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)

Twelve patients with otherwise uncomplicated acute viral hepatitis (two were HBsAg-positive) developed renal failure. Apart from dehydration due to repeated vomiting in one patient, no factor responsible for precipitating renal failure could be identified. The clinical course was characterised by renal failure with plasma urea concentrations reaching maximum values of 26-69 mmol/l (175-416 mg/100 ml). Ten patients needed dialysis for up to two weeks. Seven patients recovered completely, while the other five died from sepsis. The types of renal failure were similar to those described in fulminant hepatic failure and cirrhosis--namely, functional renal failure in five patients and acute tubular necrosis in seven. Two of the patients with functional renal failure later developed tubular necrosis. The mechanism responsible for renal failure in acute viral hepatitis is uncertain, though endotoxaemia may contribute.
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PMID:Renal failure in otherwise uncomplicated acute viral hepatitis. 68 5

The urinary excretion of D-glucaric acid, a catabolite of glucuronic acid, is considered to be a reliable index of the state of hepatic microsomal enzyme activity. Because enzyme activity may be altered in liver disease, we examined the effect of liver disease on the excretion of this metabolite and its correlation with liver function tests. We studied 89 patients with nonhemolytic jaundice, 39 with viral hepatitis, 33 with obstructive jaundice, six with cirrhosis, and 11 patients with jaundice of mixed etiology. Glucaric acid excretion was significantly increased in all these patients as compared to controls, most pronounced in the obstructive jaundice group. No correlation was found between glucaric acid excretion and concentrations of bilirubin, albumin, globulin, aspartate aminotransferase, alkaline phosphatase, cholesterol, or gamma-glutamyltransferase in serum, even though the concentrations of these analytes did vary with the type of liver disease. We suggest that this increase in glucaric acid excretion is an indication of normal or even increased glucuronidation (UDP-glucuronosyltransferase activity), which occurs in liver disease.
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PMID:Increased D-glucaric acid excretion by jaundiced patients. 69 85

329 patients with acute ouvert viral hepatitis which occurred in the Hannover area 1975 were classified according to virological data. The proportions of type A and type non A - non B hepatitis were each approximately 20 percent of the total cases (n = 60). Viral hepatitis B was the most frequent type of viral hepatitis (n = 209). 174 individuals of the 329 hepatitis patients were reexamined serologically two years after the onset of the acute disease. 7 out of 105 patients with hepatitis B (6,7%) and 5 out of 40 patients with hepatitis non A - non B (12,5%) revealed a serological pattern compatible with chronic hepatitis. In contrast none of 29 patients with hepatitis A indicated chronic liver disease. The frequency of anti-HAV was also determined in 41 patients with HBsAg positive and HBsAg negative histologically proven chronic hepatitis or liver cirrhosis. All patients were under 35 years of age. An equal proportion of anti-HAV was found in both groups. These results suggest that hepatitis A practically never results in chronic hepatitis, while hepatitis non A - non B can run a chronic course with a frequency similar to that of hepatitis B.
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PMID:[Chronic hepatitis as sequela of acute viral hepatitis A and hepatitis non A - non B (author's transl)]. 74 46

47 cases of viral hepatitis with HBs antigenemia, who were diagnosed by peritoneoscopy and biopsy, were studied. 41 cases were males, and 6 cases were females. The onset ages were mostly in 25--29 years old. The histories of blood transfusion were found in only 4.3%. On the other hand, the families clustered with HBs antigen were found in 68%. Recidivums were often seen (76%), and yet the intervals between recidivum were short (the neighborhood of 8 months). The transaminases at the recidivums were not so high (200 units or thereabout). 20 cases whom biopsies were performed more than twice, were studied histologically. 14 cases were prognessive. 5 were stationary. 1 was improved. In all of progressive cases, sublobular hepatic necrosis was seen. But in other cases, sublobular necrosis was not seen. After this sublobular necrosis, various distortion of the lobule architecture was appeared, and some of them progressed to liver cirrhosis. As to GOT and GPT, GPT was dominant before sublobular neerosis, but GOT was liable to be dominant after sublobular necrosis. Peritoneoscopically, peculiar red spots were found on liver surfaces at the time of sublobular necrosis.
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PMID:[Studies on development of viral hepatitis with HBs antigenemia (author's transl)]. 74 63

The authors have studied the frequency of an abnormal lipoprotein (LP-X), by the method presented by YAE e col. (21). The LP-X test is useful in differentiating of a cholestatic process from a non-cholestatic one, but it is not adequate to distinguish an intrahepatic cholestasis from an extrahepatic biliary obstruction. Out of the 41 icteric patients who were studied, a frequency of the presence of the LP-X was observed in 68.3% thus distributed: viral hepatitis 90,5% obstructive jaundice 85,7%, jaundice of uncertain etiology 37.6%; it was not present in 5 patients with hepatic cirrhosis and in the serum of 21 healthy volunteers. A significant association was found between the presence of LP-X and an abnormal curve of lipoproteins.
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PMID:[Frequency of lipoprotein-X (LP-X) in icteric patients. Comparison with some bioquimical data (author's transl)]. 74 47

Oxazepam (Serax) is a tranquilizer-sedative of the benzodiazepine group that is predominantly metabolized to a pharmacologically inactive glucuronide and subsequently excreted by way of the kidneys. We administered this drug as a single oral dose to seven patients with acute viral hepatitis, to six with cirrhosis, and to age-matched control subjects. Elimination half-life (T1/2) and the apparent oral plasma clearance for the drug in patients with hepatitis and cirrhosis were comparable to values obtained in age-matched controls (P greater than 0.05). In addition, the apparent volume of distribution of oxazepam, its plasma binding, blood/plasma ratio, and the rate of urinary excretion of oxazepam, predominantly as the glucuronide, were comparable (p greater than 0.05) in the two groups of patients with liver disease and their respective controls. Unlike many other sedatives, oxazepam is eliminated normally in patients with parenchymal liver disease an therefore, on pharmacokinetic grounds, seems to be an excellent sedative for use in such persons.
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PMID:Normal disposition of oxazepam in acute viral hepatitis and cirrhosis. 76 32

One hundred liver biopsies from 100 hepatitis patients were examined by the indirect immunofluorescent technique for the detection of HBsAg. Of the 60 positive specimens 52 were diagnosed as various types of chronic hepatitis and 8 were acute hepatitis. Four main distribution patterns of HBsAg were obtained: full cytoplasmic fluorescence with diffuse lobular distribution; cytoplasmic fluorescence with spotty distribution; peripheral fluorescence in the cell membrane and/or cell peripheries; and focal cytoplasmic positivity. There was an inverse relationship between the number of positive hepatocytes and the extent of liver cell necrosis. The distribution patterns of HBsAg were distinctive in each type of chronic hepatitis and in acute hepatitis. Homogeneous full cytoplasmic fluorescence, distributed diffusely in the whole liver lobule, was observed in chronic persistent hepatitis and in cirrhosis with little activity whereas peripheral liver cell membrane and/or peripheral cytoplasmic fluorescence associated with cytoplasmic positivity in a smaller number of hepatocytes was a characteristic finding in chronic aggressive hepatitis, active cirrhosis, and acute hepatitis with possible transition to chronicity. Focal cytoplasmic fluorescence was observed in acute hepatitis and a group of biopsies in chronic hepatitis in which HBsAg was detected in the liver but no antigen was detectable in the serum. The results show that the different patterns of distribution of HBsAg in the liver biopsy are helpful for the histological diagnosis of different types of HBAg positive viral hepatitis and are consistent with the hypothesis of the role of specific immune response in the pathogenesis of type B viral hepatitis.
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PMID:Distribution patterns of hepatitis B surface antigen (HBsAg) in the liver of hepatitis patients. 77 39

Diabetes mellitus is more frequently found in pateints with hepatic cirrhosis (about 10%) than in subjects without liver disease. Cirrhosis has been the main subject of interest in this respect. Very few studies have been made in viral hepatitis or steatosis. In about 40% of cases, the diabetes is identified before the cirrhosis. More often (in about 60% of cases) the diabetes is discovered at the same time as or after the finding of cirrhosis. This "post-cirrhosis diabetes" shows no clinical peculiarity. In about 80% of patients with liver cirrhosis when fasting blood glucose is normal, abnormalities of carbohydrate metabolism are to be found by the oral glucose tolerance test. Approximately 50% show an abnormal response to intravenous glucose and 30% to intravenous tolbutamide. The "mechanism" of these metabolic abnormalities in liver cirrhosis is unknown. The following abnormalities are observed: 1) With similar glycaemic response to a glucose challenge, plasma insulin levels are higher than in patients without liver disease, suggesting insulin unresponsiveness. Resistance to exogenous insulin can be demonstrated. 2) Plasma free fatty acid levels are often elevated. 3) Plasma growth hormone levels are often raised. 4) Plasma glucagon levels are high when porto-caval shunting is present. 5) Potassium is often depleted. These metabolic abnormalities, in association with porto-caval shunting and hepatocyte insufficiency may explain the insulin resistance which characterises liver cirrhosis, and the diabetes which it may precipitate in predisposed persons.
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PMID:[Diabetes mellitus secondary to liver diseases. A review (author's transl)]. 79 27

The constant and inconstant light microscopic changes in liver biopsies from patients with acute viral hepatitis are reviewed. The constant changes are essential for the diagnosis, and the distribution of ceroid (and often of haemosiderin) is important in the staging of the disease. Many and large piecemeal necroses in the acute stage are often followed by chronic aggressive hepatitis. A key to the understanding of the development of regeneration nodules - and thereby to posthepatitic cirrhosis - is portal-central bridging with subsequent formation of septa. Bridging and formation of septa is almost always preceded by piecemeal necroses in the acute stage and also by confluent necroses in 1/3 - 1/2 of the cases.
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PMID:Histological features of acute viral hepatitis. 79 96

The clinical course of acute viral hepatitis may vary from asymptomatic to fulminant, and the final outcome can be complete recovery, chronic hepatitis or cirrhosis. The two main challenges this generally benign, self limiting infection has presented for may years have been to understand 1) the progression to fulminant hepatitis, and 2) the progression to chronic hepatitis or cirrhosis. Fulminant hepatitis may appear infrequently (1-2 % of patients with clinical hepatitis) in both type A and type B infections. Nearly 10% of patients with acute viral hepatitis type B develop either chronic hepatitis or cirrhosis. The exact figures for progression to chronicity in patients with type A infections are probably less,but are still not fully known. During the acute phase of the disease, the patients with later progression to chronicity differ significantly from those with subsequent resolution in a number of serological, biochemical and morphological variables. Persistence of HBS antigenaemia for more than 13 weeks, a high concentration of circulating Dane particles, and the presence in the serum of the "e" antigenic determinant seem to be reliable prognostic markers for pregression to chronic hepatitis or cirrhosis. Such markers are prerequisites for therapeutic trials with potent drugs which are only justified for patients with fulminant hepatitis and patients with progression to chronicity. If the different outcome of viral hepatitis is a result of the individual T-cell function, these two categories of patients may represent the opposite extremes in lymphocytic function. Controlled clinical trials are required to evaluate the clinical effect of immunosuppression in fulminant hepatitis and immunostimulation in chronic hepatitis.
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PMID:Clinical course and prognosis of acute hepatitis. 79 97


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