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Craig J. Mcclain – One of the best experts on this subject based on the ideXlab platform.

  • Increased plasma interleukin-8 concentrations in Alcoholic Hepatitis.
    Hepatology (Baltimore Md.), 1993
    Co-Authors: L B M D Daniel Hill, Luis S. Marsano, Craig J. Mcclain
    Abstract:

    Patients with Alcoholic Hepatitis often have hepatic polymorphonuclear leukocyte infiltration and neutrophilia. Interleukin-8 is a cytokine that stimulates neutrophil chemotaxis and release of lysosomal enzymes. It is made by several types of cells, including fibroblasts, Kupffer cells and hepatocytes. In this study, serial plasma interleukin-8 concentrations were measured with enzyme-linked immunosorbent assay in 40 consecutive patients with moderate-to-severe Alcoholic Hepatitis over a 6-mo period. Two control groups included 10 patients without clinically important liver disease admitted for treatment of alcohol dependence and 12 healthy male volunteers. The mean plasma interleukin-8 level on admission was markedly increased: 695 ± 146 pg/ml in the Alcoholic Hepatitis patients. The alcohol-dependent control group and the normal volunteer controls had mean interleukin-8 concentrations of 106 ± 28 pg/ml and 10 ± 5 pg/ml, respectively. Initially increased interleukin-8 levels in Alcoholic Hepatitis patients decreased to a meals of 182 ± 42 pg/ml over the first month; levels had decreased further to 124 ± 79 pg/ml after 6 mo. Increased interleukin-8 concentrations in patients with Alcoholic Hepatitis suggest a role for interleukin-8 in the neutrophilia and hepatic polymorphonuclear leukocyte infiltration of Alcoholic Hepatitis. (HEPATOLOGY 1993;18:576–580.)

  • Increased plasma interleukin-6 concentrations in Alcoholic Hepatitis.
    Journal of Laboratory and Clinical Medicine, 1992
    Co-Authors: Daniell B. Hill, Luis S. Marsano, Donald A Cohen, John I. Allen, Steven I. Shedlofsky, Craig J. Mcclain
    Abstract:

    : Interleukin-6 (hepatocyte stimulating factor) is a 26 kd cytokine that plays a major role in the acute phase response, especially the hepatic aspects of the acute phase response. Patients with Alcoholic Hepatitis manifest many aspects of the acute phase response. In this 6-month study we evaluated serial plasma interleukin-6 levels in 30 consecutive patients with moderate to severe Alcoholic Hepatitis. Mean admission plasma interleukin-6 activity was markedly increased (49.8 +/- 8.5 U/ml, normal less than 5 U/ml) in patients with Alcoholic Hepatitis, and levels decreased with clinical improvement to 15.6 +/- 6.1 U/ml at 6 months. Admission interleukin-6 activity correlated significantly (r = 0.82) with the severity of liver disease as assessed by the discriminant function of Maddrey. Also measured were selected assays postulated to be regulated by interleukin-6, including serum albumin (2.3 +/- 0.1 gm/dl), which was significantly depressed; alpha 1-acid glycoprotein (52 +/- 5 mg/dl), which was within normal limits; and IgA (827 +/- 70 mg/dl) and C-reactive protein (3.03 +/- 0.51 mg/dl), which were significantly elevated. Interleukin-6 activity fell over time in a pattern similar to that of bilirubin and C-reactive protein. We suggest that plasma interleukin-6 may not only regulate many aspects of the acute phase response but also may be a marker of inflammation and severity of disease in Alcoholic Hepatitis.

  • Tumor necrosis and Alcoholic Hepatitis.
    Hepatology (Baltimore Md.), 1991
    Co-Authors: Craig J. Mcclain
    Abstract:

    Study Objective: To determine whether elevated tumor necrnecrosistor levels contribute to the clinical manifestations and complications of severe acute Alcoholic Hepatitis and to evaluate the relation between tumor necrnecrosistor and plasma levels of endotoxin and interleukin-1β. Design: Prospective, controlled study. Setting: The liver unit of a university teaching hospital. Patients: We studied 21 patients with acute severe Alcoholic Hepatitis. There were four control groups: patients with inactive Alcoholic cirrhosis, Alcoholic persons without liver disease, patients with impaired renal function, and normal subjects. Measurements and Main Results: With one exception, patients with Alcoholic Hepatitis had higher tumor necrnecrosistor levels (mean, 26.3 ng/L; 95% CI, 21.7 to 30.9) than normal subjects (6.4 ng/L; CI, 5.4 to 7.4). Patients who subsequently died had a higher tumor necrnecrosistor level (34.7 ng/L; CI, 27.8 to 41.6) than survivors (16.6 ng/L; CI, 14.0 to 19.2). In patients with Alcoholic Hepatitis, tumor necrnecrosistor levels correlated positively with serum bilirubin (r = 0.74; P = 0.0009) and serum creatinine (r = 0.81; P = 0.0003). Patients with Alcoholic Hepatitis had higher tumor necrnecrosistor levels than patients with inactive Alcoholic cirrhosis (11.1 ng/L; CI, 8.9 to 13.3) and severely Alcoholic persons without liver disease (6.4 ng/L; CI, 5.0 to 7.8). Patients with abnormal renal function had lower tumor necrnecrosistor levels (14.1 ng/L; CI, 5.4 to 22.8) than patients with Alcoholic Hepatitis. Serial samples obtained during a 1-week period from patients with Alcoholic Hepatitis showed no significant change in tumor necrnecrosistor when patients who died were compared with survivors. No correlation was found between tumor necrnecrosistor and plasma endotoxin. Levels of interleukin-1β did not exceed 20 ng/L. Conclusions: Elevations in tumor necrnecrosistor in Alcoholic Hepatitis are most marked in severe cases, suggesting that tumor necrnecrosistor plays a role in the pathogenesis. Plasma concentrations of tumor necrnecrosistor (TNF) were determined in 21 consecutive patients with severe Alcoholic Hepatitis. 10 of these patients died within 6 weeks of admission. Controls included patients with inactive Alcoholic cirrhosis, Alcoholic subjects without liver disease, patients with impaired renal function, and normal subjects. Patients with Alcoholic Hepatitis had higher plasma TNF concentrations than all but 1 normal subject. Plasma TNF concentrations positively correlated with serum creatinine, serum bilirubin, blood neutrophil count and temperature. Alcoholic Hepatitis patients having infections had higher plasma TNF concentrations than those without infection. Plasma TNF concentrations also were significantly higher in Alcoholic Hepatitis patients who subsequently died than those who survived. Patients with Alcoholic Hepatitis had significantly higher plasma TNF concentrations than did patients with inactive cirrhosis or Alcoholics having no liver disease. Patients with Alcoholic cirrhosis had mild elevations in their plasma TNF concentrations, and Alcoholics without liver disease had no significant increase in plasma TNF concentrations above normal values. Renal failure patients had modest elevations in their plasma TNF concentrations. There was no correlation found between plasma endotoxin and plasma TNF concentrations in Alcoholic Hepatitis patients. It is concluded that there is elevated plasma TNF concentrations in patients with severe Alcoholic Hepatitis, and it is suggested that TNF may play a role in the pathogenesis of this disease process.

Christophe Moreno – One of the best experts on this subject based on the ideXlab platform.

  • Alcoholic Hepatitis: Towards an era of personalised management.
    United European gastroenterology journal, 2020
    Co-Authors: Delphine Degré, Christophe Moreno, Line C Ntandja Wandji, Alexandre Louvet
    Abstract:

    Alcoholic Hepatitis should be suspected in every patient with excessive chronic alcohol consumption and recent onset of jaundice. Diagnosis of Alcoholic Hepatitis is based on clinical and laboratory findings, and confirmed by a liver biopsy when available. Several scores are available to assess severity and prognosis of Alcoholic Hepatitis. The 1-month mortality of patients with severe Alcoholic Hepatitis, as defined by Maddrey’s discriminant function, is 20-30%. Therefore, severe Alcoholic Hepatitis should be treated with a 28-day course of oral prednisolone after systematic screening for infection. In this review, we discuss diagnosis of Alcoholic Hepatitis, the different scores to assess severity of the disease, indications for corticosteroid therapy and alternative therapeutic options for non-responders to medical therapy.

  • Liver transplant for Alcoholic Hepatitis: a current clinical overview.
    Expert review of gastroenterology & hepatology, 2020
    Co-Authors: Astrid Marot, Christophe Moreno, Pierre Deltenre
    Abstract:

    Current management of severe Alcoholic Hepatitis is based on corticosteroid therapy and abstinence from alcohol. As liver transplantation is lifesaving in Alcoholic Hepatitis patients at high risk …

  • Management of Alcoholic Hepatitis
    Revue medicale de Bruxelles, 2012
    Co-Authors: Thierry Gustot, Christophe Moreno
    Abstract:

    Alcoholic Hepatitis is a severe form of Alcoholic liver disease. Diagnosis is based on the association of new onset of jaundice and a compatible liver biopsy. Alcoholic Hepatitis is severe when the Maddrey is up to 32 and, in this case, is associated with a mortality of 40-50% at 2 months. Corticosteroids improve survival of patients suffering from severe Alcoholic Hepatitis. The decrease of total bilirubin at day 7 of treatment and the Lille score are markers of response to corticosteroids. The absence of response is associated with a dramatic outcome (mortality rate of 75% at 6 months). Liver transplantation could be an alternative in a strictly selected group of non-responders.

Yasuyuki Ohta – One of the best experts on this subject based on the ideXlab platform.

  • Assay of serum interleukin 8 levels in patients with Alcoholic Hepatitis.
    Alcohol and Alcoholism, 1993
    Co-Authors: Toshikazu Masumoto, Morikazu Onji, Norio Horiike, Yasuyuki Ohta
    Abstract:

    Studies were performed to evaluate the role of interleukin 8 (IL-8) in the pathogenesis of Alcoholic Hepatitis. Using a recently developed sensitive and specific enzyme-linked immunosorbent assay, we measured serum IL-8 levels in patients with Alcoholic Hepatitis. The mean serum IL-8 level was increased significantly in patients with Alcoholic Hepatitis compared with normal controls ( P < 0.05). It was of interest to note that serum IL-8 levels were increased transiently after abstinence from alcohol in patients with Alcoholic Hepatitis. These findings suggest that there may be a correlation between IL-8 and Alcoholic Hepatitis.

Ashwani K. Singal – One of the best experts on this subject based on the ideXlab platform.

  • Current trials and novel therapeutic targets for Alcoholic Hepatitis.
    Journal of hepatology, 2019
    Co-Authors: Ashwani K. Singal, Vijay H. Shah
    Abstract:

    Alcoholic Hepatitis is a clinical syndrome in which patients present with acute-on-chronic liver failure and a high risk of short-term mortality. The current treatment of Alcoholic Hepatitis is suboptimal. Results recently published from the STOPAH study have improved our understanding of how best to design clinical trials for this condition. Although emerging data on liver transplantation for patients with Alcoholic Hepatitis are encouraging, less than 2% of these patients qualify. Clearly, there is an unmet need for novel treatments to improve the survival of these patients. Changes in the gut micrmicrobiota, inflammatory and cytokine signalling, oxidative stress and mitochondrial dysfunction, and abnormalities in the hepatic regenerative capacity alone or in combination contribute to the pathology of Alcoholic Hepatitis. In this chapter, we will describe the novel therapeutic agents targeting various pathways in the pathophysiology of Alcoholic Hepatitis. Specifically, we will describe the ongoing clinical trials in which some of these agents are being studied.

  • Grand Rounds: Alcoholic Hepatitis.
    Journal of hepatology, 2018
    Co-Authors: Ashwani K. Singal, Alexandre Louvet, Vijay H. Shah, Patrick S. Kamath
    Abstract:

    Clinical vignette A 33-year-old Caucasian male was admitted to hospital with recent onset of jaundice of 2–3 weeks duration. He reported heavy use of alcohol for the last 10 years with the last drink a day prior to the onset of symptoms. At admission, he was alert and oriented to time, place, and person, and was deeply jaundiced. His laboratory profile can be summarised as follows: haemoglobin 12.1 g/dl, white blood cell count 18,700 with 81% neutrophils, serum bilirubin 33 (direct 22) mg/dl, aspartate aminotransferase 147 IU/L, alanine aminaminotransferase 62 IU/L, alkaline phosphatase 117 IU/L, serum albumin 2.8 gm/dl, serum creatinine 0.6 mg/dl, prothrombin time 18.3 (control 14.5) seconds, and international normalized ratio 1.48. He was diagnosed with severe Alcoholic Hepatitis (Maddrey discriminant function score of 50) and treated with prednisolone for 28 days with symptomatic and biochemical improvement. His Lille score at seven days was 0.4, and his serum bilirubin had decreased to 3.5 mg/dl at the end of treatment. He was also seen by the addiction team during hospitalisation; he agreed to follow through on recommendations. He was dismissed after completing a three-week inpatient rehabilitation programme but relapsed to alcohol use three months later, and was readmitted with alcohol withdrawal. He was readmitted two months later (about six months from the first episode) for a second episode of severe Alcoholic Hepatitis. At admission, his model for end-stage liver disease score was 32 and he was treated again with corticosteroids. His Lille score at seven days was 0.6 and steroids were discontinued. The hospital course was complicated by spontaneous bacterial peritonitis and pneumonia with development of acute kidney injury. He continued to worsen, developing multiorgan failure. After a course of one month, the family’s preference was for him to receive comfort measures. This scenario raises several questions: I. Should liver biopsy have been carried out in this patient before starting treatment for Alcoholic Hepatitis? II. What should the protocol be for early diagnosis of infection? III. Are there options other than steroid therapy for severe Alcoholic Hepatitis? Should pharmacological therapy have been initiated to prevent alcohol relapse? IV. What are the determinants of short-term and long-term prognosis in Alcoholic Hepatitis? V. What is the role of liver transplantation in Alcoholic Hepatitis?

  • Alcoholic Hepatitis and concomitant Hepatitis C virus infection.
    World journal of gastroenterology, 2014
    Co-Authors: Mohamed Shoreibah, Bhupinderjit S Anand, Ashwani K. Singal
    Abstract:

    Hepatitis C virus (HCV) infection and alcohol abuse are two most important causes of chronic liver disease in the United States. Alcoholic Hepatitis is a unique clinical syndrome among patients with chronic and active alcohol abuse with a potential for high short-term mortality. About 20% of patients presenting with Alcoholic Hepatitis have concomitant HCV infection. Mortality from Alcoholic Hepatitis is increased in the presence of concomitant Hepatitis C due to synergistic interaction between HCV and alcohol in causing hepatocellular damage. Large prospective randomized studies are needed to develop guidelines on the use of corticosteroids among patients with Alcoholic Hepatitis and concomitant HCV infection. The impact of antiviral therapy on mortality and outcome in the setting of Alcoholic Hepatitis remains a novel area for future research.

Robert S. Brown – One of the best experts on this subject based on the ideXlab platform.

  • Acute Alcoholic Hepatitis as indication for liver transplantation
    Current opinion in organ transplantation, 2016
    Co-Authors: Arun Jesudian, Robert S. Brown
    Abstract:

    Purpose of review Until recently, severe acute Alcoholic Hepatitis that is refractory to medical therapy was a disease with extremely high mortality and no viable treatment options. A landmark trial of early liver transplantation in highly selected patients demonstrated a clear survival benefit and favorable posttransplant outcomes. Since then, new findings regarding medical therapy for Alcoholic Hepatitis, outcomes of early transplant, and ethical considerations as well as public percperception of this intervention have been published. Recent findings Glucocorticoids remain the best initial medical therapy for severe acute Alcoholic Hepatitis, but liver transplantation can be an acceptable and effective therapy for those who fail to respond to steroids. Recurrence of harmful drinking is a valid concern, and has been observed in long-term follow-up of patients transplanted for Alcoholic liver disease. Public percperception of early liver transplant for severe acute Alcoholic Hepatitis is overall positive. Summary Liver transplantation for refractory severe acute Alcoholic Hepatitis is a life-saving intervention and should be judiciously employed in highly selected individuals who are at low risk of recidivism.