ライフサイエンスコーパス: decompensation

1 rtality and eight for postoperative clinical decompensation).

2 identifying patients without risk of cardiac decompensation.

3 n males, erasure leads to permanent X dosage decompensation.

4 29% had at least 1 previous episode of liver decompensation.

5 nd to be independently predictive of hepatic decompensation.

6 XO females, like XY males, develop X dosage decompensation.

7 s despite SVR, indicating persistent risk of decompensation.

8 se (SVR) to therapy, remain at risk of liver decompensation.

9 palmar plantar erythrodysesthesia, and liver decompensation.

10 which could affect determination of risk for decompensation.

11 and those with cirrhosis and severe hepatic decompensation.

12 not cost-effective among those with hepatic decompensation.

13 o adverse events, patient decision, or liver decompensation.

14 estoration of liver mass, and leads to liver decompensation.

15 nts and in those with no previous history of decompensation.

16 provement after PTRAS in patients with acute decompensation.

17 -treat population and are at risk of hepatic decompensation.

18 s died, mainly from complications of hepatic decompensation.

19 ned absence to regeneration arrest and liver decompensation.

20 d ventricular contraction during hemodynamic decompensation.

21 .17; P = 0.01) were associated with death or decompensation.

22 performed at the time of the patient's acute decompensation.

23 ted with systemic inflammation and cirrhosis decompensation.

24 ic and functional protection against cardiac decompensation.

25 Gq and CaMKIIdelta recapitulates hypertrophy decompensation.

26 mainly from complications related to hepatic decompensation.

27 ervention initiated after FTC due to cardiac decompensation.

28 diplopia, motility disturbances, and corneal decompensation.

29 a clinical benefit, as it prevented hepatic decompensation.

30 respectively, and 2 patients died of hepatic decompensation.

31 ansplant without any biochemical evidence of decompensation.

32 ficant PH (CSPH) were protected from hepatic decompensation.

33 ignificantly based on severity of presenting decompensation.

34 ociated with higher risks of HCC and hepatic decompensation.

35 liver injury or clinically relevant hepatic decompensation.

36 s and patients may continue to be at risk of decompensation.

37 graphy ruled out the risk of further cardiac decompensation.

38 exposure to statins on survival and hepatic decompensation.

39 ntegrin function, augmenting disease-induced decompensation.

40 ic stenosis was also associated with cardiac decompensation.

41 based on the short-term likelihood of liver decompensations.

42 he follow-up was 0.010 eye-year (EY); cornea decompensation, 0.001 EY; ocular hypertension, 0.008 EY;

43 sease and Child-Turcotte-Pugh scores (HR for decompensation, 0.55; 95% CI, 0.39-0.78), and death (HR,

44 hite, 60% genotype 1a, 30% METAVIR F3-F4, 4% decompensation, 11% cholestatic recurrence, 7% had kidne

45 roportion of women with a history of hepatic decompensation (13%) than women with compensated cirrhos

46 nts with cirrhosis with no evidence of acute decompensation, 20 patients with septic shock but no cir

47 Among patients with HFpEF and recent decompensation, 24-week treatment with vericiguat at eit

48 loping clinical outcomes were: prior hepatic decompensations (3.42 [1.28-9.12]), pre-treatment CPT cl

49 loping clinical outcomes were: prior hepatic decompensations (3.42 [1.28-9.12]), pretreatment CPT cla

50 us 49%, P < 0.01) and lower rates of hepatic decompensation (37% versus 62%, P = 0.04) than controls.

51 The indications were corneal decompensation (39.4%), malpositioned AC IOL (28.9%), uv

52 ncluded cystoid macular edema (10%), corneal decompensation (6%), and choroidal effusion (4%).

53 a significant reduction in incident hepatic decompensation (6.5% vs. 11.6%, adjusted odds ratio [AOR

54 ections (8% vs. 6%; P = 0.47), and events of decompensation (9% vs. 10%; P = 0.78) occurred at simila

55 confidence interval, 1.56-7.73) and hepatic decompensation (9.91; 2.14-45.92).

56 SI) is involved in the pathogenesis of acute decompensation (AD) and acute-on-chronic liver failure (

57 ver failure (ACLF) is characterized by acute decompensation (AD) of cirrhosis, organ failure(s), and

58 HBV associated cirrhotic patients with acute decompensation (AD) were enrolled.

59 ACLF) in cirrhosis is characterized by acute decompensation (AD), organ failure(s), and high short-te

60 n failures (OFs) that develop after an acute decompensation (AD).

61 correlate with acute clinical heart failure decompensation (ADHF) and related adverse clinical outco

62 independently predictive of a first hepatic decompensation (adjusted hazard ratio, 3.7; 95% confiden

63 erval [CI], 0.12-0.74; P < 0.01) and hepatic decompensation (adjusted sub-HR, 0.52; 95% CI, 0.28-0.96

64 The risk of clinical relapse and hepatic decompensation after cessation of NA was explored.

65 k of 3- and 5-year mortality and of clinical decompensation after surgery for HCC.

66 However, the risk of liver decompensation after surgery is not thoroughly investiga

67 easure the incidence of the onset of cardiac decompensation after TIPS and identify the predictive fa

68 V), abdominal pain, infection, acute hepatic decompensation (AHD) and acute kidney injury (AKI).

69 currence of periprocedural acute hemodynamic decompensation (AHD) in patients undergoing radiofrequen

70 th unknown CLD presenting with acute hepatic decompensation (ALF-CLD).

71 ]) were each associated with higher rates of decompensation among co-infected patients.

72 Regression analysis revealed a lower risk of decompensation among statin users with cirrhosis due to

73 ing date of HCV therapy to the first hepatic decompensation and death due to any cause.

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

75 ine CT images allows prediction of cirrhosis decompensation and death.

76 with a more than 40% lower risk of cirrhosis decompensation and death.

77 sal normoxic conditions and in acute cardiac decompensation and enhanced mortality during transient h

78 ho are at increased risk for a first hepatic decompensation and for mortality.

79 lue of FLIS for first and/or further hepatic decompensation and for transplant-free survival was inve

80 ed penetrating keratoplasty to treat corneal decompensation and glaucoma drainage devices are preferr

81 l participants were hospitalized for cardiac decompensation and had a left ventricular ejection fract

82 the downstream signaling defects leading to decompensation and heart failure are poorly understood.

83 are an option for patients with hemodynamic decompensation and high bleeding risk.

84 LT needs to be fine-tuned to avoid clinical decompensation and improve long-term outcomes.

85 nd social isolation leading to psychological decompensation and increased drinking or relapse.

86 Statin use decreases the risk of decompensation and mortality in patients with cirrhosis

87 The reductions in hepatic decompensation and mortality suggest that future studies

88 prophylaxis has demonstrated a reduction in decompensation and mortality.

89 he association of the LSN score with hepatic decompensation and overall survival.

90 We investigated the effects of statins on decompensation and survival times in patients with compe

91 e progression and to avoid or delay clinical decompensation and the need for liver transplantation.

92 Therefore, the incidence of cardiac decompensation and the parameters associated with this c

93 ike to stress that the definition of cardiac decompensation and the time of evaluation of the patient

94 accuracy of the FLIS for predicting hepatic decompensation and transplant-free survival in patients

95 viral rebound during follow-up with hepatic decompensation and was placed on TDF therapy.

96 ring the risk of death by preventing further decompensation and/or development of acute-on-chronic li

97 ith biopsy, the adjusted subhazard ratio for decompensations and 95% confidence interval (95% CI) by

98 Thus, we aimed at evaluating the risk of decompensations and death among human immunodeficiency v

99 hich often manifests with frequent metabolic decompensations and risk of neurological injury.

100 Survivors remain at risk of metabolic decompensations and severe long term complications, nota

101 as associated with a marked decrease in HCC, decompensation, and bacterial infection incidences.

102 to complications of liver cirrhosis, hepatic decompensation, and hepatocellular carcinoma (HCC).

103 ia and statin exposure on mortality, hepatic decompensation, and hepatocellular carcinoma development

104 in parasympathetic tone, delayed hemodynamic decompensation, and improved brain perfusion following s

105 es such as hepatocellular carcinoma, hepatic decompensation, and mortality among US veterans with hep

106 ent of hepatocellular carcinoma (HCC), liver decompensation, and overall survival.

107 ates indicate patients with cirrhosis, prior decompensation, and previous protease inhibitor treatmen

108 reased HCC incidence were cirrhosis, hepatic decompensation, and soluble serum intercellular adhesion

109 The effect of diabetes on cirrhosis, its decompensation, and their time relationship in chronic h

110 months, 6 patients died, 8 experienced liver decompensations, and 7 were diagnosed with hepatocellula

111 The molecular events that drive hypertrophy decompensation are incompletely understood.

112 edure, incidence and risk factors of cardiac decompensation are poorly known.

113 s (DOACs) on all-cause mortality and hepatic decompensation as well as ischemic stroke, major adverse

114 Clinical endpoints defined as hepatic decompensation (ascites, encephalopathy, and variceal bl

115 hosis progression and development of hepatic decompensation (ascites, variceal hemorrhage and hepatic

116 The endpoint was hepatic decompensation (ascites, variceal hemorrhage, or encepha

117 rtality associated with severity of clinical decompensation assessed by the magnitude of pre-operativ

118 There were no deaths or clinical decompensations attributable to antibiotic delay.

119 osis (n = 550), a first diagnosis of hepatic decompensation before or within 12 months after initial

120 analysis, the median duration of endothelial decompensation before the regraft was 21 days (range, 2-

121 initiated ART at entry, for incident hepatic decompensation between 1996 and 2010.

122 , fibrinolytic therapy prevented hemodynamic decompensation but increased the risk of major hemorrhag

123 RT significantly reduced the rate of hepatic decompensation by 28%-41% on average.

124 ort confirms that PREsTo accurately predicts decompensation (C-statistic, 0.90; 95% confidence interv

125 pia and myopic astigmatism, although corneal decompensation can occur after implantation.

126 Children may experience an acute cardiac decompensation caused by severe inflammatory state after

127 d to estimate hazard ratios (HRs) of hepatic decompensation, comparing initiation of ART to noninitia

128 Incident hepatic decompensation, determined by diagnoses of ascites, spon

129 Clinical relapse and hepatic decompensation developed in 25 (32.5 %) and 11 (14.3 %)

130 Death from causes secondary to liver decompensation did not differ significantly between pati

131 mplications (eg, retinal detachment, corneal decompensation, dislocated intraocular lens [IOL]).

132 ed PlasmaLyte solution in limiting metabolic decompensation due to graft preparation.

133 ers a potential future therapy for metabolic decompensation due to mitochondrial CI dysfunction.

134 ated cirrhosis, 40% (129 of 326) experienced decompensation during a median follow-up period of 4.22

135 Early decompensation during the first week after TIPS was obse

136 there is a low probability of severe corneal decompensation, even in patients with a low endothelial

137 d probability of survival from first hepatic decompensation event compared with a 59.8% (95% CI, 56.3

138 sted veterans from the time of first hepatic decompensation event in multivariable survival models (h

139 ruses (HBV, HCV, HDV, respectively) on liver decompensation events (ascites, variceal bleeding, encep

140 We observed 645 hepatic decompensation events in 46 444 person-years of follow-u

141 sociated with a high rate of death and liver decompensation events in HIV-infected patients on ART.

142 r-cardioverter-defibrillator in the Reducing Decompensation Events Utilizing Intracardiac Pressures i

143 LD, defined as those with at least two liver decompensation events, were included in the analysis.

144 lated complications and 26 developed hepatic decompensation events.

145 us AEs including one death and three hepatic decompensation events.

146 r events (defined as liver-related deaths or decompensations, excluding HCC) and used Poisson regress

147 nderwent DMEK for graft failure with corneal decompensation following DSAEK were analyzed; 15 eyes wi

148 Moreover, reversible decompensations for G1 ACLF have a lower risk of G3 ACLF

149 bleeding alone; grade 4 = nonbleeding single decompensation; grade 5 = more than one decompensating e

150 = bleeding alone; grade 4=nonbleeding single decompensation; grade 5=more than one decompensating eve

151 s: severe alcoholic hepatitis as first liver decompensation (Group 1), alcoholic cirrhosis with >/=6

152 The incidence and determinants of hepatic decompensation have been incompletely examined among pat

153 fected patients had a higher rate of hepatic decompensation (hazard ratio [HR] accounting for competi

154 Statin users had a lower risk of decompensation (hazard ratio [HR], 0.55; 95% confidence

155 osis, HCV eradication reduced risk for liver decompensation, HCC, and death, regardless of whether th

156 nclusion: PREsTo accurately predicts hepatic decompensation (HD) in PSC and exceeds the performance a

157 B surface antigen (HBsAg), prevalent hepatic decompensation (HD), hepatocellular carcinoma (HCC), and

158 ression to hepatocellular carcinoma, hepatic decompensation (hepatic encephalopathy, esophageal varic

159 elated death, liver transplantation, hepatic decompensation, hepatocellular carcinoma) were observed

160 nical outcomes (liver-related death, hepatic decompensation, hepatocellular carcinoma, liver transpla

161 ASH-related cirrhosis, clinical events (e.g. decompensation, hepatocellular carcinoma, transplantatio

162 II-III symptoms, within 6 months of a recent decompensation (HF hospitalization or intravenous diuret

163 e patients present clinically with metabolic decompensation; however, this primary pathologic process

164 erval [CI], 0.19-0.43; P < .001) and hepatic decompensation (HR, 0.26; 95% CI, 0.17-0.39; P < .001).

165 than patients with stage 1 disease for liver decompensation (HR, 2.82; 95% CI, 1.73-4.59; P < .001) o

166 =2.505; 95% CI=1.609-3.897; P<0.001) and its decompensation (HR=3.560; 95% CI=1.526-8.307; P=0.003).

167 Clinical decompensation immediately prior to liver transplantatio

168 relapse occurred in 10 (19.6 %) and hepatic decompensation in 2 (3.9%).

169 f arrest was hypotension in 67%, respiratory decompensation in 44%, and arrhythmia in 19%.

170 ological features point to periodic systemic decompensation in ATP1A3-expressing organs.

171 Obesity increases the risk of clinical decompensation in cirrhosis, possibly by increasing port

172 4 score >5.88-and time to onset of cirrhotic decompensation in electronic medical records.

173 rate of hospital admission for heart failure decompensation in follow-up (HR, 1.66; 95% CI, 1.27-2.18

174 novel strategy for treating SCD and cardiac decompensation in HF.

175 ects varied widely from acute neurometabolic decompensation in late infancy to subtle neurological si

176 lost >/= 3 Snellen lines because of corneal decompensation in one and angle-closure glaucoma in the

177 PE can be a cause of decompensation in patients testing positive for COVID-19

178 catheter based parameters to predict cardiac decompensation in patients undergoing Trans jugular intr

179 Mortality after acute decompensation in patients with heart failure with prese

180 treatment HVPG on the development of hepatic decompensation in patients with PH who achieved SVR to I

181 estimated disease with a high risk for acute decompensation in the perioperative period.

182 12.6; P = .04), but not for further hepatic decompensations in patients with DACLD (adjusted hazard

183 ut advanced fibrosis are at very low risk of decompensations in the short term; deferral of HCV thera

184 ons that may further precipitate other liver decompensations including acute-on-chronic liver failure

185 No corneal decompensation, iritis, secondary glaucoma, or pupillary

186 Prevention of decompensation is a primary therapeutic target in patien

187 Prevention of decompensation is a primary therapeutic target in patien

188 heart failure and hospitalisations for acute decompensation is also of great importance.

189 Hospitalization for cardiac decompensation is observed in 20% of patients in the yea

190 ic role in patients with cirrhosis and acute decompensation is unknown.

191 r chance of a transplant attributed to liver decompensation (LD) and death.

192 Postoperative liver decompensation (LD) is the most representative and least

193 Incidences of liver decompensation (LD), hepatocellular carcinoma (HCC), and

194 f patients with HF with preserved EF reduced decompensation leading to hospitalization compared with

195 modynamically guided HF management decreases decompensation leading to hospitalization.

196 es of 1/60 OD and 6/18 OS, bilateral corneal decompensation, lens opacities and raised intraocular pr

197 to assess the influence of these factors on decompensation, liver transplantation, and death.

198 e of ordinal outcomes in trials of cirrhosis decompensation may provide more power and thus may requi

199 e of ordinal outcomes in trials of cirrhosis decompensation may provide more power and thus may requi

200 ion, including poor quality of life, hepatic decompensation, mortality in patients with cirrhosis eva

201 cirrhosis, statin use decreased the risk of decompensation, mortality, and HCC in a dose-dependent m

202 termine the effect of statin use on rates of decompensation, mortality, and HCC in HBV-, HCV-, and al

203 e association between statin use and risk of decompensation, mortality, and HCC were estimated.

204 t studies focused on the mandibular anterior decompensation movements.

205 osis without ACLF (n = 9), cirrhosis without decompensation (n = 17), or acute liver failure (n = 23)

206 rointestinal haemorrhage (n=1), neurological decompensation (n=1), and renal failure (n=1).

207 h a reduced risk of liver cirrhosis, hepatic decompensation, need for liver transplantation, and both

208 lism, mechanical ventilation, or hemodynamic decompensation needing inotropic or mechanical support w

209 s stage and a presence or history of hepatic decompensation: nonadvanced CLD, compensated advanced CL

210 an SVR (11.9%) (P = .03) or developed liver decompensation (none vs 7.1% without an SVR; P = .009).

211 l model recapitulates the cardio-respiratory decompensation observed in humans, and that EVHP appears

212 Death or hemodynamic decompensation occurred in 13 of 506 patients (2.6%) in

213 A cardiac decompensation occurred in 20% of the patients.

214 Six (11%) patients died, and hepatic decompensation occurred in 22% with advanced fibrosis an

215 Liver decompensation occurred more frequently in HCV patients

216 No episodes of clinical decompensation occurred.

217 e serious adverse event (i.e., fatal cardiac decompensation) occurred at the end of the post-treatmen

218 detect patients with severe fibrosis before decompensation occurs.

219 ndan-treatment on MPO in patients with acute decompensation of chronic heart failure over a one week

220 t beta-blockers are more suitable to prevent decompensation of cirrhosis in patients with CSPH than i

221 NGAL in 429 patients hospitalized for acute decompensation of cirrhosis in the EASL-CLIF Acute-on-Ch

222 (HR = 0.53; 95% CI = 0.29-0.98), and further decompensation of cirrhosis occurred in 52% versus 72% (

223 Patients had either ACLF (n = 41), acute decompensation of cirrhosis without ACLF (n = 9), cirrho

224 s with advanced HCC, female gender, clinical decompensation of cirrhosis, and multinodular tumor are

225 re (ACLF) syndrome is characterized by acute decompensation of cirrhosis, organ failure, and high 28-

226 reduce the risk of rebleeding and of further decompensation of cirrhosis, thus contributing to a bett

227 y volunteers) of PGE2 in patients with acute decompensation of cirrhosis.

228 Median times to decompensation of patients at high (1.76 years, n = 48),

229 rome type II, and with acute volume overload decompensation of the maternal circulation in late-onset

230 - and 5-year mortality and/or early clinical decompensation) of patients with HCC and compensated cir

231 ecreased in the serum of patients with acute decompensation or ESLD (<30 mg/dl) and appears to have a

232 occurrence of a liver complication -hepatic decompensation or hepatocellular carcinoma (HCC) - or re

233 e occurrence of a liver complication-hepatic decompensation or hepatocellular carcinoma (HCC)-or requ

234 the estimated risk of progression to hepatic decompensation or hepatocellular carcinoma was 37.2% in

235 TE and HVPG to predict the first LRE (liver decompensation or hepatocellular carcinoma).

236 and liver-related events (LREs), defined as decompensation or hepatocellular carcinoma, whichever oc

237 rongest predictors of progression to hepatic decompensation or hepatocellular carcinoma.

238 ents are diagnosed in late stages when liver decompensation or liver cancer develops.

239 ost effective treatment for those with liver decompensation or small hepatocellular carcinoma.

240 when admitted to hospital for acute cardiac decompensation or stroke.

241 that masks result in significant physiologic decompensation or that risk compensation and fomite tran

242 The primary outcome was death or hemodynamic decompensation (or collapse) within 7 days after randomi

243 continuation due to tumor progression, liver decompensation, or adverse effects.

244 p advanced liver disease: cirrhosis, hepatic decompensation, or hepatocellular carcinoma.

245 .e., hepatocellular carcinoma [HCC], hepatic decompensation, or liver-related death/transplantation)

246 y recognized syndrome characterized by acute decompensation, organ failure(s) and high short-term mor

247 an increased risk of liver cirrhosis and its decompensation over time.

248 lular carcinoma and death (P < 0.01) but not decompensation (P = 0.33).

249 Patients with hepatic decompensation, particularly those with Child-Turcotte-P

250 FU HVPG but not BL HVPG predicted hepatic decompensation (per mm Hg, hazard ratio, 1.18; 95% confi

251 nsating phase of RVH tissues but was lost in decompensation phase of RVH.

252 sition from compensating phase of RVH toward decompensation phase of RVH.

253 increased the risk of postoperative clinical decompensation (pooled OR: 3.04; 95% CI: 2.02-4.59).

254 as the only significant predictor of corneal decompensation postoperatively (P < .001).

255 1.2 mg/dL, absence of cirrhosis, and hepatic decompensation predicted SVR at 12 weeks.

256 Of borderline significance is a decreased decompensation rate in alcohol-related cirrhosis.

257 Statin use decreases the decompensation rate in both HBV- and HCV-related cirrhos

258 had a significantly reduced rate of hepatic decompensation relative to noninitiators (HR = 0.72; 95%

259 e main endpoint was the incidence of cardiac decompensation requiring hospitalization.

260 ular assist devices and may lead to clinical decompensation requiring surgical correction.

261 ned lens fragments and can evolve to corneal decompensation requiring transplantation.

262 outcomes in a hypothetical study to prevent decompensation resulted in sample size estimates 3-to 4-

263 outcomes in a hypothetical study to prevent decompensation resulted in sample-size estimates 3-to 4-

264 erged as an effective way to eliminate acute decompensation risk.

265 The main feature responsible for acute liver decompensation seemed to be heart insufficiency.

266 occurred in 49.9% of cases, including liver decompensation, severe infections in 10.4%, and death in

267 han 1000 copies/mL still had higher rates of decompensation than HCV-monoinfected patients (HR, 1.44

268 with HIV and HCV had higher rates of hepatic decompensation than HCV-monoinfected patients.

269 tension (PH) is the main driver of cirrhosis decompensation, the main determinant of death in patient

270 to minimize the duration of central corneal decompensation, the visual outcomes with secondary DMEK

271 When she faced heart decompensation, this congestive condition led to an acut

272 gle is where single vision is restored after decompensation to diplopia, during vergence range assess

273 Clinical events (death, decompensation, transplant, and hepatoma) were evaluated

274 oth Atf6 and Atf6b null mice showed enhanced decompensation typified by increased heart weight, pulmo

275 gradually evolving to a state of circulatory decompensation usually in the later stages of pregnancy,

276 ns in all these indications but also further decompensation (variceal bleeding, hepatorenal syndrome)

277 Two (4.6%) patients with SVR developed liver decompensation vs 33 (26.8%) individuals without SVR (P

278 Hepatic decompensation was defined as the first occurrence of 1

279 The incidence of hepatic decompensation was greater among co-infected than monoin

280 The incidence rate of hepatic decompensation was higher in patients with human immunod

281 with HIV/HCV-infected patients, the rate of decompensation was increased among HIV/HBV/HCV-infected

282 plantation, and clinical evidence of corneal decompensation was minimal.

283 The lowered risk of decompensation was of borderline significance among stat

284 Incident decompensation was the most common serious adverse event

285 ciated with the occurrence of severe cardiac decompensation were a prolonged QT interval corrected (4

286 (ECD) in patient 2, but no signs of corneal decompensation were detected.

287 Cirrhosis and decompensation were determined from International Classi

288 Rates of decompensation were higher for co-infected patients with

289 ses of cirrhosis and at least one feature of decompensation were included.

290 Factors independently associated with liver decompensation were non-SVR (hazard ratio [HR], 8.1; 95%

291 consecutive DMEK operations for endothelial decompensation were reviewed; 97 eyes of 84 patients met

292 nd low (6.14 years, n = 152) risk of hepatic decompensation were significantly different (P < .001).

293 age, 5-year cumulative incidences of HCC and decompensation were similar in HIV/HCV and HCV patients

294 SAEs associated with hepatic decompensation were the most frequent, with 26 SAEs occu

295 chondrial protein oxidation, and hypertrophy decompensation, which were attenuated by CaMKIIdelta del

296 ng diuretics prior to hospitalization for HF decompensation who received a discharge prescription for

297 rises those who have experienced hemodynamic decompensation with hypotension, cardiogenic shock, or c

298 d patients after the first episode of severe decompensation with no response to steroid therapy, it r

299 cohort until development of cirrhosis or its decompensation, withdrawal from insurance, or December 2

300 y can increase necroinflammation and hepatic decompensation without enhancing fibrosis progression.