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)

16 patients with acute hepatitis, 18 patients with cirrhosis and a total of 21 volunteers and patients with normal liver function received 7.32 mg/kg hexobarbital by linear intravenous infusion within 60 min. Hexobarbital was determined gaschromatographically in serial blood samples and the hexobarbital-clearance was calculated from the plasma concentration curve versus time. Additional experiments were performed in rats suffering from so called "galactosamine hepatitis". In half of the patients with acute hepatitis a normal hexobarbital clearance could be found. In the other patients this was distinctly reduced but not correlation was found to other liver function tests. Patients with cirrhosis were subdivided into two groups. The patients in group 1 were well compensated. The patients in group 2 had a decompensated state with ascites and oesophageal varices. In nearly all patients with cirrhosis the hexobarbital-clearance was diminished. This was more pronounced in group 2. Ketohexobarbital excretion in healthy subjects was in the range of 40-60% of dose. Patients with acute hepatitis excreted only 10-20% of dose and patients with liver cirrhosis only about 5% of dose. In rats with "galactosamine hepatitis" hexobarbital clearance in vivo was distinctly reduced and this could be explained by diminished microsomal cytochrome p 45- and hexobarbital oxidation rate.
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PMID:[Metabolism of hexobarbital in patients with acute hepatitis and cirrhosis (author's transl)]. 88 88

Serial measurements of complement components were performed in fifty-nine patients with acute, uncomplicated hepatitis and twelve with alcoholic cirrhosis. Thirty-one of the former group had detectable hepatitis B antigen. Abnormal complement profiles were observed in nine patients with hepatitis B and seven with antigen-negative hepatitis. Low levels of C4, C3 and factor B were common in the subjects with cirrhosis and confined to those cases with severe reduction in serum albumin and/or prothrombin index. By contrast, the complement changes in the patients with hepatitis occurred without significant alteration in these parameters; certain subjects also had reduction in C1q and C5 and a significant number had C3d detectable in fresh plasma. The pattern of abnormality suggests predominant involvement of the classical pathway and it is concluded that this results, at least in part, from an immune process evident only in the early clinical phase of hepatitis. Such gross changes in complement are likely to reflect immune-complex activity and it is proposed that these complexes may be important in the clearance of virus material. The data supports a previous suggestion that recovery from acute hepatitis is primarily dependent on host immune competence rather than viral cytotoxicity or generation of immune complexes.
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PMID:Acute hepatitis: significance of changes in complement components. 89 Oct 25

Transition from acute to chronic hepatitis has important prognostic and therapeutic implications. In 17 patients with acute viral hepatitis, observed during a period of 7 years, a liver biopsy showed changes compatible with chronic aggressive hepatitis and superimposed acute hepatitis. Follow-up biopsies showed normal liver in 14 cases, chronic persistent hepatitis in 1, and cirrhosis in 2. In 12 cases the initial biopsy which showed changes suggestive of chronicity was taken 1 month after onset of symptoms of acute hepatitis, or later. Cases developing chronic liver disease showed no characteristic clinical, laboratory, or histological features at the time of the first biopsy. If the diagnosis of chronic active hepatitis is based on histological findings alone in patients with prolonged acute hepatitis, the incidence of this condition will be grossly overestimated. The transition from acute to chronic hepatitis cannot be recognized with any degree of certainty by presently available methods.
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PMID:Significance of suspected "chronic aggressive hepatitis" in acute hepatitis. 89 54

Within 5 to 14 days of onset of grade 3 or 4 coma, liver biopsies were obtained in 14 of 15 consecutive patients who recovered from fulminant hepatitis. In 9 patients, follow-up biopsy was obtained 6 to 60 months after acute hepatitis and autopsy was performed in 2 patients who died in 4 months from complications of hepatitis (aplastic anemia) or of corticosteroid therapy (sepsis). During fulminant illness the biopsy findings were: multilobular necrosis in 4 patients, confluent (bridging) necrosis in 9, and only portal inflammation in 1. The duration or the grade of coma did not correlate with the severity of necrosis on the biopsy. Follow-up biopsy showed development of chronic (active) hepatitis in 3 of 9 patients (with cirrhosis in one of these). Chronic liver disease was not found in the two autopsies. If fulminant hepatitis is the result of vigorous cell-mediated immune attack on hepatocytes, then this process cannot always eradicate chronic hepatitis B surface antigenemia, nor can it always prevent the development of chronic (active) hepatitis or cirrhosis.
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PMID:The liver during and after fulminant hepatitis. 89 67

In the GDR mortality from liver cirrhosis decreases in contrast to most other countries though the alcohol consumption of the population is continuously increasing. In Capital Berlin and in the industrialized districts mortality from cirrhosis is higher than in the rural areas. Within a period of 6 years the number of inpatients with chronic liver diseases has risen from 11.600 to 14.200. From the epidemiologic point of view, virus hepatitis is not the main source of liver cirrhosis. The total recovery rate of acute hepatitis has increased from 80% to 94% over a period of some 8 to 10 years, liver cirrhosis was found to have developed only in 0.3%. 70% of cirrhotic patients did never suffer from virus hepatitis, as their anamnesis revealed. 73% of 1.8 million blood donors that were subjected to SGPT and HBAg-screening tests showed histologic changes of the liver. With the use of these screening methods it has been possible to register 7% persons with liver diseases among these blood donors. Early recognition and treatment of chronic liver diseases seem to result in a reduction of mortality from liver cirrhosis.
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PMID:Epidemiology of chronic liver diseases. 90 70

Hepatic insufficiency is generally caused by active liver cirrhosis with portal hypertension. The final stage is the exogenous hepatic coma. Much rarer is the endogenous hepatic coma caused by fulminant acute hepatitis or severe intoxications. In the treatment of hepatic insufficiency it is first necessary to eliminate all exacerbating factors such as too high protein-intake, gastrointestinal bleedings, abuse of alcohol and diuretics. Because hepatic encephalopathy is mainly produced by toxic intestinal protein metabolites no protein should be adminstered at the beginining of the disease. The production of toxic protein metabolites in the gut can be diminished as well by enemas with sodium acetate buffer (pH 4, 5) as by neomycin (6-8 gm daily). Because long-term treatment with neomycin reduces also the physiological intestinal bacteria combination with lactulose (70-100 gm daily) is better. Treatment with lactulose reduces not only significantly hyperammoniemia but also increases serum phenols. The same effect have so-called ammonia reducing amino acids such as arginine, ornithine and glutamic acid. In endogenous hepatic coma blood exchange transfusions, liver perfusions and charcoal perfusions are necessary. Nevertheless, the prognosis of hepatic insufficiency caused by fulminant hepatitis is very poor in the final stage of the disease. Therefore early diagnosis and treatment in special departments with intensive care is necessary.
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PMID:[Therapy of hepatic insufficiency]. 91 52

Re-evaluation of 890 consecutive liver biopsies from 1939-59 gave the diagnosis of acute hepatitis in 147 patients. A follow-up study of these patients was performed 15-37 years after the diagnostic biopsy, based on repeated liver biopsies, biochemical liver tests, autopsy reports and death certificates. Two patients died from acute liver failure, and development of cirrhosis was documented or strongly suspected in 22 patients (15 percent). A comparison between these 24 patients with a malignant course of hepatitis and 86 patients with a well documented uncomplicated disease, revealed a significantly larger number of women, a higher age, and more cases with piece-meal necrosis, confluent necrosis and marked portal inflammation in the intitial liver biopsy in the group with the poor prognosis.
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PMID:Acute hepatitis: a prognostic study with observation time up to 37 years. A follow-up of the Iversen/Roholm liver biopsy material. 92 Feb 45

Postprandial serum bile acid estimation was recently proposed as the most sensitive test of liver function. In our study, the fasting and postpranidal serum bile acid measurements were performed on 19 normal subjects, 20 patients with cirrhosis, 10 with acute hepatitis, 4 with resolving viral hepatitis, and 6 with chronic active hepatitis. A gas-chromatographic method was used. One healthy subject had postprandial serum bile acid levels above the normal range, while 7 patients with liver disease had postprandial levels within normal limits. Of the latter group, 2 had chronic active hepatitis in remission and 3 had resolving viral hepatitis. Significant correlations were seen between serum bile acid levels and most of the conventional "liver function" tests. Our data indicate that the postprandial serum bile acid determination is better than any of the other conventional tests taken separately, but no better than their combined use. No significant modification of the cholic acid/chenodeoxycholic acid ratio was observed between the fasting and the postprandial determinations.
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PMID:Fasting and postprandial serum bile acids as a screening test for hepatocellular disease. 92 Jul 3

The administration of alpha methyldopa resulted in serious liver injury to seven patients, requiring hospitalization. All patients presented with symptoms indistinguishable from viral hepatitis. Histological changes ranged from those compatible with acute hepatitis to chronic active hepatitis and subacute hepatic necrosis. One patient with subacute hepatic necrosis rapidly progressed to hepatic failure and died; autopsy revealed postnecrotic cirrhosis. Inadvertent rechallenge after recovery resulted in dramatic recurrence of symptoms in one patient, confirming the fact that a hypersensitivity phenomenon is involved. A high state of awareness among physicians of this unpredictable toxic effect of the drug may reduce its unrecognized perpetuation.
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PMID:Spectrum of methyldopa liver injury. 92 Jul 11

Sera from patients with acute hepatitis, cirrhosis or chronic hepatitis, as well as sera from healthy carriers and controls were examined for HBS antigen, DNA polymerase activity and for antibodies to HBS, HBC and DNA polymerase. The data presented suggest that in acute hepatitis the DNA polymerase test enabled us to diagnose at least 20% more cases of hepatitis B than with the RIA but that the DNA polymerase test is of little value for the screening of blood donors since all the healthy carriers gave negative results. As concerns the antibodies to DNA polymerase they appeared in at least 50% of the patients with acute hepatitis, they were transient and only detectable at the early beginning of the disease. These antibodies were also found to be different from the anti-HBS and anti-HBC antibodies.
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PMID:Transient antibodies to DNA polymerase in acute hepatitis B and related diseases. 96 84


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