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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 necrosis factor levels contribute to the clinical manifestations and complications of severe acute Alcoholic Hepatitis and to evaluate the relation between tumor necrosis factor 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 necrosis factor 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 necrosis factor 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 necrosis factor 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 necrosis factor 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 necrosis factor 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 necrosis factor when patients who died were compared with survivors. No correlation was found between tumor necrosis factor and plasma endotoxin. Levels of interleukin-1β did not exceed 20 ng/L.

    Conclusions: Elevations in tumor necrosis factor in Alcoholic Hepatitis are most marked in severe cases, suggesting that tumor necrosis factor plays a role in the pathogenesis.

    Plasma concentrations of tumor necrosis factor (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.