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Biomedical subjects

U Hopf

Publications and source records attributed to U Hopf.

At least 109 records · Page 6Linked to original sources
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↗
PubMed1989

[Indications and current developments in liver transplantation].

Today, liver transplantation has become a routine treatment in many centres and will be increasingly applied in the future. Principal indications for liver transplantation are endstage chronic liver diseases, namely cirrhoses of various origin, fulminant hepatic failure, metabolic liver disease, and rarely non-resectable malignant tumors of the liver. Clinical and biochemical parameters indicative of the indication for liver transplantation can be stated with greater confidence. Advances in organ preservation with a new cold storage solution (University of Wisconsin solution) and further refinements in surgical technique and immunosuppression with application of multimodal protocols have led to a one-year-survival rate of 70%-80% in experienced centers. Since October 1988, 32 patients underwent liver transplantation in Berlin, currently, 31 patients are alive, while one patient died due to systemic fungal infection.

Carcinoma, Hepatocellular↗
PubMed1989

[Hepatitis B in established cardiac cirrhosis--a rare indication for liver transplantation].

A 34 year old patient was diagnosed as suffering from congestive cirrhosis due to constrictive pericarditis 18 years ago. A terminal dystrophic episode of additionally acquired chronic aggressive hepatitis B led to rapidly progressive liver failure. Orthotopic liver transplantation was carried out. 10 months after transplantation the patient is alive and well. Presence of HBsAg and HBcAg can again be demonstrated in the liver graft, however, without histologic evidence of hepatitis. Problems of prognosis after liver transplantation for hepatitis B virus infection are discussed.

Adult↗
PubMed1988

Are antimitochondrial antibodies in primary biliary cirrhosis induced by R(rough)-mutants of enterobacteriaceae?

Antimitochondrial antibody (AMA)-positive serum samples from 45 patients with primary biliary cirrhosis (PBC) and AMA-negative serum samples from patients with chronic liver diseases, systemic lupus erythematosus, or rheumatoid arthritis were studied by an immunoblot technique with mitochondria from bovine heart and pig kidney and with several strains of gram-negative bacteria as antigens after separation by sodiumdodecylsulphate polyacrylamide gel electrophoresis. Serum from patients with PBC recognised up to three mitochondrial antigens with molecular weights of 70 kD, 50 kD, and 42 kD. Equivalent patterns were found with bands at 70-80 kD and 50-52 kD with Enterobacteriaceae as antigens. AMA-reactive polypeptides were localised in the ribosomal and membrane fractions from Enterobacteriaceae but differed from known outer membrane proteins. Conversely, PBC-specific mitochondrial antigens at 70 kD and 50 kD were recognised by rabbit antisera against Salmonella minnesota Rb and Rc mutants but not by antisera against wild-type Enterobacteriaceae. Absorption experiments and two-dimensional immunoblotting studies confirmed that mitochondria and gram-negative bacteria share identical PBC-specific determinants. It seems that PBC-specific antigens are expressed in gram-negative bacteria and that these antigens may be immunogenic in mutants with defective polysaccharide synthesis. The data support the hypothesis of a bacterial aetiology for PBC.

Adult↗
PubMed1988

Abnormalities of B cell activation and immunoregulation in patients with chronic inflammatory liver diseases.

The immunoglobulin production capacities of peripheral blood lymphocytes obtained from patients with various chronic inflammatory liver diseases and from normal individuals were compared. Using a reverse hemolytic plaque assay, immunoglobulin-secreting cells (ISC) were counted immediately after isolation (immediate ISC) and again after 6-day, in vitro cultivation without stimulant (spontaneous ISC) or in the presence of pokeweed mitogen, PWM (PWM-induced ISC). An increased number of immediate ISC were observed in patients with chronic active hepatitis (CAH) of the autoimmune type (n = 7) or with CAH type B (n = 32), probably reflecting a defect of the in vivo suppressor cell system as previously demonstrated. In vitro preincubation of cells with 5 x 10(-8) M prednisolone reduced the increase in the number of immediate ISC in patients with CAH of the autoimmune type. On the other hand, lymphocytes obtained from patients with CAH-type NANB (n = 9) and with primary biliary cirrhosis (PBC) (n = 12) showed an impaired capacity to generate ISC upon stimulation with PWM. Spontaneous ISC from patients' lymphocytes were not significantly different from those of normal individuals. Using allogeneic co-cultures with lymphocytes from normal individuals and from patients with CAH NANB hepatitis or primary biliary cirrhosis, we observed no increase in suppressor cell activity. Therefore, the diminished responses to PWM are probably attributable to an alteration in the peripheral helper T-cell compartment.

Antibody Formation↗
PubMed1988

The significance of high-density lipoproteins (HDL) in the clearance of intravenously administered bacterial lipopolysaccharides (LPS) in mice.

The direct immunofluorescence technique was used to study the presence of high-density lipoproteins (HDL) in the liver, spleen and kidney of mice before and after intravenous administration of purified lipopolysaccharides (LPS) from Escherichia coli O 75, Salmonella abortus equi and Salmonella minnesota R 595, as well as free lipid A. Untreated mice had small granules of HDL in the hepatocellular cytoplasm, which appeared more pronounced after oral administration of fat. After intravenous administration of LPS, hepatocellular HDL decreased continuously and was no longer visible 1 hour after injection of LPS or lipid A. Five to ten minutes after administration, smooth-form LPS were located in sinusoidal cells, and rough form LPS and lipid A were found in both parenchymal and nonparenchymal liver cells. All toxins were demonstrated in both cell populations 1-4 hours after injection. The spleen was free of HDL, while there was a strong uptake of LPS into the cells of the reticulo-endothelial system. The kidney of experimental mice had small HDL granules in the epithelial cells of the proximal tubules, with a tendency to move to the lumen 1 hour after LPS injection, while there was a transient granular deposition of LPS in the glomeruli. The results suggest that the early uptake of circulating LPS by cells of the reticulo-histiocytic system in liver and spleen, as well as by hepatocytes, is not mediated by HDL. However, HDL located in hepatocytes or present in the circulation of experimental mice seem to be eliminated through the bile and the urine, induced by LPS.

Animals↗
PubMed1988

[Frequency and clinical relevance of delta virus infection in HBsAg carriers in the Berlin area].

The frequency of delta virus infection, immunoserological parameters and degree of liver inflammation were studied in 190 HBsAg carriers in the Berlin area from 1976 to 1986. Delta infection was detected in one of 50 HBsAg carriers (2%) in the period from 1976 to 1980. In contrast 19 of 140 HBsAg carriers (14%) with delta infection were found in the period from 1981 to 1986. This group included 12 Germans, 5 Turks and 2 Italians. Only 6 of these subjects belonged to a so-called risk group: 3 drug addicts, 2 homosexuals and 1 hemophiliac. Eighteen of the 20 patients with HDV infection showed progressive liver disease in the follow-up period. Nine cases developed complete liver cirrhosis over five years. Variable transaminase levels and elevation of immunoglobulin G were recorded. Humoral autoimmune phenomena were rarely observed. The increasing frequency of HDV infection in the Berlin area is presumably related to tourism, national origin and membership in specific risk groups. The data in our study underline the importance of effective prophylaxis by active immunization with HBsAg vaccines.

Adult↗
PubMed1988

[Schoenlein-Henoch purpura in chronic HBsAG-positive hepatitis].

We report about a 40-year-old male patient suffering from a recurrent vasculitis with purpura since the age of 18. In 1983, a HBsAg-positive chronic active hepatitis with circulating immune complexes which contained HBsAg, immunoglobulin M and G as well as complement (C) was diagnosed. Serum and liver tissue were negative for HBcAg, HBeAg and hepatitis B virus (HBV) DNA; there was no evidence for HBV replication. HBsAg, IgM and C3 were demonstrable in the arteriolar walls of the skin. The results support the concept that complement activating immune complexes containing HBsAg and IgM anti HBs play a role in the pathogenesis of vasculitis as described here.

Adult↗
PubMed1987

Serological assessment of HBcAg and HBV DNA: its prognostic relevance in acute hepatitis B.

Treatment of serum precipitates with sodium thiocyanate in patients with hepatitis B virus (HBV) replication results in liberation of circulating hepatitis core antigen (HBcAg) which can be demonstrated radioimmunologically. Follow-up investigations were performed in 80 patients with acute hepatitis B. Sera were examined for HBcAg. HBV DNA and conventional HBV markers. At the time of admission to hospital 34 of 80 (42%) patients were HBeAg positive. Twenty-six (76%) of the 34 HBcAg positive patients were HBV DNA positive, and circulating HBcAg was detectable in 25 of 34 (73%) HBcAg positive cases. In patients with uncomplicated courses of acute hepatitis B the serological HBcAg assay and HBV DNA became negative 1 to 8 weeks before elimination of HBeAg and up to 12 weeks earlier than the sera became negative for HBsAg. Five patients (6%) showed transition to chronic hepatitis B with persistence of HBsAg, HBeAg, HBV DNA and HBcAg in serum. One patient with acute hepatitis B and development of chronic hepatitis suffered from acquired immunodeficiency syndrome and showed delayed formation of anti-HBc. In this case uncomplexed HBcAg was demonstrable during the acute phase of hepatitis B. With the appearance of anti-HBc HBcAg circulated in a complexed form. The data indicate that serological determinations of HBcAg and HBV DNA can serve as prognostic markers in the early phase of acute hepatitis B. The demonstration of uncomplexed HBcAg in serum of a patient with inadequate formation of anti-HBc supports the hypothesis that circulating HBcAg is usually complexed by specific antibodies.

Acute Disease↗
PubMed1985

[Immunoserologic differentiation of chronic cholestatic hepatitis. Significance of antimitochondrial antibodies and hepatic membrane antibodies].

In 22 of 45 patients with chronic cholestatic liver inflammation and humoral immune phenomena, followed over 15 years with at least one liver biopsy, there was the histological picture of primary biliary cirrhosis (PBC), stages I to IV, with constantly demonstrable antimitochondrial antibodies (AMA) of M2-type. In 12 patients there were signs of PBC and chronic active hepatitis (CAH) in the liver histology, and they were M2-positive. Six of them also had M4-antibodies and were thus classified as 'mixed form'. The other six were seropositive for liver-membrane antibodies (LMA) and (or) antinuclear antibodies (ANA) and thus demonstrated an overlap between PBC and autoimmune or lupoid CAH. In five patients there was autoimmune CAH of lupoid type, in four of them with LMA or ANA without M2- or M4-antibodies. The remaining six patients had pericholangitis with persisting ANA and increased serum concentrations of immunoglobulin M without M2- and M4-antibodies, as well as LMA. Clinically a nondestructive polyarthritis predominated without definite signs of collagenosis. The listed immunoserological parameters make it largely possible to differentiate classical PBC, mixed forms or overlap of PBC and CAH, autoimmune CAH and nonpurulent cholangitis of pericholangitic type.

Aged↗
PubMed1985

[Serologic analysis of HBc antigen in patients with HBs-antigen carrier state].

Treatment of serum with sodium thiocyanate in HBs antigen carrier patients leads to liberation of circulating HBc antigen which can be demonstrated radioimmunologically. Investigations were done in 54 HBs antigen carriers, 44 of whom had chronic inflammatory liver disease (22 patients each HBe antigen positive and negative), and in 10 patients who were asymptomatic (so-called healthy HBs antigen carriers). Out of the 22 HBe antigen positive patients 17 were HBc antigen positive serologically. In the HBe antigen negative group of HBs antigen carriers two out of 22 patients with HBc antigen in serum were detected. All 10 asymptomatic HBs antigen carriers were HBc antigen negative. In 11 out of the 40 immunohistologically assessed patients HBc antigen could be demonstrated in hepatocellular nuclei; these 11 patients also demonstrated HBc antigen in serum. The liberated HBc antigen was associated with Dane particles in the density gradient. Serologic demonstration of HBc antigen may thus be considered as direct evidence of presence of hepatitis B virus.

Carrier State↗
PubMed1985

[Binding activity of circulating HBsAg particles for polymerized human albumin in acute hepatitis B].

The binding activity of circulating HBsAg particles to polymerized human serum albumin (pHSA) was determined by radioimmunoassay in 18 patients with acute hepatitis B at follow-up and compared with other hepatitis B virus (HBV) markers. All patients had serum HBsAg particles with binding sites for pHSA during the acute phase of disease. Elimination of HBsAg particles with pHSA receptors occurred within 1 to 8 weeks in uncomplicated courses and in one case with a protracted course of 16 weeks before total elimination of HBsAg. The pHSA-test became negative after elimination of HBsAg in most instances. Three patients developed chronic hepatitis with persistence of pHSA-binding HBsAg particles. Circulating HBcAg dissociated by chaotropic ions was detectable in the first week of observation in 4 of 15 patients who recovered and persisted in 3 cases with transition to chronic disease. The results show that acute hepatitis B is associated with circulating pHSA-binding HBsAg particles which can serve as a prognostic marker of the early phase of the disease.

Adult↗
PubMed1984

Hepatocellular clearance function of bacterial lipopolysaccharides and free lipid A in mice with endotoxic shock.

Hepatic uptake of bacterial lipopolysaccharides (LPS) in defined salt forms and free lipid A was studied in C3H mice. Extracts of 14C-labeled and unlabeled LPS from Salmonella abortus equi and lipid A from Salmonella minnesota R 595 (Re) were administered intravenously in doses sufficient to induce endotoxic shock. Sixty minutes after administration of 14C-LPS, 40% of the total activity was found in the liver tissue, 10% was in the isolated nonparenchymal cells, and only 1% was in the isolated hepatocytes. However, at this time only one third of the hepatocytes could be isolated; the other two thirds were obviously damaged. After 240 minutes, 55% of the total activity was measured in the liver tissue. The nonparenchymal cells had 8% of the activity, and all hepatocytes were damaged. By use of immunofluorescence, LPS S abortus equi was localized in sinusoidal cells 5 to 10 minutes after administration, and LPS S minnesota R 595 and lipid A were found in both nonparenchymal and parenchymal liver cells. All toxins were localized in both cell populations 60 and 240 minutes after injection. After application of LPS or lipid A, the third complement component (C3) was detectable in sinusoidal cells. In decomplemented mice the hepatic deposits of LPS and lipid A were unaffected, without demonstration of C3. The data indicate that LPS and lipid A interact in vivo with Kupffer cells and hepatocytes. Hepatic clearance of endotoxin seems to be independent of complement.

Animals↗