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1 favored for carefully selected patients with alcoholic hepatitis.
2 patients with fulminant hepatic failure and alcoholic hepatitis.
3 biological markers of deleterious outcome in alcoholic hepatitis.
4 can be recommended as standard therapies for alcoholic hepatitis.
5 remain the cornerstones in the treatment of alcoholic hepatitis.
6 in formulating safe, effective therapies for alcoholic hepatitis.
7 positive cells were also greater in NASH vs. alcoholic hepatitis.
8 re markedly increased in patients with acute alcoholic hepatitis.
9 ssue and serum samples from 54 patients with alcoholic hepatitis.
10 with normal liver 11 pg/mg) in patients with alcoholic hepatitis.
11 timize the therapeutic development in severe alcoholic hepatitis.
12 17 could be a viable approach in attenuating alcoholic hepatitis.
13 ADH-specific cellular immunity is present in alcoholic hepatitis.
14 ne did not improve survival in patients with alcoholic hepatitis.
15 argeted therapies to inhibit Th1 immunity in alcoholic hepatitis.
16 er diseases such as autoimmune hepatitis and alcoholic hepatitis.
17 after liver transplantation in patients with alcoholic hepatitis.
18 l mechanism underlying IL-8 up-regulation in alcoholic hepatitis.
19 m is a potential therapeutic target in acute alcoholic hepatitis.
20 ronic-binge ethanol feeding or patients with alcoholic hepatitis.
21 be an effective treatment for patients with alcoholic hepatitis.
22 effective for the treatment of patients with alcoholic hepatitis.
23 tes to pathogenesis and clinical sequelae of alcoholic hepatitis.
24 of whom 15 had histopathological evidence of alcoholic hepatitis (10 cirrhotic) and 9 no evidence of
26 epatitis (10 cirrhotic) and 9 no evidence of alcoholic hepatitis (5 cirrhotic); other controls includ
28 PTX3 levels were increased in patients with alcoholic hepatitis, a prototypic acute-on-chronic condi
29 ed blood samples from 20 patients with acute alcoholic hepatitis (AAH), 16 patients with stable advan
30 erapy has shown some benefit in severe acute alcoholic hepatitis (AAH); however, this is limited by u
43 sessing severity of disease in patients with alcoholic hepatitis (AH) is useful for predicting mortal
47 the transcriptome analysis of patients with alcoholic hepatitis (AH), osteopontin (OPN) as one of th
48 s on effective therapeutic interventions for alcoholic hepatitis (AH), the most severe form of alcoho
51 ts based on the diagnosis of the explant (46 alcoholic hepatitis and 138 alcoholic cirrhosis) and dia
52 se (n = 58), 43 had histological features of alcoholic hepatitis and 15 (25%) did not.We aimed to det
55 s, but safe and effective therapies for both alcoholic hepatitis and alcoholic cirrhosis are still wa
56 se but safe and effective therapies for both alcoholic hepatitis and alcoholic cirrhosis have yet to
58 oholic cirrhosis were studied, 27 with acute alcoholic hepatitis and cirrhosis, in whom hepatic venou
62 n-1alpha in liver samples from patients with alcoholic hepatitis and individuals without alcoholic he
63 e interleukin-8 (IL-8) is highly elevated in alcoholic hepatitis and levels correlate with the degree
65 al hepatitis, typically in Asia, and drug or alcoholic hepatitis and variceal hemorrhage in the West.
68 osis was assessed in NASH, simple steatosis, alcoholic hepatitis, and controls without liver disease
69 e associated with obesity, type II diabetes, alcoholic hepatitis, and nonalcoholic steatohepatitis.
70 ants include bacterial and viral infections, alcoholic hepatitis, and surgery, but in more than 40% o
73 ents were stratified into two groups: severe alcoholic hepatitis as first liver decompensation (Group
74 ere heavy drinkers with severe biopsy-proven alcoholic hepatitis, as indicated by recent onset of jau
75 rinking post-OLT, and three of those died of alcoholic hepatitis at nine months, 2.5 and 3.5 years af
76 precipitating event (active alcoholism/acute alcoholic hepatitis, bacterial infection, and others); (
77 short-term and long-term survival in severe alcoholic hepatitis based on baseline disease severity,
78 ted in increasing mortality in patients with alcoholic hepatitis but the underlying mechanisms are no
79 both recommended for the treatment of severe alcoholic hepatitis, but uncertainty about their benefit
80 test the hypothesis that LBP is involved in alcoholic hepatitis by comparing LBP knockout and wild-t
81 o patients with a variety of liver diseases (alcoholic hepatitis, cirrhosis, hepatocellular carcinoma
84 tocol showed that early transplant in severe alcoholic hepatitis could improve survival with low inci
86 blood monocytes isolated from patients with alcoholic hepatitis, expression of TNFalpha mRNA was rob
87 ng organ inflammation, including in viral or alcoholic hepatitis, fatty liver disease, allograft reje
88 e spectrum of ALD includes simple steatosis, alcoholic hepatitis, fibrosis, cirrhosis, and superimpos
89 Proliferative anti-ADH immune responses in alcoholic hepatitis focused on individual epitopic regio
90 se patients with a histological diagnosis of alcoholic hepatitis from those without, and assess poten
92 ared with alcoholic cirrhosis, patients with alcoholic hepatitis have similar posttransplantation gra
93 a semiquantitative scoring system called the Alcoholic Hepatitis Histologic Score (AHHS) was develope
95 m liver biopsy showed histologic features of alcoholic hepatitis in addition to bridging fibrosis or
96 tion of lipin-1 ameliorated inflammation and alcoholic hepatitis in mice via activation of endocrine
107 that parenchymal neutrophil infiltration in alcoholic hepatitis may be determined by selective upreg
108 Forty-eight patients with moderate to severe alcoholic hepatitis (Model for End-Stage Liver Disease s
109 PBMCs were collected from 15 patients with alcoholic hepatitis (modified Maddrey's discriminant fun
110 that new therapeutic development for severe alcoholic hepatitis must target liver injury in the shor
111 ach of the histologically confirmed cases of alcoholic hepatitis (n = 43) were compared to those with
112 thrombosis (n = 6), hepatoma (n = 3), florid alcoholic hepatitis (n = 6), and refusal to give consent
113 e treatment of inflammatory diseases such as alcoholic hepatitis, nonalcoholic steatohepatitis, and p
116 ) and K2 (OR, 9.280 [95% CI, 0.987-87.250]), alcoholic hepatitis (OR, 7.435 [95% CI, 1.397-39.572]),
121 , analysis of circulating EVs from plasma of alcoholic hepatitis patients revealed increased numbers
122 ic dimethylarginine (SDMA), are increased in alcoholic hepatitis patients, and determined any relatio
123 findings that are identical to those seen in alcoholic hepatitis; patients with NASH, however, do not
124 icosteroids remain the mainstay treatment in alcoholic hepatitis pending the results from large multi
125 se results indicate that nimodipine prevents alcoholic hepatitis, possibly by inhibition of endotoxin
126 addition to being a potential biomarker for alcoholic hepatitis, PTX3 participates in the wound-heal
130 alterations in circulating albumin in severe alcoholic hepatitis (SAH) patients and their contributio
131 nfections are common in patients with severe alcoholic hepatitis (SAH), but little information is ava
132 nfections are common in patients with severe alcoholic hepatitis (SAH), but little information is ava
133 rly linked to key clinical symptoms of acute alcoholic hepatitis such as fever, neutrophilia, and was
134 mmatory Th1 responses was more pronounced in alcoholic hepatitis than in alcoholic-related cirrhosis.
136 no impact of the etiology of liver disease (alcoholic hepatitis versus alcoholic cirrhosis) on the g
137 r transplantation for a listing diagnosis of alcoholic hepatitis were matched for age, gender, ethnic
138 onsidered in a select group of patients with alcoholic hepatitis who fail to improve with medical the
139 tment of ArLD and its complications, such as alcoholic hepatitis, will allow a greater proportion of
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