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)

The clinical and histopathological evolution of 7 children with severe chronic active hepatitis and 8 with moderate chronic active hepatitis were studied. The majority (11-15) of the children had a clear past history of acute viral hepatitis. The cases of chronic active hepatitis with a moderate activity had a favorable evolution, but not the cases of severe chronic active hepatitis. Four of them developed into liver cirrhosis, in two the morphological alteration did not improve, and only one case showed a chronic presistent hepatitis.
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PMID:Clinical and histopathological evolution of active chronic hepatitis. 9 21

A double-antibody immunoprecipitation method was developed for detecting antibody to liver-specific membrane lipoprotein (anti-LSP) in sera of patients with various liver diseases and primary nonhepatic autoimmune diseases. Liver-specific membrane lipoprotein prepared from normal rat livers was labeled with 125I (chloramine-T) and monospecific antibody raised in rabbits. Cross-reactivity and absorption studies demonstrated that the assay used was highly specific. The frequency and titer of anti-LSP were similar for HBsAg-positive and -negative patients with both acute and chronic liver diseases. Patients with chronic active hepatitis had the highest frequenzy (25 of 44 cases, 57%) when compared with those with chronic persistent hepatitis (5 of 23 cases, 22%) and nonalcoholic cirrhosis (8 of 21 cases, 38%). Of the anti-LSP positive cases, the mean titer in patients with chronic active hepatitis tended to be the highest. In patients recovered from acute viral hepatitis, anti-LSP was transiently positive (7 of 20 cases, 35%) in the acute phase. In those who progressed to chronic hepatitis, a late rise as well as an early rise occurred in 6 of 10 patients before the diagnosis was made. Two of 6 patients with primary biliary cirrhosis had anti-LSP, but none of 41 patients with other nonviral liver diseases and none of 60 patients with primary nonhepatic autoimmune diseases. These data indicate that an autoimmune reaction directed against LSP can be initiated during the acute phase of viral hepatitis and it may persist in chronic hepatitis in both HBsAg-positive and -negative cases.
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PMID:Occurrence and significance of antibody to liver-specific membrane lipoprotein by double-antibody immunoprecipitation method in sera of patients with acute and chronic liver diseases. 10 59

1. The radioimmunoassay (RIA) and the competitive ligand binding assay (CLBA) are convenient routine methods for the precise and reproducible measurement of TBG in large numbers of serum samples. 2. There is an age dependent variation of the TBG-concentration in serum. There is a steady decrease of TBG with increasing age with a minimum between the 20th and 50th year. In higher age TBG increases again significantly. 3. There are significantly negative correlation between TBG-serum levels on the one hand and free T4- and T3- fractions on the other. The low TBG-level in hyperthyroid patients increases gradually to normal during treatment with thyroid blocking drugs, the elevated TBG-concentrations in hypothyroid patients decrease to normal during treatment with thyroid hormones. 4. Estrogen stimulates TBG-synthesis in the liver. During enhanced endogenous estrogen production (pregnancy) as well as during exogenous estrogen application a rise occurs in TBG-concentration in serum, which seems to be dose related. 5. Androgens induces a decrease of the TBG-concentration in serum. 6. During viral hepatitis and in compensated cirrhosis of the liver TBG-concentration is significantly elevated. In cirrhosis of the liver with poor hepatic function the TBG-concentration is decreased. 7. The T4/TBG-quotient is a good parameter to estimate free T4-concentration in serum.
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PMID:[Thyroxine-binding globulin (TBG). Clinical studies on the regulation of TBG concentration in serum and the value of TBG for the evaluation of thyroid function]. 11 50

The results of subtyping the B antigen in 551 sera from patients with viral hepatitis, chronic evolutive hepatitis and cirrhosis, chronic carriers, donors and healthy subjects, were confirmed as positive HBAg by diffusion in agar, counterelectrophoresis and radioimmunology, and characterized by the d-y and w-r determinants by rheophoresis. The high incidence of the y determinant in all nine counties investigated probably reflects the prevalence of this serotype in Romania, recalling the distribution of subtypes observed in the south of Europe.
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PMID:[Distribution of subtypes of viral hepatitis B antigen in areas of Rumania]. 13 42

The etiologic relationship of parasitic liver disease to primary liver cancer has long been debated. For this reason, a review of 4611 necropsies was carried out to determine the frequency with which hepatocellular carcinoma occurred in association with schistosomiasis. Of 227 cases of hepatocellular carcinoma, 24 (10.6%) were associated with schistosomiasis japonica. This was significantly higher than the incidence of this carcinoma without schistosomiasis (2.78%). The majority of the 24 cases exhibited the features of a mixed macronodular and micronodular cirrhosis (Gall's posthepatitic cirrhosis); this was super-imposed upon and caused a masking of schistosomiasis fibrosis. By radioimmunoassay hepatitis B antigen was positive in 27% of these cases. A review of the literature indicated that chronic schistosomiasis, on its own, is unlikely to be the cause of primary liver cell carcinoma. Histologic features resembling post-hepatitic cirrhosis combined with a high frequency of hepatitis B antigen suggest that viral hepatitis rather than S. japonicum is the more likely etiologic factor involved, or has a synergistic effect on carcinogenesis.
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PMID:Primary liver cancer coincident with Schistosomiasis japonica. A study of 24 necropsies. 16 89

Lipoprotein electrophoresis with measurement of serum lipids was performed on 115 patients with various forms of liver disease. There was a reduction in alpha-lipoproteins and an increase in beta-lipoproteins, as well as a reduced separability of pre-beta and beta fractions in those with acute viral hepatitis. All these changes regressed completely with healing. Similar changes were shown also in chronic liver disease and were most marked in acute liver failure, but also marked in decompensated liver cirrhosis and chronic progressive hepatitis, while less marked in chronic persistent hepatitis and compensated liver cirrhosis. In patients with fatty livers there were no characteristic findings other than a slight increase in pre-beta lipoproteins. On the other hand, the lipoprotein pattern was markedly changed in cases with tumour in the region of the gallbladder, but similar changes were noted also with tumours at other sites. They are, therfore, unlikely to be liver-specific.
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PMID:[Lipoprotein pattern in acute and chronic liver disease (author's transl)]. 17 52

Acute viral hepatitis has several identifiable morphologic components but the major categories are (1) cytopathic, (2) inflammatory, and (3) regenerative. Each category has independently variable characteristics. Extreme alterations related to severity of disease, alteration of immune response, or pre-existing liver disease may result in diagnostic difficulties for the pathologist. In contrast to the usual concept, patients who survive fulminant viral hepatitis rarely, if ever, develop cirrhosis and those who have severe hepatic necrosis from hepatitis also do not usually develop serious sequelae of that disease except in the older age group where the difficulty is in impaired regeneration (IR). The usual criteria for the diagnosis of chronic active hepatitis or chronic aggressive hepatitis need a thorough review since many of the variations of acute viral hepatitis result in histologic patterns that might be considered to be chronic aggressive hepatitis using the previous definitions; yet such patients recover without developing chronic liver disease. Chronic active hepatitis, a progressive hepatic disorder, is characterized by changes in the distribution of necrosis and regeneration within the lobule from that usually observed in acute viral hepatitis. Persistent viral hepatitis, a development in 10 to 12 per cent of adult patients after icteric acute disease, is characterized by a "cobblestone" hepatocellular change that resembles continued regeneration, focal hepatocytolysis, and often portal lymphoid hyperplasia. Apparently with time, these histologic features fade and the incidence, in type B PVH, of "ground glass" HBs Ag laden cells increases. This may reflect a continued adaptation of host and virus to one another.
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PMID:Viral hepatitis: a pathologic spectrum. 17 49

In the majority of instances acute viral hepatitis resolves totally without sequelae. Fulminant hepatitis is a highly lethal lesion but 20 to 25 per cent of patients, principally young patients, survive. Survivors do not appear to develop chronic liver disease. Persistent viral hepatitis follows acute icteric hepatitis, both type B and non-B, in 10 to 12 per cent of patients. Six long-term HBs Ag carriers demonstrated HBs Ag clearance after 14-73 months. Chronic active viral hepatitis often progresses to cirrhosis. This progressive hepatitis appeared as a sequelae of acute icteric type B hepatitis in 3 per cent of 429 patients. In patients with chronic active type B hepatitis, low titers of HBs Ag are common.
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PMID:Viral hepatitis: clinical aspects. 17 56

Pattern of hepatomegaly in Lusaka is studied. It appears that toxic hepatitis, viral hepatitis, hepatoma, cirrhosis and schistomasis play a major part in our set up in producing hepatic pathology.
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PMID:Hepatomegaly in Lusaka. 17 19

Activities of key carbohydrate-metabolizing enzymes were determined on biopsied liver tissues obtained from patients with acute and chronic viral hepatitis and postnecrotic cirrhosis of the liver. The results indicated that the activities of fetal or prototype enzymes, low-Km hexokinases, glucose-6-phosphate dehydrogenase and pyruvate kinase type M2 increased, while those of adult type liver enzymes, glucokinase, glucose-6-phosphatase, fructose-1, 6-diphosphatase and pyruvate kinase type L decreased in livers of these cases. Phosphofructokinase activity tended to increase only acute hepatitis. Principal component analysis revealed that the enzyme patterns of acute hepatitis and liver cirrhosis were most deviated from the control and closely resembled those of hepatocellular carcinomas.
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PMID:Undifferentiated patterns of key carbohydrate-metabolizing enzymes in injured livers. II. Human viral hepatitis and cirrhosis of the liver. 17 5


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