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)

The results of liver biopsy in 100 patients with tuberculosis are reported. In 8 patients, biopsy only occurred secondarily, during liver disease which appeared during antituberculous treatment. In five cases, the association of rifamycin and isoniazid was probably responsible and the mild histological signs noted suggested a favourable course after stopping one of the drugs or simply reducing the dose. The 3 other patients had virus hepatitis and biopsy was of prognostic interest by revealing the onset of post-hepatic cirrhosis. In 92 cases, liver biopsy was carried out before treatment. In 34 cases the liver was normal, in 38 patients there were hisotlogical changes which did not suggest tuberculosis but, probably, alcoholism. These were : steatosis, in 21 cases, cirrhosis in 8 cases, a mixture of steatosis and cirrhosis in 4 cases, and acute alcoholic hepatitis in 5 cases. Finally, in 20 cases, biopsy revealed an appearance of granulomatous hepatitis. Although this lesion is significant in the development of the disease, it is not characteristic of tuberculosis unless there is caseous necrosis, as in 2 cases, and unless culture of the biopsy material is positive, as in one case out of 9, i.e. the diagnostic interest of liver biopsy is not very great compared with prognostic interest. By determining the anatomical condition of the liver, often not obvious when simple liver function tests are carried out, it permits one to forsee to some extent the tolerance of the liver to antituberculous treatment, especially in alcoholics.
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PMID:[Information obtained by liver biopsy in 100 tuberculous patients]. 17 Jun 85

5 patients treated with perhexiline maleate, 200-400 mg/day for at least 6 months, exhibited evidence of hepatitis. The picture was very similar to acute alcoholic hepatitis, clinically, biologically and histologically with presence of necrosis, Mallory's hyaline, polynuclear infiltration and to a lesser degree, steatosis. Association with peripheral neuropathy, hypoglycemia, and renal failure appears strikingly frequently. The evolution was severe since 3 patients died within 6 months, even after treatment withdrawal. Further studies are to be done to understand the mechanisms of hepatic and neurologic toxicity, and to measure the hazards of this drug. These studies could bring a new insight to alcohol toxicity.
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PMID:Perhexiline maleate-induced hepatitis. 68 Apr 19

Needle-hepatic biopsy of 48 chronic alcoholic patients was investigated by the aid of electron microscopy. On the base of clinical and histological features five stages of the hepatic lesion could be distinguished: 1. fatty liver, 2. fatty liver with increasing activity of the mesenchymal cells, 3. acute alcoholic hepatitis ,4. chronic alcoholic hepatitis, 5. alcoholic cirrhosis. Changes of the liver cell organella and mesenchymal cells in different stages were compared. It was observed, that the damage to the hepatocytes--exept acute alcoholic hepatitis--was not parallel to the severity of the clinical picture. On the other hand proliferation of mesenchymal cells their secretory activity and fibrogenesis seem to go parallely with the progression of the hepatic lesion. Authors assume, that between alcoholic hepatitis and alcoholic cirrhosis there exists an intermedier form of the disease i.e. the chronic agressive alcoholic hepatitis ,which morphologically is similar to the chronic agressive hepatitis. This form of the hepatic lesion can be characterized not by the severity of the lesion of hepatocytes, but the by enormous proliferation of mesenchymal cells and by lymphocytic infiltration.
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PMID:[Electron microscopic study of alcoholic liver damage, with special reference to changes in the mesenchymal liver cells]. 85 35

Opsonic glycoprotein, alpha 2-HS-glycoprotein concentration was studied in the serum of 753 patients with various hematological, malignant, immunological, metabolic, endocrine and liver diseases and 68 healthy controls. Decreased serum alpha 2-HS-glycoprotein levels were detected in patients with acute leukemias, chronic granulocyte and myelomonocyte leukemias, lymphomas, myelofibrosis, multiple myeloma, metastatizing solid tumors, systemic lupus erythematosus, rheumatoid arthritis, acute alcoholic hepatitis, fatty liver, chronic active hepatitis, liver cirrhosis, acute and chronic pancreatitis, and Crohn's disease. Elevated levels were measured in patients with B and NANB/C hepatitis. Further decreased levels were observed in some groups with secondary infections. Serum alpha 2-HS-glycoprotein levels are affected by many factors, influencing the synthesis and elimination of the protein. The detection of serum alpha 2-HS-glycoprotein concentration has no specific diagnostic value as a marker for tumors or other diseases, however, its determination can be useful for the assessment of a non-specific regulator of the host defence.
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PMID:[Diagnostic value of the determination of serum alpha2-HS-glycoprotein]. 140 55

The work deals with a group of 212 patients suffering from various forms of precirrhotic alcoholic liver disease and includes a period of 8.5 years (January 1981-June 1989). At least two liver biopsies were performed in all patients. according to the histological diagnosis, the patients were distributed into 6 subgroups: simple hepatic steatosis--24 cases (11.3%), hepatic fibrosis--40 cases (18.8%), hepatic steatofibrosis--69 cases (32.5%), acute alcoholic hepatitis--18 cases (8.5%), chronic active hepatitis--43 cases (20.3%) and chronic persisting hepatitis--18 cases (8.5%). The assessed histological parameters included: fatty transformation, hepatic fibrosis, inflammatory infiltrate within the lobules and in the portal spaces, hepatocellular necrosis, cholestasis, proliferation of the bile ductules and modification of the lobular architectonic. The work is aimed at pointing out the precirrhotic hepatic histological lesions induced by alcohol and fraught with an increased risk of progression towards liver cirrhosis. The histological sequential examination of alcoholic hepatic lesions confirm the possibility of progression and installation of the cirrhotic stage for a number of these lesions. Liver cirrhosis developed in 44 patients (20.7%) within a period of 3-7 years, on an average 5.5 years. The progression toward cirrhosis occurred in 12 patients (5.7%) with steatofibrosis, in 11 (5.2%) with hepatic fibrosis, in 14 (6.6%) with an intralobular inflammatory infiltrate, in 17 (8%) with hepatocellular necrosis, in 3 (1.4%) with cholestasis, in 5 (2.3%) with proliferation of the bile ductules and in 10 patients (4.7%) with a modification of the lobular architectonic. In addition, cirrhosis was detected in 8 patients (3.8%) with alcoholic hepatitis and in 13 patients (6.1%) with chronic active hepatitis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[The criteria of histological activity and the prognosis in precirrhotic alcoholic hepatopathies]. 167 Jan 14

Life-table analysis is a suitable method for evaluating the effectiveness of therapeutical approaches to and the progression of, chronic diseases. The authors performed 324 liver biopsies in patients with liver disease between 1976 and 1986. The cumulative life-table analysis of Cutler and Ederer was applied in this retrospective study. Survival rates of different groups of patients expressed as the 7-year life expectancy were as follows: toxic hepatitis 90%, steatosis hepatitis 87%, chronic persistent hepatitis 87%, nonspecific reactive hepatitis 76%, chronic active hepatitis 72%, acute alcoholic hepatitis 66%, liver cirrhosis 40%. There seems to be a correlation between the severity of histological alteration and live expectancy. A similar correlation between the inflammatory cell infiltration and life expectancy cannot be observed. The life expectancy of patients with chronic active hepatitis has significantly improved recently. Further improvement of survival of patients with liver cirrhosis can be expected only from a reduction of alcohol consumption. The results can be regarded as a reference data for life expectancy of patients with chronic liver disease in Hungary.
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PMID:Life expectancy in chronic liver disease. 324 56

Serum catalase activity was moderately increased in fatty liver, acute alcoholic hepatitis and in the decompensated form of cardiac circulatory failure. It showed significant increase in acute yellow atrophy and in toxic hepatitis while no changes were detected in liver cirrhosis and viral hepatitis. Serum catalase activity showed a good correlation (r = 0.820) with the serum glutamate dehydrogenase activity. In accordance with our results, the inexpensive assay of serum catalase activity is suggested for the detection of severe liver cell damage.
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PMID:Serum catalase enzyme activity in liver diseases. 345 88

Sera from 71 patients with acute liver injury have been tested for antibodies to hepatocyte membrane lipoprotein complex (LSP) using a sensitive radioimmunoassay. Two main patterns of anti-LSP response were seen. In the first, seen in patients with type A and B viral hepatitis, anti-LSP antibodies were detectable at presentation, with the highest titres two to 10 days before the peak in serum aminotransferases and, in the hepatitis B patients, when viral DNA polymerase concentrations were still high, indicating active viral replication. These findings are consistent with the anti-LSP response being consequent on an interaction between T cells and neoantigens on the liver cell surface. A similar pattern was found in halothane hepatitis where immune responses to a halothane-altered liver membrane antigen are present early in the course of the disease. In the second type of response, exemplified by cases with paracetamol-induced hepatic necrosis, anti-LSP was only occasionally detectable at presentation, although present in very low titre later in the clinical course. This may be due to the release of altered antigen at the time of hepatocellular injury. The same pattern was found in a selected group of patients with uncomplicated acute alcoholic hepatitis, suggesting that in both these groups of patients the liver damage may have been due to a direct toxic effect on liver cells.
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PMID:Anti-LSP antibodies in acute liver disease. 708 6

Hepatic toxicity was observed in mice which had received Griseofulvin or Perhexilin Maleate over a period of several months. Treatment of griseofulvin alone gave rise to hepatitis with the presence of Mallory bodies (MB) whereas the same length of treatment with Perhexilin Maleate was associated with steatonecrosis with an absence of MB. When treatment was followed by a one month rest period hepatic lesions disappeared with no trace of sequelae. Cross-treatment studies showed that one week of Perhexiline Maleate was sufficient to induce MB in mice pretreated with Griseofulvin. Similarly, Griseofulvin administered to mice pretreated with Perhexilin Maleate gave rise to MB formation after one week as opposed to the usual two months incubation time (DENK et al.). The histological nature and mode of formation of these MB was identical to that encountered in acute alcoholic hepatitis. On addition, combined drug therapy employing Perhexilin Maleate suggests a particular hepatic toxicity in man in cases where the liver has become predisposed due to other therapeutic.
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PMID:[Comparative hepatic toxicity of perhexiline maleate and griseofulvin in mice]. 720 77

The precise mechanism of the pathogenesis of alcoholic hepatitis is unknown, but immune involvement may perpetuate and exacerbate the process. Heat-shock proteins, normally protective, may be immunogenic and have been shown to induce antibody formation in some inflammatory conditions. Alcohol, cellular hypoxia and tumor necrosis factor, all involved in alcoholic hepatitis, are potent inducers of heat-shock protein. In this study, we sought 60-kD heat-shock protein in liver tissue with a murine monoclonal antibody and measured circulating antibody to 60-kD heat-shock protein on ELISA. Fourteen of 20 livers from patients with acute alcoholic hepatitis expressed 60-kD heat-shock protein in hepatocyte cytoplasm in a diffuse pattern with superimposed clusters; other cell types were occasionally positive. Twelve of these patients had high-titer IgA 60-kD heat-shock protein antibody in serum. In contrast, 60-kD heat-shock protein was identified in only 2 of the 10 patients with alcoholic cirrhosis without hepatitis (p = 0.013). These two patients had severe liver disease, and one patient in this group was seropositive for IgA 60-kD heat-shock protein antibody. Eight alcoholic patients with fatty liver alone were negative for antigen, and all but one were negative for antibody. The 10 patients without liver damage were negative for antigen and antibody. The findings that 60-kD heat-shock protein is present in liver tissue of patients with acute alcoholic liver damage and that circulating IgA 60-kD heat-shock protein antibody levels are increased may point to one pathogenetic mechanism underlying development and progression of liver damage in alcoholic hepatitis.
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PMID:Hepatic 60-kD heat-shock protein responses in alcoholic hepatitis. 851 53


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