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1 redict altered risk of incident cirrhosis or portal hypertension.
2 ension (IPH) is a rare cause of intrahepatic portal hypertension.
3 giogenesis is implicated in fibrogenesis and portal hypertension.
4 ccurate noninvasive technique for estimating portal hypertension.
5 uent increased portal venous inflow leads to portal hypertension.
6 hosis, and might be a therapeutic target for portal hypertension.
7 l dysfunction in patients with cirrhosis and portal hypertension.
8 ortal inflow to contribute to development of portal hypertension.
9 ol for the diagnosis of clinically important portal hypertension.
10 asodilation, a mechanism that contributes to portal hypertension.
11 plasma-ascitic albumin gradient to diagnose portal hypertension.
12 position fails to eliminate complications of portal hypertension.
13 any signs of residual/recurrent features of portal hypertension.
14 to the arterial vasodilation associated with portal hypertension.
15 hether Nogo-B gene deletion could ameliorate portal hypertension.
16 s) modulates fibrogenesis, angiogenesis, and portal hypertension.
17 liary dysgenesis, portal tract fibrosis, and portal hypertension.
18 injury, with resultant sinusoidal damage and portal hypertension.
19 y 5) of developing severe liver disease with portal hypertension.
20 osis (CF) develops severe liver disease with portal hypertension.
21 atients with cystic fibrosis and significant portal hypertension.
22 and may be important in the pathogenesis of portal hypertension.
23 atients without liver failure or significant portal hypertension.
24 atic inflammation, fibrosis, congestion, and portal hypertension.
25 hepatorenal syndrome, or bleeding caused by portal hypertension.
26 eneficial effect of NO donors for therapy of portal hypertension.
27 progressive thrombocytopenia, suggestive of portal hypertension.
28 ntribute significantly to the development of portal hypertension.
29 bnormalities, which may lead to noncirrhotic portal hypertension.
30 patients with alcohol-related cirrhosis and portal hypertension.
31 patients with cirrhosis and complications of portal hypertension.
32 hospitalized patients with complications of portal hypertension.
33 rt and disclosed a transudate, suggestive of portal hypertension.
34 namic abnormalities typical of cirrhosis and portal hypertension.
35 parameter can be used to monitor therapy of portal hypertension.
36 gement of the complications of cirrhosis and portal hypertension.
37 namic abnormalities typical of cirrhosis and portal hypertension.
38 nosis and management of the complications of portal hypertension.
39 ology and management of the complications of portal hypertension.
40 nd control of bleeding in most patients with portal hypertension.
41 tic portosystemic shunt (TIPS) for cirrhotic portal hypertension.
42 ce to pulmonary blood flow in the setting of portal hypertension.
43 namic abnormalities typical of cirrhosis and portal hypertension.
44 roles in vascular abnormalities observed in portal hypertension.
45 ct changes, lymphadenopathy, and findings of portal hypertension.
46 nosis and management of the complications of portal hypertension.
47 namic abnormalities typical of cirrhosis and portal hypertension.
48 nosis and management of the complications of portal hypertension.
49 the injured liver and leads to intrahepatic portal hypertension.
50 ology and management of the complications of portal hypertension.
51 lular function, perisinusoidal fibrosis, and portal hypertension.
52 enerative hyperplasia (NRH) of the liver and portal hypertension.
53 he treatment of many of the complications of portal hypertension.
54 the 1980s for treatment of complications of portal hypertension.
55 ute inferior vena caval occlusion to produce portal hypertension.
56 tment attenuated burn- and endotoxin-induced portal hypertension.
57 are the earliest indicators of cirrhosis and portal hypertension.
58 lting in functional Budd-Chiari syndrome and portal hypertension.
59 ellular carcinoma (HCC), without evidence of portal hypertension.
60 odilation, which contributes to the onset of portal hypertension.
61 rhosis and liver failure but not in isolated portal hypertension.
62 eries of rats and mice with cirrhosis or/and portal hypertension.
63 lent option to treat severe complications of portal hypertension.
64 to vasodilators, with beneficial effects on portal hypertension.
65 but they do not accurately reflect degree of portal hypertension.
66 a specific cause of idiopathic noncirrhotic portal hypertension.
67 % [12 of 20]) underwent major resection with portal hypertension.
68 superior to liver elastography in predicting portal hypertension.
69 with protection against hepatic fibrosis and portal hypertension.
70 overweight/obese patients with cirrhosis and portal hypertension.
71 trary effects in cirrhotic and non-cirrhotic portal hypertension.
72 inically significant (CSPH) and severe (SPH) portal hypertension.
73 epresent risk factors for hepatic injury and portal hypertension.
74 h A, 6 Child-Pugh B, and 1 Child-Pugh C) and portal hypertension (11 males, median age 54 years (rang
75 wed by cholelithiasis in liver cirrhosis and portal hypertension (18.2%) and empyema or perforated ga
78 al IHBDD complicated with cholangitis and/or portal hypertension achieved excellent long-term patient
79 n, AQP1 promotes angiogenesis, fibrosis, and portal hypertension after bile duct ligation and is regu
81 s of human hepatopulmonary syndrome, whereas portal hypertension alone due to partial portal vein lig
82 esophageal varices result almost solely from portal hypertension, although the hyperdynamic circulati
83 esophageal varices result almost solely from portal hypertension, although the hyperdynamic circulati
84 rom 0% to 4%, 20 patients with cirrhosis and portal hypertension and 20 healthy volunteers with no kn
85 the only procedure that completely reverses portal hypertension and addresses the primary disease wh
86 es in unselected patients with cirrhosis and portal hypertension and are associated with an increased
87 04038 increases sodium excretion and reduces portal hypertension and ascites in experimental cirrhosi
89 ns, widely accepted in vivo animal models of portal hypertension and cirrhosis, and in vitro angiogen
92 nsfer exerts multifold beneficial effects in portal hypertension and cirrhosis: reduction of patholog
98 reduced endothelial fenestrae and developed portal hypertension and hepatic angiosarcoma over time.
100 ife-saving therapy to correct liver failure, portal hypertension and hepatocellular carcinoma arising
101 ohepatitis, NASH) associated with cirrhosis, portal hypertension and hepatocellular carcinoma, yet th
103 ress in understanding the pathophysiology of portal hypertension and improvements in the diagnosis an
107 to biliary cirrhosis and the development of portal hypertension and liver failure occurs in a minori
109 sfunction contributes to the pathogenesis of portal hypertension and may represent a novel therapeuti
112 in patients with PSC, noninvasive markers of portal hypertension and of advanced liver disease predic
114 irrhosis with its attendant complications of portal hypertension and potentially end-stage liver dise
116 imaging was performed in seven patients with portal hypertension and refractory ascites before and 2
117 obtained in properly selected patients with portal hypertension and relatively spared hepatic functi
119 fects 10%-30% of patients with cirrhosis and portal hypertension and significantly increases mortalit
121 This was accompanied by early-onset severe portal hypertension and twofold to fourfold increase in
122 patients (LD rate, 28.6% [85 of 297]) had no portal hypertension and underwent major resections or, i
124 , but in a certain group of patients without portal hypertension and well-preserved liver function re
125 therapeutic option, but in patients without portal hypertension and well-preserved liver function, r
126 , but in a certain group of patients without portal hypertension and well-preserved liver function, s
128 on PET), 1 patient had liver cirrhosis with portal hypertension, and 1 patient had a 5 cm abdominal
129 scarring from any cause leads to cirrhosis, portal hypertension, and a progressive decline in renal
130 with hepatic "recompensation," reduction of portal hypertension, and eventually avoidance of liver t
133 risk for HCC based on age, sex, evidence of portal hypertension, and history of blood transfusion us
134 nary arterial hypertension in the setting of portal hypertension, and is present in 5%-10% of cirrhos
135 hout (OR, 2.98; 95% CI, 1.97-4.52; P < .001) portal hypertension, and MELD score (OR, 1.79; 95% CI, 1
136 onalcoholic steatohepatitis, liver fibrosis, portal hypertension, and nodular regenerative hyperplasi
137 dure corrected liver function and eliminated portal hypertension, and the patient showed substantial
138 , FAH(-/-) pigs developed liver fibrosis and portal hypertension, and thus may serve as a large-anima
139 ere hepatosplenism, periportal fibrosis with portal hypertension, and urogenital inflammation and sca
140 rding the management of the complications of portal hypertension are reviewed, including a trial of b
141 rding the management of the complications of portal hypertension are reviewed, including trials that
143 patients with compensated cirrhosis and with portal hypertension as determined by the hepatic venous
144 Recursive partitioning analysis confirmed portal hypertension as the most important factor (OR, 2.
146 s used to act on the mechanisms that lead to portal hypertension, as well as recent advances in the d
147 transfer on angiogenesis, fibrogenesis, and portal hypertension-associated hemodynamic alterations w
148 provides evidence that vasohibin-1 regulates portal hypertension-associated pathological angiogenesis
150 er cirrhosis is complicated by bleeding from portal hypertension but also by portal vein thrombosis (
152 213 subjects with compensated cirrhosis with portal hypertension but without GEV enrolled in a random
153 213 patients with compensated cirrhosis and portal hypertension but without varices included in a tr
154 fects 10%-30% of patients with cirrhosis and portal hypertension, but the impact on functional status
156 tients with CF and severe liver disease with portal hypertension (CFLD) from 63 CF centers in the Uni
157 ality Improvement Program (NSQIP) formed the portal hypertension cohort, and were case matched to pat
159 re needed to identify clinically significant portal hypertension (CSPH) and esophageal varices (EVs)
160 CLD), the presence of clinically significant portal hypertension (CSPH) and varices needing treatment
161 Whether preoperative clinically significant portal hypertension (CSPH) has or not an impact on the o
162 nty-four patients had clinically significant portal hypertension (CSPH), of whom 59 had severe portal
163 ssociated cirrhosis and clinical significant portal hypertension (CSPH, hepatic venous pressure gradi
164 t (HVPG), and predict clinically significant portal hypertension (CSPH; HVPG >/= 10 mmHg), decompensa
167 llnesses include connective tissue diseases, portal hypertension, diet and stimulant drug use, HIV in
168 varices, which are most commonly a result of portal hypertension, downhill esophageal varices result
170 ne recipients have evidence of non-cirrhotic portal hypertension due to periportal liver fibrosis or
171 c varices (GV) occur in 20% of patients with portal hypertension either in isolation or in combinatio
172 s pressure would be valuable when diagnosing portal hypertension, evaluating patient prognosis, and m
173 ediating inherited and acquired noncirrhotic portal hypertension, expand the phenotypic spectrum of D
174 rices (EVs) or having clinically significant portal hypertension (for presurgical risk stratification
175 had cirrhosis with clinical complications of portal hypertension from all patients (n = 271,030) hosp
177 nrolled patients with compensated cirrhosis, portal hypertension (hepatic venous pressure gradient [H
178 determined any relationship with severity of portal hypertension (hepatic venous pressure gradient me
179 onitis, the cardiopulmonary complications of portal hypertension (hepatopulmonary syndrome, portopulm
180 lity were associated with the development of portal hypertension, hepatosplenomegaly, gastrointestina
181 .1; 95% CI, 2.0 to 8.3), PAH associated with portal hypertension (HR, 3.6; 95% CI, 2.4 to 5.4), modif
183 ss vary differently with respect to cause of portal hypertension (ie, congestion- or cirrhosis-induce
184 eoside analogue didanosine is known to cause portal hypertension in a subset of patients and lowers d
185 l hemorrhage is a concerning complication of portal hypertension in children, the first bleed appears
193 t leads to better control of RA secondary to portal hypertension in patients with cirrhosis, compared
194 lications related to liver insufficiency and portal hypertension in patients with heavy alcohol intak
196 nosis and management of the complications of portal hypertension in the face of an increasing burden
197 early-onset familial idiopathic noncirrhotic portal hypertension, in which Mendelian mutations may ac
198 c topics reviewed are the pathophysiology of portal hypertension (including recent findings regarding
199 m 66 children with major endoscopic signs of portal hypertension, including grade 3 esophageal varice
201 aimed at modifying the factors that lead to portal hypertension (increased intrahepatic vascular res
202 aimed at modifying the factors that lead to portal hypertension (increased intrahepatic vascular res
211 re gradient (HVPG) is based on the fact that portal hypertension is pathogenically related to liver i
218 omoting liver sinusoidal capillarization and portal hypertension, ischemic heart disease, peripheral
219 is and management of idiopathic noncirrhotic portal hypertension, its pathogenesis remains elusive.
220 lt of diffuse portomesenteric thrombosis and portal hypertension, life-threatening bleeding was unres
221 ociated with the development of noncirrhotic portal hypertension, likely owing to injury to the micro
222 portosystemic shunt (TIPS) in patients with portal hypertension may be considered as a rescue therap
223 ed with progressively developed fibrosis and portal hypertension (mean stiffness at 80 Hz and 48-week
224 t hepatic fibrogenesis and cirrhosis, marked portal hypertension, microcirculatory dysfunction, an en
225 mly assigned 213 patients with cirrhosis and portal hypertension (minimal hepatic venous pressure gra
228 nce of Nogo-B ameliorates liver fibrosis and portal hypertension, Nogo-B blockade may be a potential
230 ght subjects from six kindreds with onset of portal hypertension of indeterminate etiology during inf
231 lustrate the potential independent effect of portal hypertension on clinical outcome outside the sett
233 ections or, in case of minor resections, had portal hypertension or a MELD score greater than 9; and
234 tio [OR], 2.41; 95% CI, 1.17-4.30; P = .01), portal hypertension (OR, 2.20; 95% CI, 1.13-4.30; P = .0
235 ephalopathy, esophageal varices, ascites, or portal hypertension) or liver transplant were estimated
236 e at risk of developing liver insufficiency, portal hypertension, or bowel infarction and may experie
238 sence of a high-flow fistula, which elevated portal hypertension, patient did not qualify for the liv
239 the standard used to determine the degree of portal hypertension (PH) and an important prognostic fac
240 arkers would be useful for the assessment of portal hypertension (PH) and esophageal varices (EV) in
247 hosis, and the presence of clinical signs of portal hypertension (PH) were assessed using receiver op
259 with preoperative hierarchic interaction of portal hypertension, planned extension of hepatectomy, a
260 anulomatous inflammation in the liver causes portal hypertension, porto-pulmonary shunting, bleeding
263 within a prospective cohort of patients with portal hypertension recruited from tertiary care centers
264 oportions of patients in the LVP+A group had portal hypertension-related bleeding (18% vs 0%; P = .01
267 ntrahepatic bile ducts + 2 x dysmorphy + 1 x portal hypertension; score with gadolinium administratio
268 mic encephalopathy, is a consequence of both portal hypertension (shunting of blood through portosyst
269 emic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosyst
270 emic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosyst
271 emic encephalopathy is a consequence of both portal hypertension (shunting of blood through portosyst
273 disease; ascites plays no role in this, but portal hypertension stiffens the gastric walls and creat
275 e better control of these 2 complications of portal hypertension than standard forms of therapy.
276 nosis and management of the complications of portal hypertension that have occurred in the last year
277 osis, and management of the complications of portal hypertension that have occurred in the last year.
278 osis, and management of the complications of portal hypertension that have occurred in the past year.
280 Hepatic stellate cells (HSCs) contribute to portal hypertension through multiple mechanisms that inc
281 ne age; sex; performance status; presence of portal hypertension; tumor distribution; levels of bilir
282 t survival in patients with complications of portal hypertension undergoing elective placement of tra
283 cardiography (TEE) in patients with signs of portal hypertension undergoing orthotopic liver transpla
284 rts of patients with idiopathic noncirrhotic portal hypertension undergoing TIPS in seven centers bet
285 patients (LD rate, 4.9% [11 of 226]) without portal hypertension underwent minor resection with a MEL
286 transit in patients with liver cirrhosis and portal hypertension using a magnet-based Motility Tracki
287 scular diseases and is associated with liver portal hypertension, vascular shunting, and portal fibro
289 s induced in rats by bile duct ligation, and portal hypertension was induced by partial portal vein l
290 Cirrhosis was present in 157 patients (91%); portal hypertension was present in 139 patients (81%).
292 Hispanics hospitalized for complications of portal hypertension were less likely to undergo a pallia
294 unt is the best predictor of the severity of portal hypertension, which has early onset but is underd
295 In patients with idiopathic noncirrhotic portal hypertension who have normal kidney function or d
296 cutive patients with severe complications of portal hypertension who received placement of TIPS from
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