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1 tis, primary biliary cholangitis, and severe alcoholic hepatitis).
2 or alcoholic liver diseases and severe acute alcoholic hepatitis.
3 athologies, such as autoimmune hepatitis and alcoholic hepatitis.
4 er diseases such as autoimmune hepatitis and alcoholic hepatitis.
5 after liver transplantation in patients with alcoholic hepatitis.
6 l mechanism underlying IL-8 up-regulation in alcoholic hepatitis.
7 m is a potential therapeutic target in acute alcoholic hepatitis.
8 ronic-binge ethanol feeding or patients with alcoholic hepatitis.
9 be an effective treatment for patients with alcoholic hepatitis.
10 effective for the treatment of patients with alcoholic hepatitis.
11 tes to pathogenesis and clinical sequelae of alcoholic hepatitis.
12 favored for carefully selected patients with alcoholic hepatitis.
13 patients with fulminant hepatic failure and alcoholic hepatitis.
14 biological markers of deleterious outcome in alcoholic hepatitis.
15 can be recommended as standard therapies for alcoholic hepatitis.
16 remain the cornerstones in the treatment of alcoholic hepatitis.
17 in formulating safe, effective therapies for alcoholic hepatitis.
18 ed with increased mortality in patients with alcoholic hepatitis.
19 positive cells were also greater in NASH vs. alcoholic hepatitis.
20 re markedly increased in patients with acute alcoholic hepatitis.
21 with normal liver 11 pg/mg) in patients with alcoholic hepatitis.
22 eful to predict the outcome in patients with alcoholic hepatitis.
23 oves survival in select patients with severe alcoholic hepatitis.
24 ce showed a similar pattern as seen in human alcoholic hepatitis.
25 its deficiency in the pathogenesis of severe alcoholic hepatitis.
26 irrhosis, with highest risk in patients with alcoholic hepatitis.
27 an NASH, primary sclerosing cholangitis, and alcoholic hepatitis.
28 d with the development, but not severity, of alcoholic hepatitis.
29 utic approach is effective for patients with alcoholic hepatitis.
30 disease and with mortality in patients with alcoholic hepatitis.
31 okine ligand types 5 (CCL5) in patients with alcoholic hepatitis.
32 tion ex vivo in whole blood of patients with alcoholic hepatitis.
33 mes and increased mortality in patients with alcoholic hepatitis.
34 ssue and serum samples from 54 patients with alcoholic hepatitis.
35 timize the therapeutic development in severe alcoholic hepatitis.
36 17 could be a viable approach in attenuating alcoholic hepatitis.
37 ADH-specific cellular immunity is present in alcoholic hepatitis.
38 ne did not improve survival in patients with alcoholic hepatitis.
39 argeted therapies to inhibit Th1 immunity in alcoholic hepatitis.
40 of whom 15 had histopathological evidence of alcoholic hepatitis (10 cirrhotic) and 9 no evidence of
41 the fecal microbial ecology associated with alcoholic hepatitis, (2) relate microbiome changes to di
43 epatitis (10 cirrhotic) and 9 no evidence of alcoholic hepatitis (5 cirrhotic); other controls includ
45 PTX3 levels were increased in patients with alcoholic hepatitis, a prototypic acute-on-chronic condi
46 ed blood samples from 20 patients with acute alcoholic hepatitis (AAH), 16 patients with stable advan
47 erapy has shown some benefit in severe acute alcoholic hepatitis (AAH); however, this is limited by u
48 onsortium of Early Liver Transplantation for Alcoholic Hepatitis (ACCELERATE-AH) cohort, we aimed to
49 : recipient's age, hepatocellular carcinoma, alcoholic hepatitis, acute-on-chronic liver failure, hil
50 nically relevant progenitor markers in human alcoholic hepatitis (AH) and hepatocellular carcinoma (H
51 hat neutrophilic NCF1-dependent ROS promoted alcoholic hepatitis (AH) by inhibiting AMP-activated pro
69 sessing severity of disease in patients with alcoholic hepatitis (AH) is useful for predicting mortal
71 We found impaired autophagy both in ALD and alcoholic hepatitis (AH) mouse models and human livers w
75 lored the role of intrahepatic LCN2 in human alcoholic hepatitis (AH) with advanced fibrosis and port
78 at result in endotoxemia, such as sepsis and alcoholic hepatitis (AH), often are accompanied by chole
79 the transcriptome analysis of patients with alcoholic hepatitis (AH), osteopontin (OPN) as one of th
81 s on effective therapeutic interventions for alcoholic hepatitis (AH), the most severe form of alcoho
87 ts based on the diagnosis of the explant (46 alcoholic hepatitis and 138 alcoholic cirrhosis) and dia
88 se (n = 58), 43 had histological features of alcoholic hepatitis and 15 (25%) did not.We aimed to det
91 s, but safe and effective therapies for both alcoholic hepatitis and alcoholic cirrhosis are still wa
92 se but safe and effective therapies for both alcoholic hepatitis and alcoholic cirrhosis have yet to
94 oholic cirrhosis were studied, 27 with acute alcoholic hepatitis and cirrhosis, in whom hepatic venou
98 n-1alpha in liver samples from patients with alcoholic hepatitis and individuals without alcoholic he
99 e interleukin-8 (IL-8) is highly elevated in alcoholic hepatitis and levels correlate with the degree
102 al hepatitis, typically in Asia, and drug or alcoholic hepatitis and variceal hemorrhage in the West.
103 aceae and Ruminococcaceae) were decreased in alcoholic hepatitis, and a similar decrease was observed
106 osis was assessed in NASH, simple steatosis, alcoholic hepatitis, and controls without liver disease
108 e associated with obesity, type II diabetes, alcoholic hepatitis, and nonalcoholic steatohepatitis.
109 ants include bacterial and viral infections, alcoholic hepatitis, and surgery, but in more than 40% o
112 rule, the patients admitted for severe acute alcoholic hepatitis are not eligible for liver transplan
114 e improved 30-day survival for those with an ALCoholic Hepatitis Artificial INtelligence Ensemble sco
116 ents were stratified into two groups: severe alcoholic hepatitis as first liver decompensation (Group
117 ere heavy drinkers with severe biopsy-proven alcoholic hepatitis, as indicated by recent onset of jau
118 rinking post-OLT, and three of those died of alcoholic hepatitis at nine months, 2.5 and 3.5 years af
119 sponses in various liver diseases, including alcoholic hepatitis, autoimmune hepatitis, and primary b
120 precipitating event (active alcoholism/acute alcoholic hepatitis, bacterial infection, and others); (
121 short-term and long-term survival in severe alcoholic hepatitis based on baseline disease severity,
122 registrations and liver transplantation for alcoholic hepatitis before and during the COVID-19 pande
123 ted in increasing mortality in patients with alcoholic hepatitis but the underlying mechanisms are no
124 both recommended for the treatment of severe alcoholic hepatitis, but uncertainty about their benefit
125 test the hypothesis that LBP is involved in alcoholic hepatitis by comparing LBP knockout and wild-t
126 o patients with a variety of liver diseases (alcoholic hepatitis, cirrhosis, hepatocellular carcinoma
130 tocol showed that early transplant in severe alcoholic hepatitis could improve survival with low inci
133 blood monocytes isolated from patients with alcoholic hepatitis, expression of TNFalpha mRNA was rob
134 ng organ inflammation, including in viral or alcoholic hepatitis, fatty liver disease, allograft reje
135 e spectrum of ALD includes simple steatosis, alcoholic hepatitis, fibrosis, cirrhosis, and superimpos
136 Proliferative anti-ADH immune responses in alcoholic hepatitis focused on individual epitopic regio
137 se patients with a histological diagnosis of alcoholic hepatitis from those without, and assess poten
141 nts with alcohol-use disorder, patients with alcoholic hepatitis have increased faecal numbers of E.
142 ared with alcoholic cirrhosis, patients with alcoholic hepatitis have similar posttransplantation gra
143 a semiquantitative scoring system called the Alcoholic Hepatitis Histologic Score (AHHS) was develope
145 m liver biopsy showed histologic features of alcoholic hepatitis in addition to bridging fibrosis or
146 tion of lipin-1 ameliorated inflammation and alcoholic hepatitis in mice via activation of endocrine
147 levels, and a histologic picture similar to alcoholic hepatitis in the absence of alcohol abuse.
161 e fecal microbiome in patients with moderate alcoholic hepatitis (MAH) or severe alcoholic hepatitis
162 that parenchymal neutrophil infiltration in alcoholic hepatitis may be determined by selective upreg
163 Forty-eight patients with moderate to severe alcoholic hepatitis (Model for End-Stage Liver Disease s
164 PBMCs were collected from 15 patients with alcoholic hepatitis (modified Maddrey's discriminant fun
165 that new therapeutic development for severe alcoholic hepatitis must target liver injury in the shor
166 ach of the histologically confirmed cases of alcoholic hepatitis (n = 43) were compared to those with
167 thrombosis (n = 6), hepatoma (n = 3), florid alcoholic hepatitis (n = 6), and refusal to give consent
168 hs at 8 United States centers as part of the Alcoholic Hepatitis Network (AlcHepNet) consortium.
169 e treatment of inflammatory diseases such as alcoholic hepatitis, nonalcoholic steatohepatitis, and p
172 ) and K2 (OR, 9.280 [95% CI, 0.987-87.250]), alcoholic hepatitis (OR, 7.435 [95% CI, 1.397-39.572]),
173 expression of SEMA3C in patients with NASH, alcoholic hepatitis, or HBV-induced hepatitis discrimina
178 , analysis of circulating EVs from plasma of alcoholic hepatitis patients revealed increased numbers
179 ic dimethylarginine (SDMA), are increased in alcoholic hepatitis patients, and determined any relatio
182 tinal mycobiota in a cohort of patients with alcoholic hepatitis, patients with alcohol use disorder,
183 findings that are identical to those seen in alcoholic hepatitis; patients with NASH, however, do not
184 icosteroids remain the mainstay treatment in alcoholic hepatitis pending the results from large multi
185 se results indicate that nimodipine prevents alcoholic hepatitis, possibly by inhibition of endotoxin
186 addition to being a potential biomarker for alcoholic hepatitis, PTX3 participates in the wound-heal
191 l infiltration has been implicated in severe alcoholic hepatitis (SAH) pathogenesis; however, the mec
192 alterations in circulating albumin in severe alcoholic hepatitis (SAH) patients and their contributio
194 moderate alcoholic hepatitis (MAH) or severe alcoholic hepatitis (SAH) was compared with healthy cont
195 nfections are common in patients with severe alcoholic hepatitis (SAH), but little information is ava
196 nfections are common in patients with severe alcoholic hepatitis (SAH), but little information is ava
198 rly linked to key clinical symptoms of acute alcoholic hepatitis such as fever, neutrophilia, and was
199 holangitis, primary biliary cholangitis, and alcoholic hepatitis, suggesting IBA1 + CD163 low macroph
200 mmatory Th1 responses was more pronounced in alcoholic hepatitis than in alcoholic-related cirrhosis.
202 trated in liver specimens from patients with alcoholic hepatitis, the AR up-regulation and elevated A
203 articularly advanced ALD (cirrhosis or acute alcoholic hepatitis), total abstinence from alcohol is t
204 no impact of the etiology of liver disease (alcoholic hepatitis versus alcoholic cirrhosis) on the g
206 th bacteria from the faeces of patients with alcoholic hepatitis, we investigated the therapeutic eff
207 r transplantation for a listing diagnosis of alcoholic hepatitis were matched for age, gender, ethnic
208 priate in highly select patients with severe alcoholic hepatitis who do not respond to medical therap
209 onsidered in a select group of patients with alcoholic hepatitis who fail to improve with medical the
210 tment of ArLD and its complications, such as alcoholic hepatitis, will allow a greater proportion of