Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0019158 (hepatitis)
 30,205 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Lysozyme is a bacteriocidal enzyme which is a major stable secretory product of mononuclear phagocytes, including hepatic sinusoidal macrophages (HSM), and serves as a good marker for these cells. Patients with alcoholic liver disease (ALD) have decreased HSM function which is reflected in reduced clearance of microorganisms and endotoxin derived from the gut. The HSM population in 54 liver biopsies from patients with ALD was studied using immunoperoxidase staining of lysozyme and was compared with 15 histologically normal controls. In both groups lysozyme positive HSM were more numerous in periportal than perivenous parenchyma. In each zone there were significantly fewer positive HSM in cases of ALD than in controls, in alcoholic hepatitis than in ALD without hepatitis, and in cirrhosis than in ALD without cirrhosis. These findings suggest a decreased population of functionally active HSM in ALD which correlates with severity of liver damage. This might be due to decreased lysozyme content of the entire HSM population or to the existence of two populations, one positive and one negative for lysozyme. The observed decrease in HSM function explains many of the phenomena observed in ALD.
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PMID:Hepatic sinusoidal macrophages in alcoholic liver disease. 390 65

Amiodarone has proved very effective in the treatment of otherwise resistant cardiac tachyarrhythmias. The use of amiodarone has, however, been limited due to its serious side-effects. A patient with cholestatic hepatitis due to amiodarone treatment is presented below and a review of the hepatotoxicity of amiodarone is given. It is concluded that solid evidence exists of hepatic injury due to amiodarone treatment, including steatosis, alterations resembling alcoholic hepatitis, cholestatic hepatitis and micronodular cirrhosis of the liver. Patients receiving amiodarone should be regularly screened with respect to hepatic enzyme levels. Therapy should be discontinued on the suspicion of cholestatic injury or hepatomegaly.
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PMID:Hepatotoxicity of amiodarone. 396 37

A patient who abstained from alcohol consumption but who had asymptomatic chronic progressive hepatomegaly, mild disturbance of liver function tests and hepatitis resembling alcoholic hepatitis (nonalcoholic steatohepatitis) developed glucose intolerance several years after the hepatitis was diagnosed. The patient had a family history of both diabetes and chronic liver disease. A lesion resembling alcoholic hepatitis in a patient who denies alcohol consumption, may be diabetic or pre-diabetic in aetiology and such a patient should be followed up with glucose tolerance tests.
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PMID:Diabetic hepatitis preceding the onset of glucose intolerance. 398 46

An enzyme-linked immunosorbent assay was developed to detect insoluble liver cell membrane antigen (LMAg) which gives rise to serum LMA (anti-LM) in HBsAg-negative patients. The optical density (OD) ratio of the average LMAg level of normal subjects was less than 1.2. In HBsAg-positive cases, high LMAg levels (OD ratio greater than 2.4) were noted in 8 of 8 patients with acute hepatitis (AH), 3 of 8 with chronic persistent hepatitis (CPH), 5 of 10 with moderate chronic aggressive hepatitis (CAH), 7 of 10 severe CAH and 4 of 8 with liver cirrhosis (LC). In HBsAg-negative cases, however, high LMAg levels were noted in only 6 of 8 patients with AH, 1 of 10 with CPH, 1 of 10 with moderate CAH, 1 of of 10 with severe CAH, 0 of 8 with LC, 0 of 8 with fatty liver and 5 of 10 with alcoholic hepatitis. In micro-immunodiffusion experiments, intensively absorbed rabbit anti-rat LM precipitated two organ-specific components of rat liver homogenate, one of which was identical to liver specific protein (LSP). In immunohistochemical demonstrations of LMAg and LSP, anti-LM, prepared from the serum of a HBsAg-negative CAH patient, bound to both human and rat acetone-fixed liver cell membranes, but not to those of human or rat kidneys. Absorbed rabbit anti-rat LM also bound to liver cell membranes, but absorbed anti-rat LSP lacked organ-specificity when assayed with the immunofluorescence technique using acetone-fixed liver sections. In conclusion, the appearance of serum LMAg was associated with high-SGPT patients and HBsAg-positive CAH patients.
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PMID:Detection and clinical significance of acetone-insoluble liver cell membrane antigen in sera of patients with chronic active liver diseases. 404 Apr 88

In order to assess the specificity of transferrin molecular changes, we compared concentrations of subfractions and total transferrin in cirrhotic patients, in patients having non-alcoholic hepatitis, in patients with liver cancer, and in controls. The study was carried out in 79 patients divided into four groups: 20 patients with biopsy-proven cirrhosis of alcoholic origin, 20 patients with non-alcoholic hepatitis, 19 patients with liver cancer and 20 controls. Subfractions of serum transferrin were separated by isoelectric focusing followed by direct immunofixation. Fractions pI 5.7 percentages (expressed as percentages of one fraction over total transferrin) were significantly higher in the cirrhotic group than in the control group (p less than 0.01). Fraction pI 5.9 percentages were significantly higher in the cirrhotic group than in the hepatitis or control groups (p less than 0.05), or liver cancer group (p less than 0.01). A quantitative increase of fraction pI 5.7 was found in the cirrhotic patients. However, in this study, this parameter did not discriminate between patients with parenchymal liver diseases of alcoholic or other origin. Therefore, the value of determining fraction pI 5.7 as a marker of chronic alcohol consumption seems questionable. The elevation of fraction pI 5.9 constantly found in the cirrhotic patients could not be explained and needs further investigations.
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PMID:A study of the microheterogeneity of transferrin in cirrhotic patients. 405 85

The extractable and nonextractable collagen and glycosaminoglycuronans (GAG) were estimated and characterized in 32 dried, defatted human livers obtained at necropsy. 10 had normal livers. 22 of the 32 livers were from patients who drank in excess: 5 had fatty livers, 7 had alcholic hepatitis, and 10 had cirrhosis. Livers with alcoholic hepatitis or cirrhosis had significantly increased total and 1 N NaCl-extractable collagen. Only alcoholic hepatitis livers had significantly increased Tris-buffer-extractable GAG, but the amino acid composition of these GAG (proteoglycans) was no different from that of normal livers. The major fraction of these GAG had isoelectric pH (pI) </= 3.1 in all livers. Livers with alcoholic hepatitis or cirrhosis had significantly increased nonextractable GAG. The major GAG fraction of all livers was chondroitin-4 or -6-SO(4). Alcoholic hepatitis livers had a significant increase of hyaluronic acid and an unidentified hyaluronidase-resistant GAG. Fatty livers showed no differences from normal ones. The data indicates that alcoholic hepatitis is associated with a significantly increased fibroblast activity, but fatty livers of alcoholics are not. The changes in histologically "inactive" micronodular cirrhosis of alcoholic patients indicate continued activity of fibroblasts in the connective tissue of these cirrhotic livers.
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PMID:Natural history of alcoholic hepatitis. IV. Glycosaminoglycuronans and collagen in the hepatic connective tissue. 427 Jun 46

A group of 258 patients with various forms of alcoholic liver disease-steatosis, mild and severe hepatitis, and cirrhosis-has been studied. Severity of disease as judged histologically did not correlate very well with clinical presentation although signs of hepatocellular failure were certainly commoner in severe hepatitis and cirrhosis. Fever, pigmentation, and clubbing were also pointers to these two conditions. Alcoholic hepatitis is probably precirrhotic and carries a poor prognosis and the best laboratory indicators of this are moderate elevation of white cell count and bilirubin. Prognosis in alcoholic liver disease is significantly improved by abstinence from alcohol.
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PMID:Studies in alcoholic liver disease in Britain. I. Clinical and pathological patterns related to natural history. 436 73

Serum interferon activity was measured in 40 patients with acute viral hepatitis A, B and non-A-non-B during the acute stage of the disease and correlated with the severity, the long-term outcome and the viral etiology of the disease. Patients with alcoholic hepatitis, patients with an influenza-like illness and healthy volunteers served as controls. 80% of all patients with virus hepatitis revealed no measureable or only borderline interferon activity in their serum. No correlation was found with severity and long-term outcome of the disease, but patients with virus hepatitis A showed a stronger interferon induction than patients with hepatitis B and non-A-non-B. Further investigations of the interferon system in patients with virus hepatitis might help to improve our understanding of the different forms of the disease. The data presently available, however, do not permit as yet to define the value of interferon in the treatment of severe forms of acute virus hepatitis.
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PMID:[Interferon production in acute virus hepatitis]. 608 27

Using a leucocyte migration inhibition test sensitisation to Mallory bodies (alcoholic hyalin) was found in a statistically significant 41% of 17 patients with alcoholic hepatitis. Patients with alcohol-induced fatty liver and cirrhosis did not demonstrate sensitisation. Mallory bodies are a characteristic feature of alcohol-induced liver damage, and immunological sensitisation to them might lead to liver cell death and cell progression of the hepatitis process.
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PMID:Sensitisation to Mallory bodies (alcoholic hyalin) in alcoholic hepatitis. 616 47

Circulating antibodies reacting specifically with hepatocytes isolated from ethanol pretreated rabbits have been demonstrated by two techniques - induced cytotoxicity and immunofluorescence. In the cytotoxicity assay antibodies were found in seven of 19 (39%) of patients with alcoholic fatty liver (with or without fibrosis), six of 13 (46%) of those with alcoholic hepatitis, 15 of 36 (43%) of those with cirrhosis, and seven of 14 patients (50%) of those with hepatitis and cirrhosis. In the immunofluorescence studies, nine of 15 sera induced a granular pattern of fluorescence on the ethanol pretreated hepatocytes; two sera which induced significant cytotoxicity did not induce immunofluorescence. No ethanol related antibodies were found in normal individuals or in patients with other types of acute or chronic liver disease. These results show that antibodies directed against ethanol altered liver cell determinants are present in the serum of 43% of patients with alcoholic liver disease, and suggest a mechanism whereby chronic alcohol consumption may, by inducing antigenic changes in hepatocyte membranes, trigger a cell damaging immune reaction.
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PMID:Antibodies to alcohol altered liver cell determinants in patients with alcoholic liver disease. 619 63


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