SEARCH · PubMed Health

Results for “Hepatitis, Alcoholic”

Explore indexed PubMed citations for clinical trials, systematic reviews and public health research. Read source abstracts and follow each citation to its original PubMed record.

Quote a phrase for an exact phrase match. Source license links do not imply unrestricted reuse.

At least 19 recordsLinked to original sources

PubMed1989

[Clinical characteristics and prognostic criteria in alcoholic hepatitis and alcoholic hepatitis with cirrhosis].

A comparative study of clinical and biological features and of the immediate prognosis was made in 46 patients with alcoholic hepatitis and 19 patients with alcoholic hepatitis with liver cirrhosis. The presence of cirrhosis has different clinical manifestations and a more intense alteration of albumin, prothrombin, total bilirubin and immunoglobulins (p less than 0.01). The development of ascites, encephalopathy and hepatorenal syndrome (p less than 0.05) and albumin, prothrombin and total bilirubin values at admission (p less than 0.01) were the best parameters to identify the patients with a poorer prognosis. There were no significant differences between both groups in mortality, frequency of encephalopathy or renal failure.

Adult↗

PubMed1996

Chemokine levels in human liver homogenates: associations between GRO alpha and histopathological evidence of alcoholic hepatitis.

Alcoholic hepatitis is characterized by parenchymal neutrophil infiltration. Hepatic synthesis of the neutrophil chemokine interleukin-8 (IL-8) is highly elevated in alcoholic hepatitis and levels correlate with the degree of neutrophil infiltration. The aim of this study was to further determine the spectrum of synthesis of chemokines in liver tissue from patients with alcoholic liver disease and a range of disease control subjects. Subjects were composed of 24 patients with alcoholic liver disease of whom 15 had histopathological evidence of alcoholic hepatitis (10 cirrhotic) and 9 no evidence of alcoholic hepatitis (5 cirrhotic); other controls included; normal liver (n = 6), viral hepatitis (n = 16), primary biliary cirrhosis (n = 5), acute liver failure (n = 4), and miscellaneous liver disease (n = 13). Levels of the C-X-C neutrophil chemokine GRO alpha and the mononuclear cell C-C chemokines: macrophage inflammatory protein 1 alpha, macrophage chemotactic protein 1 and RANTES, were determined by ELISA in liver homogenates. Levels of the neutrophil chemokine GRO alpha were specifically elevated (mean 46 pg/mg, compared with normal liver 11 pg/mg) in patients with alcoholic hepatitis. GRO alpha levels correlated with IL-8 levels and were higher in patients with alcoholic liver disease and parenchymal neutrophil infiltration. Hepatic RANTES was elevated in diseased liver, with the highest levels found in viral hepatitis (mean 117 pg/mg, compared with 24 pg/mg in normal liver). No significant changes in hepatic levels of macrophage inflammatory protein 1 alpha (MIP-1 alpha) or macrophage chemotactic protein 1 (MCP-1) were found. These data provide further supportive evidence that parenchymal neutrophil infiltration in alcoholic hepatitis may be determined by selective upregulation of C-X-C chemokine synthesis.

Chemokine CCL2↗

PubMed2002

Treatment of alcoholic hepatitis.

Alcoholic hepatitis is a common disease with an overall 1-year mortality of 20%. Although the classical treatment for alcoholic hepatitis is abstinence, in some individuals abstinence alone is inadequate to promote survival and recovery. This is particularly true of patients with severe alcoholic hepatitis, who are identified by jaundice, coagulopathy and neutrophilia. Within the last two decades, several agents have been examined as treatments for alcoholic hepatitis and cirrhosis. They have targeted several key processes in the pathophysiology of alcoholic liver disease, including hypermetabolism, inflammation, cytokine dysregulation and oxidant stress. The compounds that offer the greatest survival benefit to patients with severe alcoholic hepatitis are corticosteroids. Several groups have reported excellent results with corticosteroids, but positive results are not uniform, and there remains some controversy over their efficacy. Even if corticosteroids are beneficial for alcoholic hepatitis, they are not recommended for all patients at risk. Consequently, other agents are being tested that have broader applicability to individuals with contraindications to steroids. In this regard, pentoxifylline shows some promise, as does enteral feeding with medium chain triglycerides. Independent efforts are also being directed toward treatment of chronic alcoholic liver disease and alcoholic cirrhosis. Anti-oxidants have received the greatest attention; drugs such as S-adenosyl-methionine may be of benefit. This and others are under active study.

Adrenal Cortex Hormones↗

PubMed2004

Recent understanding of immunological aspects in alcoholic hepatitis.

Alcoholic hepatitis is a rate-limiting step in the development of alcoholic liver disease into liver cirrhosis, and approximately half of the heavy drinkers with alcoholic hepatitis develop liver cirrhosis within 5 years. Immunologic mechanisms may be involved in the individual differences in the clinical course of this disease. Endotoxin from the intestine seems to play an important role in neutrophil infiltration of the liver, which induces, and at the same time is induced; by cytokines and chemokines. Kupffer cells and monocytes also have a key role in activating other cell types and producing several cytokines, chemokines, and free radicals. Both cytokines and chemokines up-regulate expression of various adhesion molecules, and adhesion molecules accelerate a cell-to-cell contact that stimulates cytotoxic lymphocytes to cause hepatocyte death. Self-antigens and adducts formed as a result of the degenerative effect of ethanol or aldehyde are targets of antibody-dependent cell-mediated cytotoxicity. Oxygen radicals, NF-kB, and AP-1 are key intracellular factors mediating hepatocyte death in alcoholic hepatitis. Viral infections and alcoholic hepatitis exacerbate each other. Integration of both human investigations and accumulated information from various animal models will gradually clarify the immunological mechanism of alcoholic hepatitis in future.

Journal Article↗

PubMed1992

[Alcoholic hepatitis].

Alcoholic hepatitis presents as an acute hepatitis in an alcoholic. No specific laboratory tests for alcoholic hepatitis exist. Therefore, the diagnosis must be based on the clinical presentation, histology and exclusion of other causes of a similar clinical picture such as viruses and drugs. Patients with elevated bilirubin, encephalopathy and coagulopathy have a poor prognosis. Steroids, infusion of insulin and glucagon, supplementation of amino-acids and other experimental therapies do not appear to be helpful with the exception of steroids which may benefit the sickest patients. Long-term prognosis depends on the extent of cirrhotic changes present after the acute episode and on the drinking habits of the patient.

Biopsy↗

PubMed1992

Is the intercellular adhesion molecule-1/leukocyte function associated antigen 1 pathway of leukocyte adhesion involved in the tissue damage of alcoholic hepatitis?

Alcoholic hepatitis is characterised histologically by an intense inflammatory cell infiltrate made up predominantly of neutrophils but including other cell types, particularly lymphocytes. Leukocyte cytotoxicity requires cell adhesion, which is mediated via receptors on the leukocyte surface including leukocyte function associated antigen-1 (LFA-1) which binds to the ligand intercellular adhesion molecule-1 (ICAM-1) on the target cell. The distribution of ICAM-1 and LFA-1 expression in liver biopsy specimens from patients with alcoholic liver disease was examined to ascertain whether this pathway of leukocyte adhesion is involved in the tissue damage of alcoholic hepatitis. Specimens were stained for ICAM-1 and LFA-1 by a three step immunoalkaline-phosphatase method using monoclonal antibodies against ICAM-1 and LFA-1. LFA-1 staining on portal tract inflammatory cells and parenchymal inflammatory cells and ICAM-1 staining on liver components were examined. ICAM-1 expression on hepatocytes was significantly greater in alcoholic hepatitis compared with fatty liver (p less than 0.001) and normal controls (p less than 0.01). ICAM-1 expression correlated with the histological degree of hepatocellular damage (tau = 0.79; p = 0.0005) and parenchymal inflammation (tau = 0.65; p less than 0.001, and with LFA-1 expression on parenchymal leukocytes (tau = 0.63; p = 0.01). The ICAM-1/LFA-1 pathway may therefore be involved in leukocyte mediated tissue damage during alcoholic hepatitis.

Antibodies, Monoclonal↗

PubMed2003

Recent developments in the treatment of alcoholic hepatitis.

Alcoholic hepatitis is a form of acute injury to liver tissue that is also a precursor of cirrhosis, and carries significant morbidity and mortality. Severe alcoholic hepatitis in particular carries a high short-term mortality, and also places an enormous burden on stretched healthcare resources. Treatment of alcoholic hepatitis has been limited to supportive management and nutritional supplementation without clear improvements in outcome, and the timing and patient selection for hepatic transplantation is problematic. The use of corticosteroids has remained controversial for many years, but probably has a role in selected patients. Various other therapeutic strategies have been tested over the decades and none has shown any consistent benefit. Recently there have been major developments in our understanding of the mechanisms of alcoholic liver injury, including the role of cytokines and hepatocyte apoptosis. For the first time, there are exciting possibilities for specific therapies for this challenging and serious condition.

Acetylcysteine↗

PubMed2003

Pathogenesis and management of alcoholic hepatitis.

Alcoholic hepatitis is a potentially life-threatening complication of alcoholic abuse, typically presenting with symptoms and signs of hepatitis in the presence of an alcohol use disorder. The definitive diagnosis requires liver biopsy, but this is not generally required. The pathogenesis is uncertain, but relevant factors include metabolism of alcohol to toxic products, oxidant stress, acetaldehyde adducts, the action of endotoxin on Kupffer cells, and impaired hepatic regeneration. Mild alcoholic hepatitis recovers with abstinence and the long-term prognosis is determined by the underlying disorder of alcohol use. Severe alcoholic hepatitis is recognized by a Maddrey discriminant function >32 and is associated with a short-term mortality rate of almost 50%. Primary therapy is abstinence from alcohol and supportive care. Corticosteroids have been shown to be beneficial in a subset of severely ill patients with concomitant hepatic encephalopathy, but their use remains controversial. Pentoxifylline has been shown in one study to improve short-term survival rates. Other pharmacological interventions, including colchicine, propylthiouracil, calcium channel antagonists, and insulin with glucagon infusions, have not been proven to be beneficial. Nutritional supplementation with available high-calorie, high-protein diets is beneficial, but does not improve mortality. Orthotopic liver transplantation is not indicated for patients presenting with alcoholic hepatitis who have been drinking until the time of admission, but may be considered in those who achieve stable abstinence if liver function fails to recover.

Hepatitis, Alcoholic↗

PubMed2006

Alcoholic hepatitis.

Alcoholic hepatitis is a form of hepatic injury that carries a significant morbidity and mortality. The clinical presentation is that of fatigue, malaise, and jaundice in individuals who have abused excessive quantities of alcohol. Severity at presentation, traditionally calculated using the Maddrey Discriminant Function, determines outcome; the short-term mortality can be exceptionally high, with many persons dying within 1 month of hospitalization. This article summarizes the epidemiology, pathogenesis, pathology, and clinical features of alcoholic hepatitis. Prognostic scoring systems and therapeutic options receive special emphasis.

Hepatitis, Alcoholic↗

PubMed1981

Abnormal apolipoprotein composition in alcoholic hepatitis.

Alcoholic hepatitis leads to major derangements in lipoprotein metabolism. This study defines the characteristics of the abnormal high density lipoprotein and very low density lipoprotein in relation to the severity of the disease. In severely affected subjects very low density lipoprotein apolipoproteins were deficient in apolipoprotein E and apolipoprotein C. The concentration of high density lipoprotein was markedly reduced, although the proportion of high density lipoprotein 1 was substantially elevated when compared to normal subjects. High density lipoproteins were deficient in apolipoprotein AI and apolipoprotein AII but enriched in apolipoprotein E, apolipoprotein E complexes and apolipoprotein C, and contained a mixture of particles. The high density lipoprotein of subjects with alcoholic hepatitis contained a high proportion of material which bound to heparin affinity columns. This bound fraction contained a group of particles rich in apolipoprotein E, apolipoprotein E complexes and apolipoprotein C and was deficient in apolipoprotein AI and apolipoprotein AII. Examination by electron microscopy showed the presence of both discoidal and spherical particles, which varied in concentration according to the severity of the disease. Another fraction of high density lipoprotein, not bound to heparin, contained reduced amounts of apolipoprotein AI and apolipoprotein AII, consisted of disc-shaped particles and showed a higher esterified: free cholesterol ratio than the other high density lipoprotein fraction.

Apolipoprotein A-I↗

PubMed1998

Distinct patterns of chemokine expression are associated with leukocyte recruitment in alcoholic hepatitis and alcoholic cirrhosis.

Alcoholic liver disease is associated with three histologically distinct processes: steatosis (parenchymal fat accumulation), alcoholic hepatitis (characterized by parenchymal infiltration by neutrophil polymorphs), and alcoholic cirrhosis (in which chronic inflammation and fibrosis dominate). Chemokines are cytokines that promote subset-specific leukoycte recruitment to tissues and could therefore play a crucial role in determining which leukocyte subsets are recruited to the liver in alcoholic liver disease. This paper reports that chemokine expression is increased in the liver of patients with alcoholic liver disease and, moreover, that distinct patterns of chemokine expression are associated with the different inflammatory responses to alcohol. Interleukin-8 (IL-8), monocyte chemoattractant protein-1 (MCP-1), macrophage inflammatory protein-1 alpha (MIP-1 alpha), and MIP-1 beta were all detected in the parenchyma at sites of inflammation in alcoholic hepatitis, whereas in alcoholic cirrhosis, chemokines were restricted to inflammatory cells and endothelium in the fibrous septa and portal tracts. In alcoholic hepatitis, chemokine transcription was localized to sinusoidal cells, leukocytes, and fibroblasts in areas of parenchymal inflammation, but hepatocytes, despite staining strongly for chemokine protein, were negative. In alcoholic cirrhosis, chemokine mRNA was detected in portal tract endothelium, leukocytes, and fibroblasts. Thus, alcoholic hepatitis and alcoholic cirrhosis are associated with distinct patterns of chemokine expression that are likely to be important factors in determining whether a patient develops acute parenchymal inflammation and alcoholic hepatitis, or chronic septal inflammation and alcoholic cirrhosis.

Chemokine CCL2↗

PubMed1996

The treatment of alcoholic hepatitis.

Alcoholic hepatitis is a precirrhotic lesion; it develops in only a minority of chronic alcohol abusers even after decades of abuse. The clinical spectrum of disease varies from asymptomatic hepatomegaly to florid hepatocellular failure with gastrointestinal bleeding and hepatic encephalopathy. Corresponding variation is observed both in morbidity and mortality. The majority of individuals with mild to moderate alcoholic hepatitis improve significantly following abstinence from alcohol and the provision of a diet sufficient to meet their nutritional requirements; their long-term outcome is determined largely by their ability to maintain abstinence from alcohol. Individuals with severe alcoholic hepatitis require intensive nutritional support and vigorous management of the complications of their liver injury; their outcome is generally poor. A small, carefully selected subgroup of these very sick patients may benefit, at least in the short-term, from treatment with corticosteroids; the place of orthotopic hepatic transplantation, in this patient group, is still the subject of debate. No other treatment modalities have been shown to confer benefit consistently. A number of new therapeutic approaches have been proposed and need to be explored.

Adrenal Cortex Hormones↗

PubMed1980

[Alcoholic hepatitis].

Alcoholic hepatitis is defined by histological findings, i.e. Mallory bodies, necrosis and polynuclear infiltration. It may be accompanied by steatosis and more or less advanced fibrosis. The clinical picture is variable, ranging from a total absence of symptoms to high fever, jaundice and encephalopathy. Laboratory findings reveal high polynuclear white cell counts, SGOT (but not SGPT) and glutamate dehydrogenase levels. The prognosis varies according to the series studied. The pathogenesis is unclear but cellular and humoral immunity mechanisms may play a role. Therapeutic possibilities are limited, corticosteroids only being useful in very serious cases. Alcoholic hepatitis is not a nosological entity but an acute inflammatory reaction of the liver due to cell necrosis caused by alcohol, and can therefore occur at any stage of alcoholic liver.

Adult↗

PubMed1990

Alcoholic hepatitis.

Alcoholic hepatitis is a serious consequence of alcohol misuse and the usual precursor of cirrhosis. Risk factors, histology, pathogenesis, clinical features, prognosis and treatment are discussed in this review.

Biopsy↗

PubMed2001

Alcoholic Hepatitis.

Alcoholic hepatitis is a multisystem disease seen in individuals who chronically abuse alcohol. When severe, it is associated with a very high mortality rate, with nearly 50% of severely affected persons dying within 1 month of hospitalization. Primary therapy is complete alcohol abstinence and supportive care. Corticosteroids have been shown to be beneficial in a subset of severely ill patients with alcoholic hepatitis and concomitant hepatic encephalopathy. Pentoxifylline has been shown to improve short-term survival rates. Other pharmacologic interventions, including colchicine, propylthiouracil, calcium channel antagonists, and insulin with glucagon infusions, have not been proven to be beneficial. Nutritional supplementation with high-calorie, high-protein diets does not improve mortality rates. Orthotopic liver transplantation is highly controversial in this population of patients and currently is not indicated as definitive treatment. Extracorporeal liver support devices are still in their developmental stage and are only experimental.

Journal Article↗

PubMed1976

Alcoholic hepatitis.

Alcoholic hepatitis is the precursor of cirrhosis. Susceptibility is independent of amount and duration of ethanol intake or of diet. Centrilobular hyalin, the key morphologic abnormality, sensitizes lymphocytes to secrete factors which may account (in part) for necrosis, liver cell destruction, increased collagen synthesis and development of cirrhosis. Diagnosis may be facilitated by detection of alcoholic hyalin antigen (AHAg) and antibody (AHAb) in serum of patients with alcoholic hepatitis. Treatment requires abstinence. Steroids have not reduced mortality rates. Measures to improve immunologic reactivity may be helpful. Persons unable to abstain should be enrolled in a surveillance group.

Alcoholism↗

PubMed2002

Alcoholic Hepatitis.

Alcoholic hepatitis is a common clinical problem confronting gastroenterologists and hepatologists alike. The fundamental issue regarding treatment of this disease is its recognition on the part of the physician. Chronic alcohol abuse, fever, leukocytosis, jaundice, and encephalopathy are key symptoms and signs that should prompt consideration of this diagnosis. Nutrition and abstinence from alcohol are the cornerstones of therapy. In addition, management of seriously ill, hospitalized patients should include prophylaxis for withdrawal and delirium tremens. Alcoholic hepatitis (AH) induces a profound catabolic state, resulting in net negative nitrogen balance. In part, because of malnutrition, AH carries a considerably high mortality rate. Therefore, nutrition remains a key aspect of therapy. In the absence of encephalopathy and in the presence of a functioning gastrointestinal tract, oral intake or nasogastric feedings should be given. If the gastrointestinal tract cannot be used (ie, because of paralytic ileus), then total parenteral nutrition is absolutely essential for recovery. A select subset of patients, based on multiple clinical trials and several meta-analyses, can be treated with corticosteroids provided that the patient does not have active gastrointestinal bleeding and does not have an active infection. The subset of patients with AH who should receive corticosteroids is based on calculation of a modified Maddrey discriminant function, which incorporates the patient's prothrombin time and total serum bilirubin as variables in this equation. Generally, a 4-week course of prednisone or prednisolone is administered. d-penicillamine, colchicine, anabolic steroids, propylthiouracil, and antioxidants have not been shown to be effective in AH and cannot be recommended. After acute illness, patients should be discharged to an inpatient alcohol rehabilitation unit to ensure continued abstinence.

Journal Article↗

PubMed2004

Alcoholic Hepatitis.

Alcoholic hepatitis (AH) is a common disease associated with significant morbidity and mortality. Most often the diagnosis is suggested by a history of heavy alcohol excess in a patient with features of hepatic decompensation. In its purest form, AH is a histologic diagnosis of acute hepatic inflammation in response to alcohol. The primary objective of treatment for AH is to support long-term alcohol abstinence and to achieve adequate nutrition with lifestyle modification; goal setting and education are integral to long-term medical management. Severity at presentation (calculated by way of the Maddrey score) determines outcome. Patients with AH represent a heterogeneous group with regard to severity and pathogenesis, with various therapeutic interventions assessed in patients with severe AH. To date, corticosteroids have been studied most, and despite remaining controversial, warrant a place in the treatment of selected patients. Recent advances in unraveling the aspects of disease pathogenesis in AH have raised the possibility of targeted therapies, such as anti-tumor necrosis factor-a monoclonals and pentoxifylline. Orthotopic liver transplantation is not recommended for patients with severe acute AH, as most have an unclear long-term prognosis in the context of ongoing excess alcohol ingestion at presentation.

Journal Article↗