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At least 19 recordsLinked to original sources
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↗
PubMed1977

[Acute alcoholic hepatitis].

Acute alcoholic hepatitis is an anatomical (fatty liver with sclerosing hyaline necrosis) and a clinical (hepatomegaly with a variety of symptoms of hepatic failure) entity arising out of chronic alcoholism, and of a typically 'pre-cirrhotic' state. Although fatal in 25% of acute cases due to failure of homeostasis, it often leaves a centrilobular scarring necrosis which in more than 60% of cases progresses to nodular cirrhosis. Continued alcoholism worsens the prognosis. Alcoholic hepatitis may be confused with acute abdominal catastrophes or with a hepatoma. The characteristic Mallory bodies found on liver biopsy are found rarely in non-alcoholic hepatitis. There is no effective treatment for this disease except reduction of alcohol intake; indeed, the disease may become self-perpetuating.

Acute Disease↗
PubMed1977

Alcoholic hepatitis with and without alcoholic hyaline.

Sixteen cases of alcoholic hepatitis with alcoholic hyaline (Group I) and 13 cases without alcoholic hyaline (Group II) have been collected since 1970. These were most frequently found in the fifth decade in both groups. One female was found in Group I. Cases of about two-thirds of both groups were comsumers of 110 g or more of alcohol per day. No significant differences except fever and erythrocyte sedimentation rate were found in clinical and laboratory changes between both groups. Fatty change in liver biopsy specimens were more frequently seen in Group I than in Group II. The wedged hepatic venous pressure was markedly elevated in alcoholic hepatitis with cirrhosis and moderately elevated in alcoholic hepatitis without cirrhosis. Wedged hepatic venography showed the main portal trunk and extrahepatic collaterals, namely, reversal of the portal flow or such tendency in 2 out of 5 patients of Group I.

Adult↗
PubMed1977

Difference of hepatic circulation between alcoholic and non-alcoholic hepatic cirrhosis.

Comparisons were made of hepatic circulation between alcoholic and non-alcoholic cirrhosis. The wedged hepatic venous pressure and per cent intrahepatic shunt measured by the method of continuous infusion of D-galactose-1-14C were similarly markedly increased. On the other hand, the wedged hepatic venography showed the main portal trunk and extrahepatic collaterals, namely, the tendency of reverse or stagnant portal flow, more frequently in alcoholic cirrhosis than in non-alcoholic cirrhosis. The nodules shown by slow low-pressure hepatic sinusoidography were larger in non-alcoholic cirrhosis than in alcoholic cirrhosis.

Blood Pressure↗
PubMed1976

Alcoholic hepatitis. Cell-mediated immunological response to alcoholic hyalin.

Immunological reactivity in alcoholic hepatitis has bben attributed to alcoholic hyalin, the histological hallmark of this disease. A purified isolate of alcoholic hyalin with electron microscopic, biochemical, and serological characteristics documented previously was added to lymphocytes from healthy subjects and patients with alcoholic hepatitis or other hepatic disorders. Production of migration inhibition factor (MIF) in response to this material was used as an index to lymphocyte reactivity. MIF was significantly increased in lymphocytes obtained from patients with alcoholic hepatis, as compared to the healthy controls (P less than 0.001), and persons with other liver diseases (P less than 0.005). These observations indicate that immunological hyperreactivity to alcoholic hyalin occurs in patients with alcoholic hepatitis; such activity may be of key importance in the pathogenesis or sequelae (or both) of this disease.

Alcoholism↗
PubMed1979

[Lymphocytotoxicity in alcoholic hepatitis: evalutation of effector cells].

Alcohol induced liver damage has been recently suggested to occur in some cases as a consequence of a true autoimmune reaction. However the nature of the effector cells is still debated. Microlymphocytotoxicity "in vitro" test against rabbit hepatocytes has been performed in 29 patients with alcoholic cirrhosis and 8 with acute alcoholic hepatitis. The diagnosis has been done on clinical and histological grounds. The mean cytotoxicity index (CI) of subjects with alcoholic cirrhosis was 15.12 +/- 14.18 and with acute alcoholic hepatitis 62.49 +/- 16.33 (normal range: 0 -37.90). To further characterize the effector cells in our system, the test has been performed again either using T-enriched fractions of peripheral lymphocytes or after pronase-induced digestion of SmIg of total lymphocytes in 5 patients with acute alcoholic hepatitis and high CI. In both instances a disappearance of citotoxic activity has been observed. These data suggest: a) autoimmune reaction can occur only in patients with acute alcoholic liver damage; b) non T-cells are responsible for cytotoxicity; c) the immune reaction appears to be of cell-mediated antibody-dependent type.

Adolescent↗
PubMed1975

Post-jejunoileal-bypass hepatic disease. Its similarity to alcoholic hepatic disease.

The authors studied serial hepatic biopsies of five patients who developed hepatic failure following jejunoileal bypass for extreme obesity, with autopsies of two. The hepatic histologic changes included centrilobular or focal alcoholic hyalin, intrasinusoidal collagenosis, fatty hydropic degeneration, and neutrophilic infiltrate. At least two of the patients were abstinent from alcohol, both prior to and after the surgical procedures. The others, after the bypass procedures, had reduced alcohol consumption from previous levels. All patients developed hepatic failure and histologically progressive hepatic disease with alcoholic hyalin and other changes indistinguishable from alcoholic hepatic disease in 21/2 to 5 months, in spite of hyperalimentation and re-establishment of intestinal continuity in four. Nausea, vomiting, abdominal pain and ascites were prominent complaints. Four of the five patients died in hepatic failure. The authors conclude that these cases of progressive hepatic disease with histologic changes simulating those found in livers of alcoholic patients offer evidence that heavy alcohol consumption may affect the liver in an indirect fashion.

Adult↗
PubMed1978

Depressed delayed cutaneous hypersensitivity in alcoholic hepatitis.

Delayed cutaneous hypersensitivity was studied in 10 patients with severe alcoholic hepatitis, 9 patients with either inactive alcoholic cirrhosis or alcoholic fatty liver, and 10 agematched controls. The mean response of the alcoholic hepatitis group was significantly less compared to controls for SK-SD (P less than 0.001), mumps (P less than 0.001), trichophyton (P less than 0.025), and Candida albicans (P less than 0.025). Upon clinical recovery, the response of the 6 surviving patients with alcoholic hepatitis was similar to controls for 4 of the 5 antigens tested, and the improvements in response to SK-SD and Candida albicans were significant (P less than 0.02 and P less than 0.05). The mean percentage and absolute numbers of thymus-derived lymphocytes were significantly less in the alcoholic hepatitis group compared with controls. Both the alcoholic hepatitis patients and patients with less advanced alcoholic liver disease had a diminished response to concanavalin A and phytohemagglutinin. This study demonstrates a reversible depression of delayed cutaneous hypersensitivity in alcoholic hepatitis. Several mechanisms may help account for this finding. We recommend that skin tests in patients with alcoholic hepatitis be interpreted with this phenomenon in mind.

Antigens↗
PubMed1977

Alcoholic hyalin, microfilaments and microtubules in alcoholic hepatitis.

The alcoholic hyalin which is composed of light and dark occasionally swollen and conglomerating filaments, is found to be surrounded by proliferated RER, hypertrophied Golgi apparatus and mitochondria containing enlarged matrical granules. Besides, microfilaments and some microtubules are seen in relation to the hyaline bodies. In biopsies where hyaline bodies are scarce, hepatocytes without alcoholic hyalin present similar changes and the Golgi apparatus is seen to contain very low density lipoprotein-like particles. These ultrastructural changes are suggested to be related to an early stage in the development of alcoholic hyalin. The abundance of microfilaments indicates an increased motility of the hepatocytes, possibly as a part of the regenerative processes. It can hardly be precluded that microfilaments disintegrate and accumulate in the alcoholic hyaline mass.

Adult↗
PubMed1979

Hyperalimentation in alcoholic hepatitis.

Enteral hyperalimentation in four patients with severe alcoholic hepatitis and anorexia increased spontaneous food intake, increased their nitrogen balance and the patients improved clinically. Seven patients with alcoholic hepatitis, who were clinically ill and able to eat only 410-1,100 calories per day, were given a 900 mosM/l. parenteral "hyperalimentation" solution by a peripheral vein (P-900). The intravenous nutrition provided daily 51.6-77.4 gm. amino acids in addition to oral intake. All patients improved. None developed detectable encephalopathy after 16-42 days of P-900 therapy. Five additional patients had ascites and alcoholic hepatitis. The daily infusion of 2,000 ml. P-900 was not associated with hyponatremia, renal failure or encephalopathy in four of these five patients who improved and continued their diuresis. P-900 therapy was discontinued in one because of progressive hyponatremia. The observations indicate that over and above the maximum tolerable oral nutrition, intravenous nutrition can be effectively utilized by clinically ill, jaundiced patients with alcoholic hepatitis without precipitating encephalopathy or interference with standard therapy of ascites.

Hepatitis, Alcoholic↗
PubMed1976

Sclerosing hyaline necrosis in noncirrhotic chronic alcoholic hepatitis.

A group of 18 chronic alcoholic patients who had sclerosing hyaline necrosis in noncirrhotic livers was compared with a group of 12 similar individuals with acute alcoholic hepatitis, but no centrilobular fibrosis. In cases with sclerosing hyaline necrosis, the most characteristic features were portal hypertension with very large, tender livers and unusually high glutamic-oxalacetic transaminase values; these were associated with centrilobular fibrosis and abundant alcoholic hyalin. Three of these patients died within two years and in two of these, early cirrhosis was found at necropsy. In the cases of acute alcoholic hepatitis, hepatomegaly was the most conspicuous finding, and only a single patient died; death here was unrelated to hepatic disease, the liver being unremarkable at necropsy. Patients who had sclerosing hyaline necrosis tended to remain ill for significantly longer periods. These observations, in conjunction with evidence gathered from the literature, seem to suggest that sclerosing hyaline necrosis is an obligatory step in the natural evolution of alcoholic hepatic disease, especially in cases that evolve into cirrhosis.

Alcoholism↗
PubMed1978

Corticosteroid therapy of alcoholic hepatitis.

Fifty-five patients with alcoholic hepatitis were studied in a 28- to 32-day randomized double blind treatment trial comparing prednisolone (40 mg per day) with placebo therapy. Of 31 placebo-treated patients, 4 died during the study interval and 2 more died within 5 days of study completion. Only 1 of 24 prednisolone-treated patients died during the same interval (Fisher exact test; P = 0.10). Stepwise discriminant analysis of laboratory factors associated with death revealed independently significant associations with prolongation of prothrombin time and height of serum bilirubin at the initiation of the study. When treatment was included as a variable in this discriminant analysis, it was found that corticosteroid therapy significantly decreased mortality (P less than 0.05). The corrected wedged hepatic venous presure decreased to a similar extent in the two groups. These studies suggest that corticosteroid therapy does decrease early mortality in patients with severe alcoholic hepatitis, but has no short term effect on the development of portal hypertension.

Adult↗
PubMed1977

Alcoholic hyalin antigen (AHAg) and antibody (AHAb) in alcoholic hepatitis.

Complement fixation (CF) and immune adherence (IA) hemagglutination tests demonstrate antigen (Ag) and antibody (Ab) to alcoholic hyalin (AH) in serum of patients with alcoholic hepatitis. Immunoglobulins from postmortem liver of patients dying of alcoholic hepatitis show antibody activity against AH. Isolated purified AH was used to produce AHAb in rabbits. Rabbit antiserum was added to heat-inactivated human serum to detect AHAg; purified AH was added to serum and tissue elutes to detect AHAb. AHAg was present in serum of each of 15 patients with early phase alcoholic hepatitis in CF titers of 8 to 64 and IA titers of 16 to 2048. AHAg became negative within 3 to 5 weeks with abstinence from alcohol and was followed by transient appearance of AHAb. AHAb was present in 11 patients with advanced phases of alcoholic hepatitis in CF titers of 8 to 640 and IA titers of 16 to 4096. Four patients in this group exhibited concomitant AHAb and AHAg. Investigations of liver tissue elute reveal that patients with advanced alcoholic hepatitis or active alcoholic cirrhosis have AHAg-reactive immune complexes containing IgG and IgA immunoglobulins.

Animals↗
PubMed1979

[Acute tubular necrosis in acute alcoholic hepatitis with cardiac beriberi (author's transl)].

In one case of fulminant hepatic failure by acute alcoholic hepatitis, renal failure seemed to be related to active renal vasoconstriction by systemic endotoxemia due to impaired hepatic clearance of toxins, associated with or complicated by a located intravascular coagulation with acute tubular necrosis. The associated thiamin deficiency may have accentuated this renal vasoconstriction.

Acute Disease↗
PubMed1977

Lymphocyte cytotoxicity in alcoholic hepatitis.

Studies were undertaken to evaluate the cytotoxicity of peripheral lymphocytes obtained from patients with alcoholic hepatitis. Lymphocyte cytotoxicity to Chang liver cells was investigated by a microcytotoxicity test, and that to autologous liver cells obtained by percutaneous liver biopsy was studied using a 51Cr release assay. Lymphocytes from patients with alcoholic hepatitis were found to be highly cytotoxic to Chang liver cells and autologous liver cells when compared to those of healthy subjects (P is less than 0.001). Cell-free supernatant fluid of lymphocytes from patients with alcoholic hepatitis incubated with purified alcoholic hyalin for 5 days was significantly cytotoxic to Chang liver cells (P is less than 0.01), indicating that a cytotoxic factor is elaborated by sensitized lymphocytes. A significant reduction in cytotoxicity was noted with disappearance of clinical features or direct addition of a purified isolate of alcoholic hyalin or its preincubation with lymphocytes. Preincubation of sensitized lymphocytes with acetaldehyde increased cytotoxicity for autologous liver beyond that obtained by the combined effects of lymphocytes alone and acetaldehyde alone (P is less than 0.001), interpreted as evidence that ethanol toxicity and hyperactivity of lymphocytes independently and collectively contribute to development of cirrhosis in patients with alcoholic hepatitis who continue to imbibe alcohol.

Acetaldehyde↗