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 records of 192 cadaver renal allotransplants were reviewed in order to evaluate the role of the hepatitis B antigen (HBsAg) carrier state on graft function, patient survival, and the incidence of severe hepatic dysfunction. Twenty-one allografts were placed into patients with hepatitis B antigenemia. After follow-up ranging from 1.5 to 8 years (mean 4.7), graft and patient survivals were not statistically different from antigen-negative patients. In addition, the acquisition of HBsAg after grafting did not seem to affect the rate of graft failuue or death. Neither cirrhosis not fatal hepatic failure developed in the HBsAg carrier group, whereas five HBsAg-negative recipients died of hepatic disease. Among HBsAg-positive recipients, nine with functioning renal allografts and five with graft failures, there was a low incidence of e antigen, suggesting low infectivity. This may explain the lack of correlation of the surface antigen with serious liver disease. Severe hepatic disease developing in renal graft recipients is most likely attributable to causes other than hepatitis B infection. The presence of hepatitis B antigenemia alone should not be a deterrent to renal transplantation.
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PMID:The effect of hepatitis B antigenemia on long-term success and hepatic disease in renal transplant recipients. 33 36

Kidney tissue from 99 unselected necropsy cases of various forms of hepatitis and liver cirrhosis was examined by histology and direct immunofluorescence. Glomerular deposits of hepatitis B surface antigen (HBsAg), IgG, IgM, and complement were found in nine of 59 cases (15%) of acute and subacute hepatitis and in seven of 40 cases (17%) of chronic aggressive hepatitis and liver cirrhosis. Different amounts of granular hepatitis B surface antigen immune deposits were distributed along glomerular capillary walls and/or in mesangial areas. Glomerular lesions found in these cases consisted of thickening of glomerular capillary walls, a slight increase in glomerular cellularity, and an increase of mesangial matrix. These glomerular lesions are considered to result from the humoral immune elimination of circulating viral surface antigen immune complexes.
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PMID:Kidney glomerular pathology in various forms of acute and chronic hepatitis. 36 29

A patient suffering from chronic active hepatitis with macronodular cirrhosis, positive for hepatitis B surface antigen (HBsAg), was treated with an orthotopic liver allograft. The HBs antigenemia, as measured with several precipitation tests and by complement fixation, became negative after transplantation and remained so for about 2 1/2 months. During the interval, very low titers of the antigen were detectable by radioimmunoassay. At about three months after transplantation, she had an attack of acute hepatitis, at which time HBsAg became detectable by all tests. She recovered, but progressive liver disease developed during the remaining 1 1/2 years of her life. She died of disseminated nocardiosis and candidiasis with deteriorating hepatic function. The homograft at autopsy showed no evidence of rejection, but was the site of chronic active liver disease, although of a different pathologic pattern than that affecting her native liver. The differences in histology may reflect the influence of chronic immunosuppression on the features of chronic active hepatitis.
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PMID:Liver allograft. Its use in chronic active hepatitis with macronodular cirrhosis, hepatitis B surface antigen. 36 34

In a study of apparently normal, healthy Korean Army recruits performed in 1962, we found that 42 of 1,906 screened subjects had elevations of their serum glutamic pyruvate transaminase. Liver biopsies were obtained from 32 of these subjects and 9 of these had a "novel" antigen present, which reacted specifically with a convalescent serum from a case of serum hepatitis. We have recently tested frozen serum obtained from 8/9 of these cases and found that all 8 had HBsAg in their serum which, in some cases, persisted for at least three months. We reviewed the histological specimens from the original 32 cases using newly defined criteria: 18 were diagnosed as chronic active hepatitis and the 8 HbsAg positive cases with the "novel" antigen were in this group. In four of these cases the lesion appeared to progress to cirrhosis during a 3--4 month follow-up period. Since none of the cases had a prior history of hepatitis and no symptoms developed during the follow-up period, our findings emphasize the significance of chronic hepatitis B virus carrier state in the etiology of cryptogenic cirrhosis.
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PMID:The etiology of chronic active hepatitis in Korea. 37 25

Single liver biopsies from 102 clinically diagnosed hepatitis patients were examined by immunofluorescence for the presence of hepatitis B surface antigen (HBsAg) and hepatitis B core antigen (HBcAg), complement and immunoglobulin deposition, and for their capacity to fix human complement in vitro. Of the sixty-five HBsAg positive livers, fifty-three were histologically diagnosed as chronic hepatitis, three as acute hepatitis, five as acute hepatitis with signs of transition to chronicity, and four as 'near normal liver'. In the group with chronic hepatitis, HGcAg was observed in thirty-nine livers, all of which also had HBsAg. Thirty-five of these thirty-nine cases also had the ability to fix complement in vitro in the hepatocyte nuclei and/or cytoplasm. Of these thirty-five cases, twenty-nine were positive for immunoglobulin deposition on the nuclei. All of these cases had antibody to HBcAg in the blood, but only five had anti-HBs. The frequency of in vitro complement fixation and immunoglobulin deposition was higher in active forms of the disease, such as chronic aggressive hepatitis and active cirrhosis, than in non-active disease such as chronic persistent hepatitis and mild cirrhosis. By the application of double fluorescent staining techniques, complement fixation was observed in some HBcAg-positive nuclei. In the 'near normal liver' cases there was no intrahepatic accumulation of HBcAg, and despite the presence of anti-HBc in the blood, in vitro complement fixation and immunoglobulin deposition were both absent. The group of three HBsAg ositive 'acute hepatitis with signs of transition to chronicity' cases behaved similarly to those with chronic aggressive hepatitis and had circulating anti-HBc, in vitro complement fixation and immunoglobulin deposition in the hepatocytes. None had circulating anti-HBs. In the group sith HBs-positive acute hepatitis, anti-HGc in the blood was the only other evidence of hepatitis B virus infection.
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PMID:Hepatitis B core antigen immune complexes in the liver of hepatitis B patients. 38 86

Two hundred four volunteer blood donors with hepatitis B surface antigen found in their blood were followed for 3 to 44 months. The annual clearance rate of this antigen was 1.7%. Liver enzyme levels (aminotransferase) were elevated in 45 (22.1%) on at least one occasion, in 26 (12.7%) for one month or more, and in 13 for more than six months. Liver biopsies were performed on 17 chronic carriers with normal enzymes and nonspecific histologic abnormalities were found in 14 and mild diffuse hepatitis in three. Seventeen carriers with abnormal enzymes were biopsied, and specimens revealed chronic active hepatitis (CAH) in seven, including two with bridging necrosis and three with cirrhosis. CAH was found in 7 of 26 (26.9%) carriers with abnormal liver enzymes persisting for at least one month and 4 of 13 (30.8%) with abnormal liver enzymes for more than six months.
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PMID:The liver histology and frequency of clearance of the hepatitis B surface antigen (HBsAg) in chronic carriers. 42 95

Lymphocytes from patients with HBs-Ag-positive and -negative acute, chronic-persistent, and chronic-active hepatitis, from healthy controls and from patients with alcoholic liver cirrhosis were tested under standardized conditions. These included use of a single charge of Phytohemagglutinin (PHA-P) dissolved and diluted in one operation, of a single pool of homologous serum of the major blood group AB found free of HBs-Ag and cytotixic factor, and elaboration of PHA dose response curves in the presence of autologous and homologous serum in each case examined. During the early phase of acute virus hepatitis B and non-B, and in HBs-Ag-positive chronic persistent and active hepatitis, hyperresponsiveness of lymphocytes to PHA was observed independently of the source of the serum present in the culture. Lymphocyte responsiveness returned to normal in the later phase of acute hepatitis and depressed in alcoholic liver cirrhosis and in cases of HBs-Ag-positive chronic active hepatitis in which cirrhosis had developed. Although the cause of these alterations in lymphocyte responsiveness is not completely understood, the central role of a primary change of the lymphocytes themselves affecting their ability to react to PHA seems probable.
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PMID:Lymphocyte proliferation to phytohemagglutinin (PHA) in hepatitis B antigen-positive and -negative hepatitis. 44 26

Twenty-six untreated patients with chronic persistent hepatitis were followed prospectively for one to 17 years (mean 5.6 years). The patients developed no clinical features of chronic liver disease. Raised serum transaminase levels were usually, but not consistently, the only biochemical abnormality; gamma globulin values were normal. Serum markers of past or present hepatitis B infection were found initially in 14 patients: another two developed markers during their follow-up. Nine patients progressed to a mild or moderate chronic active hepatitis as shown by serial needle liver biopsies but there was no evidence of cirrhosis. This progression was not associated with any clinical or biochemical deterioration. Seven of these patients had presented with insidious symptoms, seven had serum markers of hepatitis B infection, and the four who were HBsAg positive had relatively lower serum HBsAg concentrations than did those patients who continued with chronic persistent hepatitis.
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PMID:Chronic persistent hepatitis: hepatitis B virus markers and histological follow-up. 46 67

Immune complexes (IC) were investigated in sera from 208 individuals with various clinical types of viral hepatitis diagnosed by clinical and laboratory criteria, including liver biopsy. Immune complexes were assessed by platelet aggregation (PI A) and by radioimmunoassay (RIA). The data were related to autoimmune phenomena (especially rheumatoid factors) and to the role that the IgM class of hepatitis B (HB) antibody might have in IC formation. Although the highest frequency of P1 A was in the few sera from patients with cirrhosis or hepatoma, the next highest was in sera from acute hepatitis patients (71%), and the lowest in sera from chronic active (57%) and chronic persistent (46%) hepatitis patients. A proportional number of patients with IC's were positive for hepatitis B surface antigen (HBs). A parallel prevalence was noted between P1 A and autoantibodies, with anti-Ig's being found more frequently in sera from acute hepatitis and chronic active hepatitis patients. The relationship between RIA results for complexes and RIA results for anti-IgG was inverse, as though anti-IgG interfered with IC reactivity by RIA. Anti-IgM pre-incubated with sera increased the amount of P1 A in sera from patients with acute hepatitis as well as in those from patients with chronic persistent hepatitis, suggesting a more frequent IgM involvement in IC's in these diseases than in chronic active hepatitis. Whereas liver cell damage in acute and active hepatitis may reflect elevated autoantibodies, the IgM class of HBs antibody may be involved in acute as well as chronic persistent hepatitis.
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PMID:Autoimmune implications of immune complexes in clinical variants of hepatitis B. 49 83

The clinical course of a 26 year old female patient with acute liver necrosis and coma due to hepatitis B is reported. The disturbances of conciousness had improved. The patient survived 41 days after the beginning of the coma and developed liver cell regeneration and an acute post-hepatitic liver cirrhosis. As a grave complication a septicemia with aspergillus was observed. The patient died because of gastro-intestinal hemorrhage. At autopsy there were no signs of brain edema. The treatment consisted in: daily infusions with coenzyme A, nicotinamid-adenin-dinucleotide, alpha lipoic acid and cocarboxylase to improve the metabolic disorders and the clinical picture; mannitol intravenously to prevent and to treat cerebral edema; 33 charcoal-hemoperfusions to remove toxic substances of acute liver failure. Treatment of the aspergillus infection with 5-fluorocytosine and amphotericine B and infusion of concentrated ascites led to a decompensation of liver functions. From this observation the following conclusions can be drawn: after an acute viral hepatic necrosis, new synthetic functions and improvements of the disturbed intermediary metabolism in regenerated liver-cells can eventually be seen only after twenty-four to thirty days. With systematically applicated mannitol infusions it is possible to treat cerebral edema effectively.
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PMID:Treatment of fulminant hepatic failure with infusions of Co-factors and mannitol and charcoal-hemoperfusions during Forty-one days. 50 61


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