ライフサイエンスコーパス: cirrhosis

1 he reversal of bouts of OHE in patients with cirrhosis.

2 s at follow-up examinations of patients with cirrhosis.

3 male, 82% were treatment naive, and 20% had cirrhosis.

4 results, and various grades of fibrosis and cirrhosis.

5 88) had severe fibrosis, and 9% (n = 38) had cirrhosis.

6 biopsy, transient elastography, and clinical cirrhosis.

7 tion and progression of PVT in patients with cirrhosis.

8 itis C virus (HCV) infection and compensated cirrhosis.

9 an be observed in patients with pre-existing cirrhosis.

10 ed MRI for diagnosis of HCC in patients with cirrhosis.

11 s of SVR in patients with HCV genotype 3 and cirrhosis.

12 ors of the absolute risk for alcoholic liver cirrhosis.

13 mpensation rate in both HBV- and HCV-related cirrhosis.

14 H), hereditary dyslipidaemia, or cryptogenic cirrhosis.

15 >/=10 000 IU/mL) with or without compensated cirrhosis.

16 eased decompensation rate in alcohol-related cirrhosis.

17 nfection, particularly among persons without cirrhosis.

18 rovided a high level of SVR in those without cirrhosis.

19 irst-degree relatives of probands with NAFLD-cirrhosis.

20 D, from steatosis to hepatic inflammation to cirrhosis.

21 infection, including those with compensated cirrhosis.

22 liver cancer stem cells together with liver cirrhosis.

23 least moderate fibrosis and, in some cases, cirrhosis.

24 options that are applicable to patients with cirrhosis.

25 e men, 48 (45%) were black, and 19 (18%) had cirrhosis.

26 ings, suicide, and chronic liver disease and cirrhosis.

27 subtype 3a HCV and 39 (35%) had compensated cirrhosis.

28 nged after excluding subjects with suspected cirrhosis.

29 ompared with 68 of 72 (94%) patients without cirrhosis.

30 the leading cause of death in patients with cirrhosis.

31 groups, 46% of the patients had compensated cirrhosis.

32 orated in prognostic scores in patients with cirrhosis.

33 C remained high in patients with established cirrhosis.

34 m, similar to the Child-Pugh-Score for liver cirrhosis.

35 ia-lowering therapy to reverse sarcopenia of cirrhosis.

36 infections other than HBV and HDV, or liver cirrhosis.

37 are infrequently performed in patients with cirrhosis.

38 e 1, 2, 4, 5, or 6 infection and compensated cirrhosis.

39 , and HCC in HBV-, HCV-, and alcohol-related cirrhosis.

40 d by steatosis, inflammation, and eventually cirrhosis.

41 processes impact the risk for NASH and NASH cirrhosis.

42 atocellular carcinoma (HCC) in patients with cirrhosis.

43 indeterminate liver nodules in patients with cirrhosis.

44 ted in 20.6% of patients but no patients had cirrhosis.

45 ically disadvantaged cohort of patients with cirrhosis.

46 tients infected with HCV genotype 1b without cirrhosis.

47 tes to thrombotic complications occurring in cirrhosis.

48 on for advanced liver fibrosis (0.9-2.0%) or cirrhosis (0.1-1.7%) narrowed the estimates of prevalenc

49 nce of advanced liver fibrosis (0-27.9%) and cirrhosis (2.4-4.0%) than those in the general populatio

50 specialty care, 11 had advanced fibrosis or cirrhosis, 20 started treatment, and 9 achieved sustaine

51 Of the 39 patients with cirrhosis, 31 (79%) achieved SVR12, compared with 68 of

52 Results In patients with compensated cirrhosis, 40% (129 of 326) experienced decompensation d

53 1.5 times the upper limit of normal 13%; and cirrhosis 6%.

54 ull cohort with compensated or decompensated cirrhosis, 61% (504 of 830) died during the median follo

55 rior treatment experience and/or compensated cirrhosis achieved high SVR12 rates following 12 or 16 w

56 vs 0.34/100 person-years in patients without cirrhosis; adjusted hazard ratio, 4.73.

57 Projected changes in NAFLD-related cirrhosis, advanced liver disease, and liver-related mor

58 as a new treatment for renal dysfunction in cirrhosis, although further validation in patients with

59 Cirrhosis among patients was associated with an MRR of 4

60 ly different among patients with (i) Child-A cirrhosis and (ii) single HCC lesion, although DFS was w

61 h SVR was 0.37 (0.22-0.63) for those without cirrhosis and 0.54 (0.31-0.92) for those with cirrhosis

62 prospective cohort of 26 probands with NAFLD-cirrhosis and 39 first-degree relatives.

63 system and inflammation in 59 patients with cirrhosis and 59 age-matched controls.

64 liver samples from 12 patients with ALD and cirrhosis and 9 healthy individuals (controls) and analy

65 in patients with cirrhosis; in patients with cirrhosis and an indeterminate mass, there were insuffic

66 No studies examined whether adults with cirrhosis and an indeterminate nodule are best evaluated

67 Among patients with cirrhosis and an occurrence of HE, 38% (n = 445) had a h

68 tiveness in patients with Child-Pugh class B cirrhosis and any moderating effects of health system ch

69 death in a national cohort of patients with cirrhosis and ascites in their last year of life.

70 We randomized 54 stable outpatients with cirrhosis and ascites to rifaximin 550 mg twice a day (n

71 prove systemic hemodynamics in patients with cirrhosis and ascites; rifaximin did not affect glomerul

72 care institutes in India, 370 patients with cirrhosis and bouts of OHE were screened.

73 disease progression to advanced fibrosis or cirrhosis and cancer.

74 the liver, including inflammation, fibrosis/cirrhosis and cancer.

75 ction in the liver, which could develop into cirrhosis and cancer.

76 ntegrated Research Database on patients with cirrhosis and chronic liver failure (CLF) from 2006 thro

77 : Patients with hepatitis C virus-associated cirrhosis and clinical significant portal hypertension (

78 nd validated a GFR equation specifically for cirrhosis and compared the performance of the new derive

79 matrix by myofibroblasts that often leads to cirrhosis and consequently liver dysfunction and death.

80 6 patients with hepatitis C virus-associated cirrhosis and CSPH who had SVR to interferon-free therap

81 tive therapy for patients with decompensated cirrhosis and fulminant liver failure.

82 B (CHB), Hepatitis B virus (HBV)-associated cirrhosis and HBV-associated carcinoma are high and incr

83 han in Class A and Class B in HBV-associated cirrhosis and HBV-associated HCC groups.

84 sociated with HCV infection is implicated in cirrhosis and HCC, but the molecular players and signali

85 implicating ATX/LPA in the causative link of cirrhosis and HCC.

86 ed States, where they are a growing cause of cirrhosis and hepatocellular carcinoma (HCC) and increas

87 lay an important role in the pathogenesis of cirrhosis and hepatocellular carcinoma (HCC), most cases

88 ple in the world and it is a common cause of cirrhosis and hepatocellular carcinoma (HCC).

89 us (HCV) infection is a major cause of liver cirrhosis and hepatocellular carcinoma and the leading i

90 V can cause severe liver diseases, including cirrhosis and hepatocellular carcinoma, and is one of th

91 y liver disease (NAFLD), a common prelude to cirrhosis and hepatocellular carcinoma, is the most comm

92 to others and disease progression, including cirrhosis and hepatocellular carcinoma.

93 m around the world and often causes fibrosis/cirrhosis and hepatocellular carcinoma.

94 nic liver infection, which may lead to liver cirrhosis and hepatocellular carcinoma.

95 and mortality due to complications of liver cirrhosis and hepatocellular carcinoma.

96 The association of advanced fibrosis/cirrhosis and incident CHF persisted regardless of HIV/H

97 phalopathy (HE) is a serious complication of cirrhosis and is associated with gut dysbiosis.

98 SH), which is associated with progression to cirrhosis and is rapidly becoming the leading indication

99 Patients who have liver cirrhosis and liver cancer also have reduced farnesoid X

100 , blood donation) and cause hepatitis, liver cirrhosis and liver cancer.

101 hepatitis (NASH) has become a major cause of cirrhosis and liver-related deaths worldwide.

102 ive strategy for patients with decompensated cirrhosis and MELD score greater than 13.

103 ant retrospective study, adult patients with cirrhosis and Model for End-Stage Liver Disease (MELD) s

104 l pressure in overweight/obese patients with cirrhosis and portal hypertension.

105 ction and renal dysfunction in patients with cirrhosis and portal hypertension.

106 ic inflammation that promotes progression to cirrhosis and predisposes to the development of hepatoce

107 ce rebleeding and mortality in patients with cirrhosis and previous variceal bleeding stratified by c

108 atic review and meta-analysis, patients with cirrhosis and PVT who receive anticoagulant therapy have

109 or warfarin vs no therapy) in patients with cirrhosis and PVT; these studies reported rates of compl

110 to increase the proportion of patients with cirrhosis and recurrent ascites who survive transplantat

111 to increase survival times of patients with cirrhosis and refractory ascites.

112 er validation in patients with more advanced cirrhosis and renal dysfunction is required.

113 s for developing physical disorders, such as cirrhosis and sleep disorders, were also noted as well a

114 RI or gadoxetate-enhanced MRI in adults with cirrhosis and suspected HCC.

115 al therapies, particularly for patients with cirrhosis and those who are treatment experienced, where

116 ivity in human patients diagnosed with liver cirrhosis and to determine the effectiveness of a chemic

117 als of adults (>18 years) with decompensated cirrhosis and type 1 hepatorenal syndrome that compared

118 h the progression from CHB to HBV-associated cirrhosis and ultimately to HBV-associated HCC.

119 26 patients with alcoholic cirrhosis and variceal haemorrhage were studied prior to

120 To investigate the association between cirrhosis and various stroke types.

121 A total of 3410 patients with CHC (1014 with cirrhosis), and 67 315 matched individuals were included

122 One patient had cirrhosis, and 42 did not; in 57 patients the degree of

123 ients (KT = 60, LT = 347, DLK = 36); 42% had cirrhosis, and 54% had failed prior antiviral therapy.

124 ent demographics, comorbidities, presence of cirrhosis, and annual surgical hospital volume.

125 epatic inflammation leads to liver fibrosis, cirrhosis, and cancer in a significant number of patient

126 vely leads to cholestasis, hepatic fibrosis, cirrhosis, and eventually liver failure.

127 atients who are treatment-naive, do not have cirrhosis, and have a pretreatment viral load <6,000,000

128 carriers are at risk of developing fibrosis, cirrhosis, and hepatocellular carcinoma.

129 V is a major cause of viral hepatitis, liver cirrhosis, and hepatocellular carcinoma.

130 t microbiota may be altered in patients with cirrhosis, and may further change after administration o

131 onic lower respiratory tract diseases, liver cirrhosis, and spinal disc herniation); causes of mortal

132 drug poisonings), chronic liver disease and cirrhosis, and suicide.

133 The latter leads to steatohepatitis, cirrhosis, and the formation of hepatic adenomas and car

134 cularly nonalcoholic fatty liver disease and cirrhosis, and this was true even among patients without

135 4 HCV infection, with or without compensated cirrhosis, and with an estimated glomerular filtration r

136 Index score 1.45-3.25 [44%] and >3.25 [17%, cirrhosis]) and 30% were HCV treatment experienced.

137 sease, nonalcoholic fatty liver disease, and cirrhosis (any etiology).

138 determine whether or not NASH progresses to cirrhosis are also unclear.

139 ients with HCV genotype 1b infection without cirrhosis are limited; shortening the treatment duration

140 HCC in populations where viral hepatitis and cirrhosis are prevalent.

141 th chronic HCV genotype 1b infection without cirrhosis (as assessed by liver biopsy, transient elasto

142 Cirrhosis, as defined by a validated diagnosis code algo

143 assessed correlates of significant fibrosis/cirrhosis at 1 year on ART.

144 ere more likely to have significant fibrosis/cirrhosis at 1 year on ART.

145 -naive patients with and without compensated cirrhosis at 15 sites in Canada.

146 udy of patients with documented or suspected cirrhosis at a large safety-net health system from Decem

147 2016, for studies that enrolled adults with cirrhosis awaiting LT and treated with bridging or down-

148 ional study includes cohort of patients with cirrhosis before liver transplantation (cohort A) and a

149 ibrosis was noted in 26.8%, whereas 5.4% had cirrhosis but were clinically compensated.

150 cute kidney injury in patients with advanced cirrhosis, but current therapy with systemic vasoconstri

151 ersons were more likely to be obese and have cirrhosis, but less likely to have stage 3-5 chronic kid

152 is safe and effective in patients with liver cirrhosis, but no adequately powered randomised controll

153 ion; these changes in LV function related to cirrhosis can be assessed using robust echocardiographic

154 PIs), frequently prescribed to patients with cirrhosis, can contribute to small-bowel bacterial overg

155 ge-animal model of HT1, develop fibrosis and cirrhosis characteristic of the human disease.

156 Turcotte-Pugh scores ( P < .001), and higher Cirrhosis Comorbidity Index scores ( P = .01).

157 irrhosis and 0.54 (0.31-0.92) for those with cirrhosis compared with their respective counterparts wi

158 dary to portal hypertension in patients with cirrhosis, compared with an 8-mm stent, without increasi

159 Portal vein hypertension (PVH) in liver cirrhosis complicated with portal venous thrombosis (PVT

160 lifestyles and can progress to fibrosis and cirrhosis contributing to premature death.

161 tly approved for patients with decompensated cirrhosis (DC) secondary to hepatitis C virus (HCV), is

162 atocellular carcinoma (HCC) or decompensated cirrhosis (DCC).

163 omographic (CT) images, allows prediction of cirrhosis decompensation and death.

164 stiffness suggestive of significant fibrosis/cirrhosis decreased following ART initiation-regardless

165 in percentages of patients with compensated cirrhosis (decreases in percentages of patients with cir

166 ving cirrhosis; the remainder did not have a cirrhosis determination.

167 ndence) during 1998-2002 for alcoholic liver cirrhosis development (n = 36,044).

168 LV systolic function is enhanced in cirrhosis due to augmented adrenergic tone and modulated

169 ecompensation and mortality in patients with cirrhosis due to hepatitis C virus (HCV).

170 ed to cirrhosis in the general population or cirrhosis due to other causes, such as hepatitis B virus

171 ividuals aged 50 years with well-compensated cirrhosis entering surveillance.

172 ected with all HCV genotypes with or without cirrhosis, except patients with genotype 3 and cirrhosis

173 Over one fourth of patients with cirrhosis experience physical harm for false-positive or

174 ir F0-F1), significant fibrosis (F2-F3), and cirrhosis (F4).

175 Patients with cirrhosis followed at a large urban hospital were invite

176 dothelial cell therapy in a porcine model of cirrhosis for liver regeneration.

177 -year cumulative incidences of decompensated cirrhosis from 12.2% to 4.5%, hepatocellular carcinoma f

178 s (decreases in percentages of patients with cirrhosis from HCV or ALD, but increase in percentages o

179 ng rates due to hepatitis C and emergence of cirrhosis from non-alcoholic fatty liver disease.

180 but increase in percentages of patients with cirrhosis from nonalcoholic steatohepatitis [NASH]), CLF

181 cancer screening in patients with high-risk cirrhosis generates positive and negative predictive val

182 ssment in cirrhosis, the Royal Free Hospital cirrhosis GFR, using readily available variables; this r

183 carnitine level was higher in HBV-associated cirrhosis group than in other two groups.

184 fibrosis (8.0-12.3 kPa) and severe fibrosis/cirrhosis (>12.3 kPa).

185 lustering, and microbiota from patients with cirrhosis had less marked alpha diversity.

186 However, patients with cirrhosis had lower abundances of five phyla, namely Ten

187 All 19 patients with cirrhosis had SVR12.

188 Patients with cirrhosis had the highest annual incidence of HCC after

189 irst-degree relatives of probands with NAFLD-cirrhosis have a 12 times higher risk of advanced fibros

190 e consequences, including the development of cirrhosis, hepatic failure, and hepatocellular carcinoma

191 w disease progression and reduce the risk of cirrhosis, hepatocellular carcinoma (HCC), and CHB-assoc

192 lly progresses from chronic HCV to fibrosis, cirrhosis, hepatocellular carcinoma (HCC), and death.

193 including nonalcoholic fatty liver disease, cirrhosis, hepatocellular carcinoma, gallstones, acute p

194 uses progressive fibrosis leading to biliary cirrhosis; however, its cause(s) and early pathogenesis

195 (HR, 1.40; 95% CI, 1.24-1.58), decompensated cirrhosis (HR, 1.49; 95% CI, 1.30-1.70), and treatment i

196 n intraportal technique for the treatment of cirrhosis in a porcine model.

197 MRs among patients with CHC with or without cirrhosis in Denmark compared with the general populatio

198 erum-based fibrosis markers for detection of cirrhosis in patients with hepatitis C virus (HCV), hepa

199 The IRR for alcoholic liver cirrhosis in the cohort relative to the general populati

200 er this beneficial effect can be extended to cirrhosis in the general population or cirrhosis due to

201 ted as the incidence rate of alcoholic liver cirrhosis in these patients relative to the general popu

202 patitis (NASH) and NAFLD-related fibrosis or cirrhosis in these patients than in individuals without

203 teatohepatitis (NASH), which can progress to cirrhosis in up to 20% of NASH patients.

204 disease, including those with decompensated cirrhosis, in routine practice (all currently approved r

205 preferred for HCC diagnosis in patients with cirrhosis; in patients with cirrhosis and an indetermina

206 patients with HCV infection and compensated cirrhosis included in the CirVir cohort who achieved an

207 tients with HCV genotype 1 infection without cirrhosis, including those with HIV co-infection.

208 In cirrhosis, increased intrahepatic vascular resistance (I

209 GROUND & AIMS: Surveillance of patients with cirrhosis increases early detection of hepatocellular ca

210 , we found that use of PPIs in patients with cirrhosis increases the risk for HE; risk increases with

211 py to patients with HCC and well-compensated cirrhosis instead of primary LT because it may lead to b

212 as significantly higher in patients who knew cirrhosis is a risk factor for developing HCC (odds rati

213 Acute-on-chronic liver failure (ACLF) in cirrhosis is an increasingly recognized syndrome charact

214 Cirrhosis is associated with hemorrhagic and thrombotic

215 liver failure (ACLF) in patients with liver cirrhosis is associated with high mortality rates.

216 Decompensated cirrhosis is characterized by disturbed systemic and spl

217 t gold-standard monitoring for patients with cirrhosis is cost-effective, attributed to a higher prob

218 thogenesis of hepatic encephalopathy (HE) in cirrhosis is multifactorial and ammonia is thought to pl

219 ellular carcinoma (HCC) for individuals with cirrhosis is recommended.

220 Alcoholic liver cirrhosis is usually preceded by many years of heavy dri

221 lic fatty liver disease and cirrhosis (NAFLD-cirrhosis) is unknown and needs to be systematically qua

222 ak = 2), or severe (Ishak = 3,4) fibrosis or cirrhosis (Ishak = 5,6).

223 Advanced stages of liver cirrhosis lead to a dramatically increased mortality.

224 ents with HIV/HCV coinfection, decompensated cirrhosis, liver and kidney transplants, and end-stage l

225 PRMT1 loss in individuals with cirrhosis may contribute to their immune defects.

226 059 beneficiaries, 15586 patients (1.0%) had cirrhosis (mean [SD] age, 74.1 [6.9] years; 7263 [46.6%]

227 Among 26,577 patients with cirrhosis (median follow-up = 4.7 years), the mean PTUDS

228 inical outcomes in patients with hepatitis C cirrhosis (n = 216), suggesting it may have a protective

229 ts with nonalcoholic fatty liver disease and cirrhosis (NAFLD-cirrhosis) is unknown and needs to be s

230 mellitus, AIDS, end-stage renal disease, and cirrhosis), need for intensive care, and mortality.

231 year of transplantation, underlying cause of cirrhosis, neutrophil-lymphocyte ratio, history of locor

232 = 0.29-0.98), and further decompensation of cirrhosis occurred in 52% versus 72% (HR = 0.68; 95% CI

233 lcoholic liver disease (65.1%), fibrosis and cirrhosis of the liver (23.7%), and mental and behaviora

234 6, we enrolled 146 patients with compensated cirrhosis, of whom 48 (33%) had genotype 1a HCV infectio

235 ents, particularly in those with compensated cirrhosis; older age (especially >/=50 years), lower pla

236 ten has adverse consequences (development of cirrhosis or liver cancer).

237 eating HCV genotype-4 infected patients with cirrhosis or postliver transplantation.

238 fibrosis, and 16.3% (95% CI, 7.0-35.1) with cirrhosis (P < 0.01).

239 Gut microbiota from cirrhosis patients and controls showed differential clus

240 product) was higher in SAH versus alcoholic cirrhosis patients and healthy controls (P < 0.05).

241 Cirrhosis patients at risk for 3-month postdischarge mor

242 mal MELD threshold below which decompensated cirrhosis patients should receive HCV treatment while aw

243 elates of surveillance benefits and harms in cirrhosis patients undergoing HCC surveillance.

244 Ex vivo studies showed that platelets from cirrhosis patients were more responsive to the agonists

245 ronic liver scarring from any cause leads to cirrhosis, portal hypertension, and a progressive declin

246 eases the risk of clinical decompensation in cirrhosis, possibly by increasing portal pressure.

247 suggesting it may have a protective role in cirrhosis progression.These findings reinforce the value

248 Patients with decompensated cirrhosis receiving DAAs present lower response rates an

249 ion of MPV, 98 patients diagnosed with liver cirrhosis related thrombotic total occlusion of MPV and

250 niques and clinical outcome of TIPS on liver cirrhosis-related thrombotic total occlusion of MPV, 98

251 TIPS is safe and effective in treating liver cirrhosis-related thrombotic total occlusion of MPV.

252 luation of cardiac function in patients with cirrhosis remains a challenge.

253 nd, if untreated, can progress eventually to cirrhosis requiring liver transplantation (LT) before th

254 .0-67.7) with moderate, severe fibrosis, and cirrhosis, respectively (P < 0.01).

255 re significant predictors of alcoholic liver cirrhosis risk in men and women, whereas civil status, e

256 and previous variceal bleeding stratified by cirrhosis severity (Child A versus B/C) by means of indi

257 Among patients with cirrhosis, statin use decreased the risk of decompensati

258 in rat models and exploratory study in human cirrhosis suggest the therapeutic potential of selective

259 nd may predispose to HCC in patients without cirrhosis, suggesting it should be evaluated in future p

260 Among those with cirrhosis, SVR12 was achieved by 98% (39/40; 95% CI, 87-

261 lic strain rate were higher in patients with cirrhosis than in controls (median [1st-3rd quartile], 4

262 uent, potentially reversible complication in cirrhosis that adversely affects clinical outcomes.

263 ere are specific cardiovascular responses in cirrhosis that can be detrimental to the LT candidate.

264 yperammonemia is a consistent abnormality in cirrhosis that results in impaired skeletal muscle prote

265 patients with normal ALP and no evidence of cirrhosis, the 5-year incidence rate of PBC was 16%.

266 0.47-0.79) among patients with decompensated cirrhosis, the median survival benefit was 31 days, and

267 d a new accurate model for GFR assessment in cirrhosis, the Royal Free Hospital cirrhosis GFR, using

268 Forty percent were assessed as not having cirrhosis; the remainder did not have a cirrhosis determ

269 in patients with acutely decompensated liver cirrhosis, though determining CysC at day 3 did not prov

270 ss, is present in up to 30% of patients with cirrhosis, thus challenging perioperative management.

271 3, lysoPC a C20:4) were observed from CHB to cirrhosis to carcinoma; lower levels of lysoPC a C20:4 w

272 , in increasing the numbers of patients with cirrhosis undergoing surveillance for HCC in a racially

273 l disease, and 327 consecutive patients with cirrhosis underwent the ANT1 .

274 It is a challenge to treat patients with cirrhosis using anticoagulants, because of the perceptio

275 SVR12 in GT3-infected patients with cirrhosis was 83% (10 of 12) after 12 weeks of treatment

276 Liver cirrhosis was already present in 62 patients at first pr

277 The risk of cirrhosis was highest among patients with PsO with an ST

278 Cirrhosis was predictive of reduced SVR (0.51 [95% confi

279 was not associated with lower SVR rates, but cirrhosis was.

280 rrhosis, except patients with genotype 3 and cirrhosis, was designed to test the noninferiority of 8

281 sociated with HCC incidence in patients with cirrhosis were age, antiviral treatment, and high sICAM-

282 From 1994 to 2012, all R&T HCC patients with cirrhosis were enrolled in the SLT strategy.

283 Few patients with HCV genotype 1a and cirrhosis were enrolled.

284 A total of 1350 patients with cirrhosis were enrolled.

285 Patients with cirrhosis were identified from a representative cohort o

286 irst-degree relatives of probands with NAFLD-cirrhosis were odds ratio 14.9 (95% CI, 1.8-126.0, P = 0

287 gylated interferon therapy) patients without cirrhosis were randomized 1:1 to receive 12 or 16 weeks

288 A total of 50 patients without cirrhosis were randomized to three arms: 200 mg GLE + 80

289 ibrosis) and FIB-4 > 3.25 (advanced fibrosis/cirrhosis) were associated with CHF (hazard ratio [95% c

290 patients had HCV infection and biopsy-proven cirrhosis, were Child-Pugh class A, and had no prior liv

291 atohepatitis (NASH) can lead to fibrosis and cirrhosis, which permanently damage the liver.

292 with genotype 1b infection with and without cirrhosis who received coformulated ombitasvir, paritapr

293 Among participants with cirrhosis who were infected with genotype 3, SVR12 for t

294 tify LT-eligible patients with decompensated cirrhosis who would benefit (and not benefit) from pre-L

295 f at least 10 000 IU/mL, without evidence of cirrhosis, who had not received previous treatment for H

296 rn that the cured patient with decompensated cirrhosis will find themselves in "MELD purgatory" with

297 Patients with cirrhosis with controlled variceal bleeding were randomi

298 ent in a consecutive series of patients with cirrhosis with refractory ascites (RA).

299 d compensated liver disease (with or without cirrhosis) with severe renal impairment, dependence on d

300 eased portal pressure (PP) in both models of cirrhosis without changes in portal blood flow, suggesti