safety concerns.

259 ties, especially no vascular constriction or thrombotic signs as well as no retinal detachment.

260 haemic strokes (n = 8) associated with a pro-thrombotic state (four with pulmonary thromboembolism),

261 ulation occur with progression of ALI: a pro-thrombotic state progresses to hypocoagulability.

262 Experimental models of thrombotic stroke induced by either intra-arterial throm

263 ole of PKal on cerebral outcomes in a murine thrombotic stroke model treated with tPA.

264 in the percentage of patients with the post-thrombotic syndrome (47% in the pharmacomechanical-throm

265 primary outcome was development of the post-thrombotic syndrome between 6 and 24 months of follow-up

266 n did not result in a lower risk of the post-thrombotic syndrome but did result in a higher risk of m

267 The post-thrombotic syndrome frequently develops in patients with

268 Moderate-to-severe post-thrombotic syndrome occurred in 18% of patients in the p

269 Severity scores for the post-thrombotic syndrome were lower in the pharmacomechanical

270 hypothesized to reduce the risk of the post-thrombotic syndrome.

271 However, multiple factors contribute to the thrombotic tendency, including gender, mutational profil

272 omplications (inflammatory, co-infection and thrombotic) that are identifiable by analytics patterns.

273 A3 pathway may be a relevant target for anti-thrombotic therapy.

274 Congenital thrombotic thrombocytopenic purpura (cTTP) is an ultra-r

275 By studying 20 patients with congenital thrombotic thrombocytopenic purpura (cTTP) who cannot cl

276 Insights into immune-mediated thrombotic thrombocytopenic purpura (iTTP) pathophysiolo

277 odies in plasma samples from immune-mediated thrombotic thrombocytopenic purpura (iTTP) patients.

278 ssociated with increased mortality in immune thrombotic thrombocytopenic purpura (iTTP).

279 on during the acute phase of immune-mediated thrombotic thrombocytopenic purpura (iTTP).

280 Acquired thrombotic thrombocytopenic purpura (TTP) and hemolytic

281 Its aims are: to rule thrombotic thrombocytopenic purpura (TTP) in or out, wit

282 Immune-mediated thrombotic thrombocytopenic purpura (TTP) is a life-thre

283 Thrombotic thrombocytopenic purpura (TTP) is a life-thre

284 Thrombotic thrombocytopenic purpura (TTP) is a microangi

285 Thrombotic thrombocytopenic purpura (TTP) is a rare and

286 Thrombotic thrombocytopenic purpura (TTP) is an acute, l

287 and effective treatment, most patients with thrombotic thrombocytopenic purpura (TTP) survive the ac

288 ma ADAMTS13 activity is the primary cause of thrombotic thrombocytopenic purpura (TTP) whereas overwh

289 In acquired thrombotic thrombocytopenic purpura (TTP), an immune-med

290 13 (ADAMTS13) revolutionized our approach to thrombotic thrombocytopenic purpura (TTP).

291 characterised by thrombotic microangiopathy, thrombotic thrombocytopenic purpura is distinguished by

292 13 to make management decisions in suspected thrombotic thrombocytopenic purpura, new evidence suppor

293 us define a new 2-component paradigm wherein thrombotic tone is regulated by both COX1 and COX2 throu

294 ses and a long-term follow-up, especially on thrombotic total occlusion of main portal vein (MPV).

295 ients diagnosed with liver cirrhosis related thrombotic total occlusion of MPV and treated with TIPS

296 l outcome of TIPS on liver cirrhosis-related thrombotic total occlusion of MPV, 98 patients diagnosed

297 ffective in treating liver cirrhosis-related thrombotic total occlusion of MPV.

298 protected from thrombosis, forming less pro-thrombotic TxA(2) and PGE(2) .

299 nd complement responses but can also lead to thrombotic vascular occlusion.

300 crease in exposure on the ln-scale) of fetal thrombotic vasculopathy (FTV) both with increasing PM2.5