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1 e systemic immune responses in patients with decompensated cirrhosis.
2 te exacerbation of the SI already present in decompensated cirrhosis.
3 ot been extensively studied in patients with decompensated cirrhosis.
4 should be used with caution in patients with decompensated cirrhosis.
5 response in patients with HCV infection and decompensated cirrhosis.
6 on, including transplantation for those with decompensated cirrhosis.
7 rgery with excellent outcomes for those with decompensated cirrhosis.
8 ould be considered in patients admitted with decompensated cirrhosis.
9 patients with genotypes 2 or 3 infection and decompensated cirrhosis.
10 annual number of IDUs developing HCV-related decompensated cirrhosis.
11 g mortality in patients with compensated and decompensated cirrhosis.
12 nt of patients admitted to the hospital with decompensated cirrhosis.
13 in the prevalence of cirrhosis (1.7%-2.2%), decompensated cirrhosis (1.1%-1.2%), and HCC (0.03%-0.13
14 in the prevalence of cirrhosis (3.5%-13.2%), decompensated cirrhosis (1.9%-5.8%), and HCC (0.07%-1.6%
15 produced the largest absolute reductions in decompensated cirrhosis (16%) and hepatocellular carcino
16 is hypothesis and included 522 patients with decompensated cirrhosis (237 with ACLF) and 40 healthy s
17 32% had a diagnosis of cirrhosis (9.9% with decompensated cirrhosis), 36% had a Fibrosis-4 index sco
18 ort screening leads to 84,000 fewer cases of decompensated cirrhosis, 46,000 fewer cases of hepatocel
19 Among the full cohort with compensated or decompensated cirrhosis, 61% (504 of 830) died during th
21 could prevent approximately 124,200 cases of decompensated cirrhosis, 78,800 cases of hepatocellular
22 cs of systemic inflammation in patients with decompensated cirrhosis and ACLF, with special emphasis
25 the only effective therapy for patients with decompensated cirrhosis and fulminant liver failure.
26 V, the number of individuals with cirrhosis, decompensated cirrhosis and HCC will continue to increas
27 f patients developing HCV-related cirrhosis, decompensated cirrhosis and HCC will increase substantia
29 long the survival of rats with irreversible, decompensated cirrhosis and may be useful in the treatme
30 st cost-effective strategy for patients with decompensated cirrhosis and MELD score greater than 13.
33 c function in over half of the patients with decompensated cirrhosis and replicating HBV, and may con
34 re now presenting in increasing numbers with decompensated cirrhosis and the need for liver transplan
35 controlled trials of adults (>18 years) with decompensated cirrhosis and type 1 hepatorenal syndrome
36 ons of portal hypertension is a harbinger of decompensated cirrhosis and warrants consideration for l
37 ver function in patients with compensated or decompensated cirrhosis, and delay or obviate the need f
38 lculated the annual prevalence of cirrhosis, decompensated cirrhosis, and HCC in a national sample of
39 time trends in the prevalence of cirrhosis, decompensated cirrhosis, and hepatocellular carcinoma (H
40 ency is common among patients with HCV, with decompensated cirrhosis, and in the posttransplant setti
41 treatment of CHB in pregnancy, coinfection, decompensated cirrhosis, and posttransplant is safe and
42 interferon-alpha, the cost of treatment for decompensated cirrhosis, and quality of life in patients
43 patient with hemochromatosis, alcohol abuse, decompensated cirrhosis, and spur cell anemia who had a
44 nd decreased renal blood flow, patients with decompensated cirrhosis are very susceptible to developi
45 ents with cirrhosis, particularly those with decompensated cirrhosis, are at increased risk of bacter
47 advanced liver disease, including those with decompensated cirrhosis before and after liver transplan
48 advanced liver disease, including those with decompensated cirrhosis before or after liver transplant
50 erial infections are common complications in decompensated cirrhosis, but their relationship with hem
51 tes incubated with plasma from patients with decompensated cirrhosis carrying the protective SNP geno
52 ficial effect of lamivudine in patients with decompensated cirrhosis caused by replicating hepatitis
53 ected with HCV genotypes 1 through 6 who had decompensated cirrhosis (classified as Child-Pugh-Turcot
54 therapy, recently approved for patients with decompensated cirrhosis (DC) secondary to hepatitis C vi
55 hronic HCV only, 9% with cirrhosis, 12% with decompensated cirrhosis (DCC), 2% with liver cancer, 2%
57 re grouped into HBV-related (subdivided into decompensated cirrhosis [DCC] and hepatocellular carcino
61 ecrease the 15-year cumulative incidences of decompensated cirrhosis from 12.2% to 4.5%, hepatocellul
62 ificantly larger proportion of patients with decompensated cirrhosis given a combination of G-CSF and
63 nt-reported outcomes (PROs) in patients with decompensated cirrhosis given a fixed-dose combination o
65 f HCV incidence, prevalence, compensated and decompensated cirrhosis, hepatocellular carcinoma, liver
66 H-fibrosis, NASH-compensated cirrhosis, NASH-decompensated cirrhosis, hepatocellular carcinoma, liver
67 esponse, chronic HCV, compensated cirrhosis, decompensated cirrhosis, hepatocellular carcinoma, liver
68 ge IV disease (HR, 1.40; 95% CI, 1.24-1.58), decompensated cirrhosis (HR, 1.49; 95% CI, 1.30-1.70), a
69 The number of IDUs developing HCV-related decompensated cirrhosis in Scotland is estimated to doub
72 advanced liver disease, including those with decompensated cirrhosis, in routine practice (all curren
73 , for patients admitted to the hospital with decompensated cirrhosis, individuals who were managed by
76 including patients with HIV/HCV coinfection, decompensated cirrhosis, liver and kidney transplants, a
77 ging from early, ambulatory-phase disease to decompensated cirrhosis necessitating liver transplantat
80 ical treatments that can halt progression to decompensated cirrhosis or even reverse cirrhosis are cu
81 ction of any genotype and either compensated/decompensated cirrhosis or posttransplantation recurrenc
82 al need is great, treatment of patients with decompensated cirrhosis or with recurrent hepatitis C af
83 eatening liver disease (acute liver failure, decompensated cirrhosis, or severe hepatitis flare) and
84 nsideration are patients with compensated or decompensated cirrhosis, organ transplantation, acute he
85 utive patients admitted to the hospital with decompensated cirrhosis over a 1-year period were identi
86 underwent liver transplantation at UCLA for decompensated cirrhosis owing to a jejunoileal bypass we
87 that the optimal MELD threshold below which decompensated cirrhosis patients should receive HCV trea
90 Three patients are described who developed decompensated cirrhosis requiring retransplantation desp
91 CI], 2.62-4.49; P < .001, log-rank test) and decompensated cirrhosis (RR = 4.11; 95% CI, 2.95-5.70; P
92 [CI]=1.11-2.11; log-rank test; P<0.001) and decompensated cirrhosis (RR=2.01; 95% CI=1.07-3.79; log-
93 prospective study, consecutive patients with decompensated cirrhosis seen at the Institute of Liver a
94 0.61; 95% CI, 0.47-0.79) among patients with decompensated cirrhosis, the median survival benefit was
95 ended in specific patient groups: those with decompensated cirrhosis, those coinfected with human imm
96 e probability of survival after diagnosis of decompensated cirrhosis was 81.8 and 50.8% at 1 and 5 ye
98 ASTRAL-4) in which patients with HCV-related decompensated cirrhosis were randomly assigned to an all
99 th fibrosing cholestatic hepatitis (FCH) and decompensated cirrhosis who had a life expectancy of 1 y
100 Os was observed in patients with HCV-related decompensated cirrhosis who were given sofosbuvir and ve
101 ve was to identify LT-eligible patients with decompensated cirrhosis who would benefit (and not benef
102 ) correlates with mortality in patients with decompensated cirrhosis, who are almost invariably sarco
103 ere is a concern that the cured patient with decompensated cirrhosis will find themselves in "MELD pu
105 after their primary HCV infection developed decompensated cirrhosis within 17 months to 6 years afte
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