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)

To aid understanding of markers of disease and predictors of outcome in alcohol-exposed systems, we undertook a literature survey of more than 700 articles to view the morphological characteristics and the clinical and experimental epidemiology of the Mallory body. Mallory bodies are filaments of intermediate diameter that contain intermediate filament components (e.g., cytokeratins) observable by conventional light microscopy or immunohistochemical methods, identical in structure regardless of initiating factors or putative pathogenesis. Although three morphological types can be identified under electron microscopy (with fibrillar structure parallel, random or absent), they remain stereotypical manifestations of hepatocyte injury. A summary of the conditions associated with Mallory bodies in the literature and their validity and potential etiological relationships is presented and discussed, including estimates on the combined light microscopic and immunohistochemical prevalences and kinetics. Emphasis is placed on proper confounder control (in particular, alcohol history), which is highly essential but often inadequate. These conditions include (mean prevalence of Mallory bodies in parentheses): Indian childhood cirrhosis (73%), alcoholic hepatitis (65%), alcoholic cirrhosis (51%), Wilson's disease (25%), primary biliary cirrhosis (24%), nonalcoholic cirrhosis (24%), hepatocellular carcinoma (23%), morbid obesity (8%) and intestinal bypass surgery (6%). Studies in alcoholic hepatitis strongly suggest a hit-and-run effect of alcohol, whereas other chronic liver diseases show evidence of gradual increase in prevalence of Mallory bodies with severity of hepatic pathology. Mallory bodies in cirrhosis do not imply alcoholic pathogenesis. Obesity, however, is associated with alcoholism and diabetes, and Mallory bodies are only present in diabetic patients if alcoholism or obesity complicates the condition. In addition, case studies on diseases in which Mallory bodies have been identified, along with pharmacological side effects and experimental induction of Mallory bodies by various antimitotic and oncogenic chemicals, are presented. Mallory bodies occur only sporadically in abetalipoproteinemia, von Gierke's disease and focal nodular hyperplasia and during hepatitis due to calcium antagonists or perhexiline maleate. Other conditions and clinical drug side effects are still putative. Finally, a variety of experimental drugs have been developed that cause Mallory body formation, but markedly different cell dynamics and metabolic pathways may raise questions about the relevance of such animal models for human Mallory body formation. In conclusion, the Mallory body is indicative but not pathognomonic of alcohol involvement. A discussion on theories of development and pathological significance transcending the clinical frameworks will be presented in a future paper.
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PMID:The Mallory body: morphological, clinical and experimental studies (Part 1 of a literature survey). 792 9

Alcoholism alone, or in combination with other etiologic factors, is a common cause of liver failure because of hepatitis, cirrhosis, and/or hepatocellular cancer. Encountered morphologic and functional alterations are due to immunologic reactivity to cell injury evoked by acetaldehyde, other noxious factors, and nutrient deficits. Less than 20% of subjects who consume over 90 g/d of ethanol for years develop progressive liver damage and cirrhosis. Alcoholism should be interrupted in patients with subclinical hepatic abnormalities. Although early alcoholic hepatitis and cirrhosis respond to abstinence and symptomatic therapy, available measures have little influence on functional and morphologic abnormalities in end-stage alcoholic liver disease. Resection is desirable for localized hepatocellular cancer, and liver transplantation should be considered for cirrhosis. Transplantation is appropriate for patients with uncomplicated end-stage alcoholic cirrhosis in whom evidence of liver failure can be controlled during a 6-month period of rehabilitation. Continuous psychosocial support is required to prevent recividism in the posttransplant immunosuppressed alcoholic.
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PMID:Alcoholic liver disease. 813 22

Fulminant hepatic failure (FHF) is a poorly understood condition in which total liver failure occurs and is thought to be caused by a variety of conditions including Reye's syndrome, hepatitis, drug overdoses, and vascular insufficiency. While this condition is an uncommon one, it carries with it a high fatality rate and must therefore be diagnosed as rapidly as possible. Six patients have been observed over a two-year period with biopsy and/or autopsy-confirmed FHF: one with acute hepatitis B-delta; three with histories of alcoholism, two of them with cirrhosis; one with acute tylenol overdose; and one with hepatic vascular insufficiency. All of these patients, except one, exhibited a rapid, fatal downhill course after onset of symptoms. In all of these patients, a consistent elevation was observed in serum levels of aspartate aminotransferase (AST) or serum glutamate oxaloacetate transaminase (SGOT) and alanine aminotransferase (ALT) or serum glutamate pyruvate transaminase (SGPT) such that the ratio of AST to ALT was significantly greater than 1 and in serum levels of ammonia. Other liver function tests were found to be abnormal but not in so consistent a pattern, although total protein and albumin were found to be significantly decreased in all of these patients. The stereotypical elevation of the transaminases with high AST-to-ALT ratios and the rise in ammonia appear to characterize this life-threatening illness most reliably.
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PMID:Serum analyte pattern characteristic of fulminant hepatic failure. 820 19

One hundred and ninety-nine cases of hepatic injury related to antituberculous treatment were analysed in order to assess the role played by each drug and to look for predisposing factors. This is a retrospective study of 169 cases reported in the literature and 30 cases reported to the regional pharmacovigilance centre of Paris Saint-Antoine. The mortality rate was related to the dose of isoniazid: it was 43 percent with a daily dose higher than 300 mg, and 9 percent with a daily dose of 300 mg or less (P < 0.001). Hepatic injury appeared significantly earlier in the case of rifampicin combination: 11 weeks without rifampicin and 2 weeks with rifampicin (P < 0.01). The role of pyrazinamide was difficult to determine because isoniazid and pyrazinamide were always used in combination. The influence of a preexisting liver disease could not be evaluated because of the small number of cases reported (8 cases). Alcoholism did not increase the mortality rate. Our results confirm the dose-dependent toxicity of isoniazid. Because of the short time elapsed before the apparent onset of hepatitis observed with the rifampicin combination, a close supervision of the patients should be exerted during the first weeks of treatment.
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PMID:[Hepatic toxicity of antitubercular agents. Role of different drugs. 199 cases]. 824 40

Neurologic manifestations of severe infectious complications of drug abuse and chronic alcoholism are reviewed in this article. Portals of entry from cutaneous postinjection infections and multiple vascular injection sites may lead to pyomyositis, tetanus, infective endocarditis, meningitis, brain abscesses, and vertebral osteomyelitis. Chronic intranasal abuse of cocaine may be followed by frontal osteomyelitis, botulism, brain abscess, and visual loss. Problems of hepatitis, malaria, and syphilis in drug abusers are discussed also.
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PMID:Infections other than AIDS. 837 45

After undergoing withdrawal treatment for alcoholism as an in-patient for one year a 49-year-old woman was started on disulfiram, 250 mg daily, her liver function tests being normal. Except for vitamin B1 she received no further medication. Jaundice developed 13 days after onset of treatment and acute liver failure was diagnosed on the 18th day after a total disulfiram dose of 4.5 g (Quick value < 10%; bilirubin 460 mumol/l; GPT 5099 U/l; GOT 4142 U/l), as well as early renal failure (creatinine 300 mumol/l). An acute viral infection, autoimmune hepatitis and a metabolic liver disease were excluded by biochemical, serological and molecular biology tests. All toxicological tests were negative. The patient died 25 days after the onset of disulfiram treatment in hepatic coma due to a fulminant hepatitis with hepatorenal syndrome. Both a liver biopsy and the autopsy showed the signs of an acute hepatic dystrophy without cirrhosis. The temporal relationship between the disulfiram intake and onset of the illness, the exclusion of other causes of the fulminant hepatitis and the liver histology, which was compatible with a chemical-toxic hepatitis, indicate that this was a case of disulfiram-induced hepatitis. The hepatotoxicity of disulfiram is a very rare idiosyncratic reaction which is often fatal. Disulfiram administration must be discontinued at once if there is a rise in liver enzyme activity or jaundice occurs.
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PMID:[Fulminant hepatitis caused by disulfiram]. 840 76

We measured serum levels of carbohydrate deficient transferrin (CDT) in 420 subjects: 100 healthy blood donors, 82 healthy employees, 70 abstaining patients with different chronic nonalcoholic liver disease, 16 abstaining patients with alcoholic fatty liver, 50 abstaining patients with alcoholic liver cirrhosis, 25 abusing patients with alcoholic fatty liver, 41 abusing patients with alcoholic liver cirrhosis, and 36 patients with alcohol dependence syndrome with a daily ethanol consumption of 173 +/- 120 g the last 4 weeks before blood was drawn. In controls the serum level of CDT was significantly higher in females compared with males (17.7 +/- 5.1 and 13.7 +/- 3.8 units/liter, respectively), and the upper normal limit was defined as 27 and 20 units/liter. Sixty-two of 102 (60.8%) abusing patients with alcoholic liver disease had increased levels of CDT compared with 1 of 66 abstaining (1.5%) patients with alcoholic liver disease, and 10 of 70 (14.3%) abstaining patients with nonalcoholic liver disease among them 3 with primary biliary cirrhosis and 2 with chronic autoimmune hepatitis. No correlation was found between serum CDT and gamma-glutamyltranspeptidase (GGT), AST, ALT, and mean red cell volume (MCV). The sensitivity and specificity for serum CDT was 61 and 92%, respectively, compared with 85 and 18% for GGT and 70 and 66% for MCV. No advantage was gained by using the CDT/transferrin ratio. Our study confirms that CDT is a specific marker for chronic alcohol abuse, except in few patients with other chronic liver diseases. Serum CDT seems to be a better indicator of abstention than GGT; AST and MCV in patients with alcoholic liver disease. However, in our hands CDT is not so sensitive for alcohol abuse in patients with liver disease as reported earlier in unselected alcoholics.
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PMID:Serum carbohydrate-deficient transferrin as a marker of alcohol consumption in patients with chronic liver diseases. 848 62

Liver biopsy (n = 35) and autopsy (n = 71) specimens from HIV infected HCV-positive and HCV-negative haemophiliacs and non-haemophiliacs and liver biopsies (n = 33) from HIV-negative HCV-infected haemophiliacs and non-haemophiliacs were studied by histo- and immunohistochemistry to investigate the influence of HIV-coinfection on chronic C hepatitis (> 10 years duration). Almost all HIV-infected patients had a CD4 cell counts < 200/microns3. In biopsies and autopsies HCV-infection lead to stronger portal, periportal and lobular inflammatory changes independent from HIV-infection and haemophilia. However, HIV-infected patients with HCV-coinfection showed much more granulocytic infiltrates, particularly in the small bile ducts. In biopsies and autopsies HCV infection was associated with a stronger (centrilobular) fibrosis, particularly in HIV-positive haemophiliacs, and significantly stronger compared to HCV-negative patients. In the autopsy group half of the HIV-infected and HCV-positive haemophiliacs (n = 20) had developed posthepatitic liver cirrhosis due to C hepatitis, contrasted by two liver cirrhosis in HCV-infected non-haemophiliacs (n = 6) due to chronic B and C hepatitis and chronic alcohol abuse; no liver cirrhosis was observed in HIV-positive HCV-negative non-haemophiliacs (n = 45). Cholestasis and mild granulocytic cholangiolitis was a predominant feature in HIV/HCV-coinfection and similar distributed in haemophiliacs and non-haemophiliacs. The findings are suggestive that HIV-coinfection aggravates the course of a preceding hepatitis C virus infection, by a more granulocytic inflammatory infiltrate, stronger (centrilobular) fibrosis followed by a high incidence of posthepatitic cirrhosis--particularly in multitransfused haemophiliacs--and by cholestatic hepatopathy.
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PMID:[Hepatitis and posthepatic cirrhosis in AIDS]. 860 Jun 88

All patients with a positive reaction to the tuberculin skin test should be evaluated for weight loss, night sweats, fever, chronic cough and other signs of active tuberculosis. Chest radiographs should also be obtained in these patients. All converters receiving isoniazid should be examined monthly for signs of hepatitis and neurotoxicity. Liver function tests should be obtained at initiation of isoniazid therapy and again during the first two to four months in patients age 35 or older or with a history of alcoholism, liver disease or intravenous drug use. All cases of active tuberculosis should be reported to the local public health department. Most patients with active tuberculosis should receive isoniazid, rifampin, ethambutol and pyrazinamide daily for two weeks, followed by directly observed administration twice weekly for six additional weeks. If sputum cultures show no resistance after two months of therapy, pyrazinamide and ethambutol may be discontinued, with isoniazid and rifampin taken for an additional 16 weeks. Patients with human immunodeficiency virus infection or acquired immunodeficiency syndrome should receive the initial treatment for at least nine to 12 months, and isoniazid and rifampin for at least six months after culture conversion has occurred.
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PMID:Outpatient management of tuberculosis. 862 77

The aim of the present study was to analyze on chronic alcoholic patients the effect of ethanol (EtOH) withdrawal on the immune system through the investigation of the distribution of PB lymphoid subsets, using multiple-stainings with monoclonal antibodies and flow cytometry. For this purpose a group of 20 patients with active alcoholism without liver disease, negative for hepatitis virus, and without malnutrition was analyzed and followed for 9 months after alcohol consumption had been discontinued. Twenty-five age- and sex-matched healthy volunteers were included in the study. The following panel of monoclonal antibodies combinations (FITC/PE/PerCP or PE-Cy5) was used: TCR alpha beta/CD3/HLA DR, CD25/CD56/CD3, TCR gamma delta/CD3/HLA DR, CD45RA/CD45R0/CD4, CD3/CD8, CD19/CD5, and CD3/CD11c. Analysis was performed on at least 1,500 events/tube at flow cytometry using the Lysys II software program. During the alcohol intake period, the most striking findings were a significant (P < 0.05) expansion of the CD8+ T-lymphocyte subset, which coexpresses the activation associated antigens HLA DR and CD11c, as well as a significant increase in both NK-cells (CD3-/CD56+) and the T-cell subset with NK activity coexpressing CD3 and CD56 (P < 0.05 and P < 0.01, respectively). In addition, a decrease in the CD5+ B-cells (P < 0.05), associated with reduced serum gamma-globulin levels, was also observed. During alcohol withdrawal, a rapid decrease towards normal values of activated CD8+/HLA DR+ and CD11c+ T-lymphocytes was observed as well as a normalization of CD19+/CD5+ B-cells and gamma-globulin serum levels; these changes might be directly related to EtOH suppression. Surprisingly, however, new immunological imbalances emerged in spite of the absence of alcohol intake. Thus, a progressive and significant expansion (P < 0.05) of CD4+ T-cells associated with an increased expression of the CD25 activation-related antigen and a preferential use of the CD45R0 isoform by CD4+ T-cells were observed. In parallel, there was an even more evident increase (P < 0.01) in the number of PB NK-cells. Our results show that EtOH consumption induces changes in the immune system, its effects persisting or even becoming more evident after suppression of EtOH intake for a 9 month period.
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PMID:Long lasting immunological effects of ethanol after withdrawal. 897 26


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