Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0023890 (cirrhosis)
 42,195 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma antidiuretic hormone (ADH) and urinary prostaglandin E2 excretion (UPGE2V) were measured in basal conditions, after water restriction, and after water-loading in 10 normal subjects (free water clearance after the water load, CH2O, 9.6 +/- 0.8 ml/min) and in 27 patients with cirrhosis and ascites (13 with a positive CH2O: 3.6 +/- 0.5; 14 with a negative CH2O: -0.37 +/- 0.007). Plasma ADH and UPGE2V were significantly increased in patients with a positive CH2O as compared with normal subjects. Patients with a negative CH2O showed a significantly higher plasma ADH and a lower UPGE2V and GFR than did normal subjects and patients with the positive CH2O. In 18 additional subjects (6 normal and 12 with cirrhosis, ascites, and a positive CH2O) submitted to a sustained water overload, the i.v. administration of 450 mg of lysine acetylsalicylate (LAS) induced a marked reduction of UPGE2V, but it had no effect on plasma ADH. LAS did not alter GFR and CH2O in normal subjects; however, it reduced CH2O in all the 12 patients (from 5.1 +/- 0.4 to 0.6 +/- 0.3) and the GFR in only 6 of these patients. These results suggest (a) that renal PGE2 plays an important role in the maintenance of water excretion in cirrhosis with ascites, and (b) that impaired ability to dilute the urine in cirrhosis may be a consequence of the simultaneous occurrence of impaired renal hemodynamics, nonostomic hypersecretion of ADH, and reduced renal production of PGE2.
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PMID:Evidence that renal prostaglandins are involved in renal water metabolism in cirrhosis. 643 91

To evaluate the potential carcinogenic effects of formaldehyde, we examined the proportionate mortality experience of embalmers licensed to practice in California. Mortality was significantly elevated for total cancer, arteriosclerotic heart disease, and suicide, whereas significant deficits were noted in mortality from diseases of the respiratory and genitourinary systems. Deaths from cancers of the brain, colon, and prostate and leukemia were significantly higher than expected. No increased mortality was seen for cancers of the respiratory tract, including the nasal passages, where an effect might be expected based on animal studies. A parallel mortality survey of embalmers from New York State showed similar findings, with excesses of brain tumors, leukemia, colon cancer, arteriosclerotic heart disease, and cirrhosis. Further investigation is needed to determine whether any of these outcomes is related to formaldehyde exposure.
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PMID:Cancer and other causes of death among embalmers. 646 19

In a study of the mortality of Ontario undertakers, a cohort of 1,477 men first licensed during 1928 through 1957 was followed up until the end of 1977. Numbers of observed and expected deaths were determined for the period 1950 through 1977, using mortality rates of Ontario men as the standard. In all, 319 persons had died, compared with 322 expected. Ontario undertakers were not at increased risk of death from cancers at sites of contact with formaldehyde. Cirrhosis of the liver (standardized mortality ratio, 238) and chronic rheumatic heart disease (standardized mortality ratio, 199) were the only causes of death found to be significantly in excess. The data are discussed in the context of current epidemiologic information on the mortality experience of persons exposed to formaldehyde.
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PMID:The mortality of Ontario undertakers and a review of formaldehyde-related mortality studies. 649 80

To investigate different staining techniques for demonstration of hepatitis B-surface antigen a series of 250 liver biopsies were stained with direct immunofluorescence (I.F.) on frozen tissue and indirect immunoperoxidase (I.P.), direct I.F., orcein and haema toxylin-eosin (H.E.) on paraffin embedded tissue. Examination of different fixatives and various fixation times of formalin fixed tissue on the demonstration of HBsAg was performed on liver tissue from one case with large amounts of HBsAg in the tissue. Among 70 HBsAg sero-positive cases only 27 were tissue positive. In 51 sero-positive AVH cases, 11 were positive with I.F., 3 with I.P., one with orcein and none with H.E. In the remaining 19 sero-positive cases, representing 9 cases with chronic hepatitis, 6 cases with cirrhosis, 3 cases with non-specific reactive changes and one case without pathological changes, 15 cases were positive with I.F. as well as with I.P., 9 with orcein and 5 with H.E. Membrane related staining reaction was best preserved when using Bouin's and Clarke's fixative. No difference was observed between different fixatives as regards intracytoplasmic staining reaction. Formalin fixation for more than 7 hours duration caused a decrease in the amount of demonstrable HBsAg, which only to a limited extent could be restored by pre-treatment with proteolytic enzyme.
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PMID:Methods for localization of hepatitis B surface antigen in liver tissue. An evaluation of different staining- and tissue preparation methods. 661 83

The kinetics of plasma and breath elimination of aminopyrine after 14C-aminopyrine given orally were studied using an open one-compartment model and first order rates of elimination. The study comprised eight healthy volunteers and two groups with histologically verified chronic liver diseases (cirrhosis, n = 12, and chronic aggressive hepatitis, n = 12). Elimination rates from plasma and breath were significantly reduced in the group with cirrhosis, but only so in chronic aggressive hepatitis when they were expressed relative to each other. Monomethylaminopyrine was eliminated more rapidly compared to aminopyrine, and the rate of formaldehyde formation was positively correlated to the excretion rate of CO2 (r = 0.53, P less than 0.002). No correlation was found with clinical or other laboratory data in the groups of liver diseases studied. The test is a quantitative indicator of the drug metabolizing mixed function oxidases of the endoplasmatic reticulum of the liver, and may reflect the degree of damage to this system in chronic liver disease.
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PMID:The determination of aminopyrin elimination for control of the metabolic capacity of the liver in man. 680 87

Default risk assessment procedures use threshold models for non-carcinogens and a non-threshold model for carcinogens. This a priori distinction reflects the fact that the default procedures do not consider mechanisms of action of specific chemicals. When mechanisms are considered, the distinction is not necessary. Starting with the premise that the goal of risk assessment is to identify actual risk for specific chemicals, three major, generic components of the overall mechanism translating exposure into a response of regulatory interest are identified. These are the specific mechanisms linking (1) exposure with dose to target tissue, (2) target tissue dose with short-term responses such as cytolethality or mutation, and (3) short-term responses with ensuing long-term responses such as cancer or cirrhosis. (Short-term responses may be regulatory end points of interest, or they may be intermediate steps on the way to longer-term sequelae). On-going research on formaldehyde and chloroform is described to illustrate how these three components of the overall mechanism can be examined experimentally and used in specific models. The impact of mechanism-based risk assessment on uncertainty is also considered. Uncertainty is a function of the extent to which the model used for risk assessment misspecifies the actual mechanism of action for the chemical in question. There is a trade-off between (a) mechanism-based models that may reduce uncertainty but are expensive and time-consuming to develop and (b) default models that are not chemical-specific but can be used with minimal data sets. Experience with mechanism-based risk assessment may allow modification of default procedures to minimize this trade-off. A future default procedure for carcinogen risk assessment might allow specification of mode of action. For example, while DNA reactive-carcinogens would still be assumed to have linear low-dose risk, carcinogens acting through purely cytotoxic mechanisms might be assumed to have sharply non-linear or even threshold dose-response curves.
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PMID:Cancer and non-cancer risk assessment: not so different if you consider mechanisms. 748 52

Polymerase chain reaction (PCR) has been used to study liver biopsy tissue in patients with known or suspected hepatitis C virus (HCV). Recent studies of cryptogenic cirrhosis using PCR have been based on study of sera, and HCV has not been shown. The failure to show HCV in patients so studied has left unanswered the question of whether or not patients with cryptogenic cirrhosis could still harbor the virus in the liver. The authors studied liver tissue, obtained at the time of orthopic liver transplantation from 10 patients clinically diagnosed as having end-stage liver disease without demonstrable origin, so-called cryptogenic cirrhosis, using reverse transcription (RT)-PCR to try to recover HCV-RNA. Formalin-fixed, paraffin-embedded tissue was used. For comparison, the authors also studied similarly obtained samples from 10 patients with typical hepatitis C-associated cirrhosis and 10 patients with end-stage liver disease resulting from autoimmune hepatitis. The authors recovered HCV-RNA from 9 of 10 livers from patients with cirrhosis resulting from HCV, and 3 of 10 livers from patients with autoimmune hepatitis. HCV-RNA was not recovered from any of the livers of the 10 patients designated as having cryptogenic cirrhosis.
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PMID:Hepatitis C virus is not recoverable from liver tissue in cryptogenic cirrhosis: failure to identify hepatitis C virus-RNA using reverse transcription-mediated polymerase chain reaction. 891 25

Formalin-fixed sections from the brains of 36 patients (30 alcoholic and 6 nonalcoholic) with autopsy-proven cirrhosis who died while in a hepatic coma were stained with hematoxylin and eosin, and examined for the presence of diencephalic, cerebellar, pontine, and basal ganglia lesions. Significant neuropathology was identified in 23 of 36 cases consisting of mammillary body and thalamic lesions characteristic of Wernicke encephalopathy (WE) (9 cases, all alcoholic patients) and cerebellar degeneration (20 cases, 17 alcoholic and 3 nonalcoholic patients). Clinical diagnosis of WE had been entertained during life in only 2 of these patients. All cases, alcoholic and nonalcoholic, manifested mild to severe Alzheimer's type II astrocytosis. No cases of central pontine myelinolysis nor acquired (non-Wilsonian) hepatocerebral degeneration were found. These findings show that the brains of a high proportion of cirrhotic patients with end-stage liver disease manifest concomitant unsuspected diencephalic and cerebellar pathology. The high incidence of WE underscores the need for early sustained treatment of alcoholic cirrhotic patients with vitamin B1. Evaluation of the neurological sequelae of liver transplantation, particularly of alcoholic patients with end-stage liver disease, may require a careful neurological and radiological assessment both before and after surgery.
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PMID:Diencephalic and cerebellar pathology in alcoholic and nonalcoholic patients with end-stage liver disease. 932 1

The pathogenesis of portal hypertensive gastropathy has not yet been thoroughly elucidated. Changes in the gastric surface mucus layer in prehepatic portal hypertensive and cirrhotic rat models were studied by observing frozen sections fixed with formaldehyde vapor and stained with hematoxylin and eosin. We produced prehepatic portal hypertensive rats by partial ligation of the portal vein, and cirrhotic rats by prolonged administration of carbon tetrachloride (CCl4) and phenobarbital sodium. The thickness of the corporal and antral gastric surface mucus was significantly reduced in prehepatic portal hypertensive and cirrhotic rats compared with the values obtained in control rats for portal hypertension (subjected to sham operation) and control rats for cirrhosis (treated with phenobarbital but not CCl4). These results indicate that the hemodynamic changes associated with portal hypertension reduce the thickness of the gastric surface mucus layer and may be one of the causes of the gastropathy associated with portal hypertension.
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PMID:Reduced gastric surface mucus layer in experimental portal hypertension. 943 8

To assess the possible involvement of canine adenovirus type 1 (CAV-1) in naturally occurring cases of canine chronic liver disease, a polymerase chain reaction (PCR)-based assay was developed to detect a conserved region of the major core protein gene (pVII) of CAV-1 in formalin-fixed, paraffin-embedded liver sections. Results were compared with a standard avidin-biotin immunoperoxidase complex technique that detected CAV-1 antigens using a commercial monoclonal anti-adenovirus antibody. Seventeen cases of cirrhosis and 28 cases of chronic hepatitis with piecemeal necrosis and progressive fibrosis were selected for the study. Formalin-fixed, paraffin-embedded liver sections of 2 cases of infectious canine hepatitis (ICH) and crude DNA extract from CAV-1 (ATCC VR 293 Utrecht strain) served as positive controls. A 411-base-pair viral region was amplified and sequenced as CAV-1 pVII in both cases of infectious canine hepatitis and in the CAV-1 crude DNA extract. The 2 ICH cases were positive for CAV-1 antigens by the immunoperoxidase method. CAV-1 DNA or antigens were not detected by either technique in any of the 45 cases of chronic liver disease selected for the study. These results indicate that both PCR and immunohistochemistry are reliable and rapid techniques for detecting CAV-1 in formalin-fixed, paraffin-embedded liver sections of dogs with ICH. Several possibilities may explain the negative results obtained with both techniques in this study, including the noninvolvement of CAV-1 in canine chronic hepatitis and cirrhosis and the possibility that the virus causes initial damage, provokes a self-perpetuating chronic liver disease, and disappears.
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PMID:Use of polymerase chain reaction and immunohistochemistry for detection of canine adenovirus type 1 in formalin-fixed, paraffin-embedded liver of dogs with chronic hepatitis or cirrhosis. 978 18


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