PubMed Health⌕ Search

Biomedical subjects

U Hopf

Publications and source records attributed to U Hopf.

At least 37 records · Page 2Linked to original sources
PubMed1992

[Orthotopic liver transplantation in hepatic cirrhosis: on the problem of infection of the transplant with persistent hepatitis viruses].

269 orthotopic liver transplantations (OLT) were performed in 253 patients at our institution from September 1988 to May 1992. 121 patients had end-stage cirrhosis secondary to viral hepatitis type B, delta, or type non-A non-B and C respectively. Reinfection of the graft by persistent viruses is a potential complication in these cases. Passive immunization with anti-HBs hyperimmunoglobulin (HIg) can prevent clinically relevant reinfection of the graft in patients with hepatitis B virus (HBV) infection and low replication rates. Patients with high replication rates will rarely benefit from OLT. Patients with hepatitis delta virus (HDV) infection usually experience HDV reinfection of the graft with subsequent chronic hepatitis although prophylaxis with anti-HBs-HIg was performed. Treatment with interferon alpha had no apparent effect on the incidence of graft reinfection with HBV in this series, but the replication rate of HDV was reduced. Persistent hepatitis C viruses (HCV) usually infect the graft; this was demonstrated in 17 patients by means of the polymerase chain reaction. HCV infection usually causes a mild form of acute hepatitis with transition to a chronic course. Therefore the significance of persistent viral infection lies in the potential for chronic hepatitis in the transplanted organ rather than in the danger of acute injury of the allograft.

Biopsy, Needle↗
PubMed1991

Follow-up of recurrent hepatitis B and delta infection in liver allograft recipients after treatment with recombinant interferon-alpha.

Reinfection of the graft with hepatitis B virus (HBV) and hepatitis delta virus (HDV) is a potential complication in patients undergoing orthotopic liver transplantation (OLT). Therefore, we added recombinant interferon-alpha (rIFNa) to the standard immunosuppressive regimen in 11 patients who received transplants following liver failure attributed to cirrhosis B (n = 10, with HDV co-infection in four cases) or fulminant hepatitis B (n = 1). Patients were treated with rIFNa for periods ranging from 2 to 3 months between the first and the 13th month after OLT. All patients received immunosuppressive treatment with low-dose corticosteroids, azathioprine and cyclosporine. Anti-HBs hyperimmune globulin was also administered. None of the patients showed evidence of severe allograft rejection. Seven patients suffered HBV reinfection of the graft with histological signs of acute hepatitis in five cases and transition to chronic hepatitis in one patient. Treatment with rIFNa did not prevent or reduce HBV replication. Reinfection of the graft with HDV was demonstrated by PCR in four patients co-infected with HDV. During treatment with rIFNa liver biopsy specimens from three reinfected patients were transiently negative for HDV antigen but not for HDV RNA, and the sera from two patients were transiently negative for HDV RNA. The data indicate that rIFNa can reduce HDV replication in reinfected liver allografts.

Adrenal Cortex Hormones↗
PubMed1991

[Non-tropical sprue and chronic inflammatory rectal stenosis in a patient with abuse of ergotamine-containing suppositories].

A 51 year old Yugoslavian patient was admitted to our hospital in reduced general condition with distinct hypocalcemia, osteomalacia, and with rectum stenosis. Our investigations led to the diagnosis of a malabsorption syndrome due to non-tropical sprue. The most likely cause of the rectum stenosis is an abuse of ergotamine-containing suppositories for several years. A gluten-free diet and the interruption of the use of the suppositories improved her general condition remarkably.

Bone Density↗
PubMed1990

Ursodeoxycholic acid-induced changes of plasma and urinary bile acids in patients with primary biliary cirrhosis.

Ursodeoxycholic acid treatment of patients with primary biliary cirrhosis may lead to relief of pruritus and improvement of biochemical liver tests. The changes in serum and urinary bile acids induced by ursodeoxycholic acid treatment were studied. After 29 patients with primary biliary cirrhosis were treated with ursodeoxycholic acid (750 to 1,000 mg/day) for 6 to 12 mo because of an increase in ursodeoxycholic acid, total plasma bile acids increased from 30.5 +/- 6 mumol/L (mean +/- S.E.M.) to 52.7 +/- 11.7 mumol/L (p less than 0.01). The increase in total plasma bile acids correlated significantly with concentrations of plasma bile acid before treatment (p less than 0.01). The concentrations of endogenous bile acids decreased, mainly because of a decrease of cholic acid. During treatment, glycine conjugation increased and taurine conjugation decreased, whereas sulfation and glucuronidation of bile acids were unchanged. In 10 patients with primary biliary cirrhosis in stages III and IV, urinary excretion of bile acids was also studied. After treatment, ursodeoxycholic acid and its 3-beta isomer and C-1-hydroxylated and C-6-hydroxylated derivatives were also excreted. During treatment, urinary excretion of endogenous bile acids decreased. The increase of ursodeoxycholic acid and the decrease of endogenous bile acids may both be related to the improvement of biochemical liver tests in precirrhotic stages of the disease. In cirrhosis, endogenous bile acids in plasma remained high and changes in liver tests were small.

Bile Acids and Salts↗
PubMed1990

Long-term follow-up of posttransfusion and sporadic chronic hepatitis non-A, non-B and frequency of circulating antibodies to hepatitis C virus (HCV).

The natural course of chronic hepatitis non-A, non-B (HNANB) was documented for 3-20 yr (mean 8 yr) in 86 patients, who attended our special ambulance between 1981 and 1988. Sixty five of the 86 patients (75%) were positive for circulating antibodies against hepatitis C virus (HCV) (anti-HCV). Twenty four patients had chronic posttransfusion (PT)-HNANB (18 anti-HCV-positive; 75%), and 62 patients had sporadic (S)-HNANB (47 anti-HCV-positive; 75%). Twenty nine per cent of patients with chronic PT-HNANB had sustained normalization of aminotransferases after a period up to 5 yr, 55% demonstrated chronic persistent hepatitis (CPH) and 16% progressed to chronic active hepatitis (CAH) with transition to cirrhosis. In the group with chronic S-HNANB, 2% of patients showed remission, 43% had stable CPH and 55% progressed to CAH or cirrhosis. However, development of cirrhotic complications required many years. Transition from CAH to CPH or remission was not observed. The results indicate that 75% of both patients groups with chronic PT- and S-HNANB are infected with the same agent, of which antibodies are detected by the new anti-HCV assay. There was no statistical association between the severity of the disease and the presence of anti-HCV. The different proportions of progressive courses in chronic PT- and S-HNANB might be explained by the patient recruitment.

Blood Transfusion↗
PubMed1990

Liver membrane antibodies (LMA) recognize a 26-kD protein on the hepatocellular surface.

Sera from 82 patients with chronic inflammatory liver diseases and from patients with systemic lupus erythematosus (SLE), rheumatoid arthritis (RA) and Hashimoto's thyroiditis were studied by immunoblotting against purified liver plasma membranes (LPM) and soluble liver protein (SLP) fractions from different species after previous separation by SDS-PAGE. Eighteen of 19 sera with LMA of IgG type in immunofluorescence assay and six LMA-negative sera (three sera from patients with RA) showed antibodies of the IgG or IgM classes against a protein with a molecular weight of 26 kD which was present in LPM and SLP fractions from rats, rabbits, pigs and humans. The reaction with 26-kD liver protein did not correlate with other known autoantibody-antigen systems. All sera were negative in the 26-kD region with liver mitochondria, liver microsomes and soluble proteins of kidney (with one exception), heart and gut from the rat. The 26-kD protein was purified by affinity chromatography on immobilized anti-26-kD protein antibodies from patients, eluted from the 26-kD band of immunoblots. Studies with purified 26-kD liver protein and with SLP as antigens after separation in two-dimensional electrophoresis confirmed that patient serum and experimental rabbit antiserum react with the same protein. Eluted patient antibodies and rabbit antisera showed a linear fluorescence pattern on isolated hepatocytes from rat and rabbit. The data indicate that one of the target antigens of LMA is a species-nonspecific 26-kD protein located on the hepatocellular surface.

Adolescent↗
PubMed1990

Antibody activity against lipopolysaccharides, lipid A and proteins from Enterobacteriaceae in patients with chronic inflammatory liver diseases.

These studies are concerned with detection of circulating antibodies against various defined enterobacterial antigens in patients with chronic inflammatory liver diseases such as chronic hepatitis type B (n = 46), chronic active hepatitis (CAH) of autoimmune type (n = 10), alcoholic cirrhosis (n = 24) and primary biliary cirrhosis (PBC) (n = 24) as well as in healthy individuals (n = 39). Anti-LPS and anti-lipid A were determined by hemolytic and hemagglutination assay. Immunoblot technique was used to investigate the antibody activity against plasmid encoded proteins from Yersinia enterocolitica. Persistent titers of anti-LPS up to serum dilution 1:32.768 were found with hemolytic and hemagglutination assay in patients with alcoholic cirrhosis or PBC and in healthy control. In contrast nearly 50% of patients with chronic hepatitis B had no hemolytic antibodies against the two LPS E. coli serotypes at the time of liver biopsy. Anti-lipid A was detectable in 58% of patients with alcoholic cirrhosis but in low titers in less than 10% in the other groups (p less than 0.001). Alcoholic cirrhosis was also associated with a high frequency of IgG and IgA antibodies against plasmid encoded proteins from Yersinia enterocolitica. The data indicate that the O-polysaccharides as strong antigens are physiologically exposed to the immune system while lipid A and enterobacterial proteins are solely immunogenic under abnormal conditions.

Adult↗
PubMed1990

Experimental liver membrane antibodies (LMA) and antibodies against "liver specific protein (LSP)"--a comparative in vitro study.

Experimental antisera against the 26 kD rat liver protein--recently defined as a target antigen of LMA--and against "LSP" were tested on tissue sections and isolated hepatocytes from rat as well as with a variety of subcellular fractions as antigens. Anti-26 kD protein resulted in sharp immunofluorescence staining of hepatocellular plasma membranes in liver sections and on isolated hepatocytes, while the antiserum did not react with intracellular structures and was also negative with tissue sections from kidney and heart. Anti-"LSP" stained the plasma membranes of isolated hepatocytes, the cytoplasma of liver and kidney sections as well as the connective tissue of heart sections. In Western blot studies anti-26 kD protein showed a single band at 26 kD when liver plasma membranes and soluble liver protein fractions were used as antigens; a weak reaction was observed with microsomes and soluble kidney protein fractions, but there was no reaction with mitochondria or soluble heart proteins. Anti-"LSP" reacted with various proteins of the subcellular fractions between 16 and 116 kD. The 26 kD protein was found in peak II of Sepharose 6B chromatography of soluble liver protein fractions but was absent in the "LSP" fraction (peak I). We conclude that experimental LMA and anti-"LSP" recognize different epitopes of the hepatocellular plasma membrane.

Animals↗
PubMed1990

Glycoproteins of rat liver plasma membranes: their hepatocellular, intestinal and renal expression in rat, rabbit and human.

Expression of six glycoproteins (Mr = 60,000 (gp 60), 80,000 (gp 80), 110,000 (gp 110), 120,000 (gp 120), 140,000 (gp 140), 160,000 (gp 160)) recently purified from rat liver plasma membranes (LPM) were compared in the liver, small intestine and kidney of the rat, rabbit and human. Immunoblotting studies with monospecific antisera showed that five of the six glycoproteins (gp 60, gp 80, gp 110, gp 120, and gp 140) were expressed not only in LPM of the rat but also in LPM from the rabbit and human with Mr corresponding to those of the glycoproteins isolated from the rat. In contrast, the glycoprotein gp 160 was only detected in rat liver. The same pattern of expression was found by immunofluorescence on isolated hepatocytes from the three species. In rat liver, the glycoproteins were localized primarily either in the bile canalicular domain (gp 80, gp 110, gp 120), or in the sinusoidal domain (gp 60, gp 140), or they were distributed over the whole hepatocellular surface (gp 160). In rat, but not in rabbit or human, the glycoproteins gp 110, gp 120 and gp 140 were also found in the small intestine localized either in the brush border membrane (gp 110, gp 120) or over the whole surface membrane of enterocytes (gp 140). Gp 120 was also detected in the luminal pole of tubular epithelial cells of rats kidney. The data show that LPM of different mammalian species share several common glycoprotein antigens. These glycoproteins, that are also partly expressed in extrahepatic tissues, may represent plasma membrane structures conserved among mammalian species.

Animals↗
PubMed1990

[Long-term treatment of cryptogenic hepatitis C using recombinant interferon alpha].

In a pilot study 15 patients with cryptogenic chronic hepatitis non-A, non-B received human recombinant interferon alpha (rIFNa) at a dosage of 5 million units 3 times per week for periods of up to 4 months, followed by an additional 4-month course of treatment with 2 million units 3 times per week after an observed reduction in serum aminotransferase levels. Ten of the 15 patients demonstrated antibodies to hepatitis C virus (HCV). Pretreatment histological examinations revealed evidence of chronic aggressive hepatitis in 12 patients, 4 with signs of cirrhosis, and chronic persistent hepatitis (CPH) in the remaining 3 cases. Normalization of serum aminotransferase levels was documented in 9 patients (7 anti-HCV-positive), and a significant reduction occurred in 2 additional anti-HCV-positive cases. Follow-up biopsy at 8 months in 7 of the 11 responders documented improved histological findings in every case. Five patients with CAH in the initial study had discrete residual portal inflammation or mesenchymal reaction in the second histological examination. Clinical follow-up is currently at 12 month, and 3 anti-HCV-positive responders have normal aminotransferase levels. The data show that a subset of patients with chronic hepatitis C will demonstrate remission of disease after an 8-month course of treatment with rIFNa.

Adult↗
PubMed1989

Relation between Escherichia coli R(rough)-forms in gut, lipid A in liver, and primary biliary cirrhosis.

Since antimitochondrial antibodies (AMA) specific to primary biliary cirrhosis (PBC) recognise enterobacterial proteins and can be induced by R(rough)-mutants of enterobacteriaceae a study was done to find out the prevalence of enterobacterial R-forms in stool samples of patients with chronic inflammatory liver diseases. Liver biopsy specimens were also examined for lipid A, a common antigenic component of the cell wall in gram-negative bacteria. In all stool samples from the 21 patients with PBC Escherichia coli R-forms constituted up to half of the total amount of E coli. In contrast E coli R-forms were detectable in the stools of only 1 healthy control (n = 20), and in 25% of patients with other cholestatic diseases (n = 10), chronic hepatitis type B (n = 15), type non-A, non-B hepatitis (n = 15), or chronic pancreatitis and fat malabsorption (n = 8). An immunoblot technique showed that E coli R-forms isolated from patients' stools contained PBC-specific AMA-reactive proteins with molecular weights of 70-80 kD and 50 kD. Deposits of lipid A, located primarily in the cytoplasm of hepatocytes, were found in 11 patients with PBC but not in the liver of patients with chronic viral hepatitis. Circulating antibodies against lipid A were found rarely and in low titres. The data support the hypothesis that intestinal enterobacterial R-forms are aetiologically important in PBC and that antigens released from the bacterial cell wall contribute to the pathogenesis of the disease.

Adult↗
PubMed1989

HBcAg expressed on the surface of circulating Dane particles in patients with hepatitis B virus infection without evidence of anti-HBc formation.

Circulating immune complexes composed of HBcAg and anti-HBc have been demonstrated recently in patients with hepatitis B virus replication. After dissociation of immune complexes by chaotropic ions, HBcAg was quantified radioimmunologically. In the present study, we describe 10 patients with hepatitis B virus replication, absent or delayed anti-HBc formation and exposed HBcAg in serum. Four of the 10 patients had acute hepatitis, and six patients had chronic persistent hepatitis. In seven of 10 patients, a secondary immune defect was apparent due to acquired immunodeficiency syndrome, leukemia, histiocytosis X, sarcoidosis or end-stage renal disease. Electron microscopy demonstrated that Dane particles from anti-HBc-negative patients were agglutinated after addition of monoclonal anti-HBc antibodies, whereas Dane particles from anti-HBc-positive sera did not show agglutination. Monoclonal HBsAg-specific antibodies aggregated Dane particles independent of the presence of anti-HBc. Circulating HBcAg was always associated with the Dane particle fraction after density gradient separation. Hepatitis B virus core proteins from patients with and without anti-HBc studied by immunoblotting after sodium dodecyl sulfate-gel electrophoresis showed identical patterns. Hepatocytes from anti-HBc-negative patients were positive for HBcAg but negative for immunoglobulin G by immunofluorescence technique. The data indicate that HBcAg may also be expressed on the surface of Dane particles, where it is commonly masked by anti-HBc.

Acute Disease↗