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Biomedical subjects

F Bonino

Publications and source records attributed to F Bonino.

At least 145 records · Page 8Linked to original sources
PubMed1991

Serological diagnosis of hepatitis B and delta virus (HBV/HDV) coinfection.

Diagnosis of acute hepatitis B virus/hepatitis delta virus (HBV/HDV) coinfection is currently based on detection of anti-HD, however this antibody may be undetectable during the acute phase of hepatitis. To evaluate the entity of misdiagnosis of HBV/HDV coinfection in acute HBsAg-anti-HBc IgM positive hepatitis we examined sera from 245 consecutive patients obtained at admission and day 30, 60, 120, 210 and 400 of their follow-up. Anti-HD was detected in the serum of 26 out of 245 patients (10.6%). In 15% of cases it was present at admission, while in 92% it was found after 30 days. The combined detection of HDV-RNA, HDAg and IgM anti-HD in acute phase sera allowed a correct etiologic diagnosis in 69% of the cases. These findings suggest that the prevalence of HBV/HDV coinfection is underestimated when anti-HD is the only marker to be detected during the acute phase of disease. A correct etiologic diagnosis can only be made by testing acute phase sera for all the available markers of HDV. However, the best cost-effective procedure is to test any patient with HBV markers at presentation for anti-HD, 30-40 days after the onset of symptoms.

Adult↗
PubMed1991

Treatment with interferon of chronic hepatitis B associated with antibody to hepatitis B e antigen.

Persistence of HBV replication (serum HBV-DNA and intrahepatic HBcAg) and markers of HBV-induced (IgM anti-HBc positive) liver disease in anti-HBe-positive patients characterize a peculiar form of chronic hepatitis B. This form of hepatitis B prevails in the Mediterranean Basin, Middle and Far East and is associated with the infection of an HBV variant that lacks the capacity to produce HBeAg. We analysed the results of interferon treatment of 90 patients with chronic anti-HBe-positive hepatitis included in four randomized controlled trials. Interferon inhibited viral replication to undetectable levels and ALT normalized in about 70% of patients. However, the effect was transient in the majority of cases and hepatitis B relapsed in 41 to 90% of patients. A discrepancy in the rate of relapses could be explained by a significant difference in patients populations with a higher prevalence of cirrhotic patients in studies with poorer response. Therefore, in advanced anti-HBe-positive chronic hepatitis B, interferon shows a lower efficacy than in HBeAg-positive patients. The earlier treatment starts, the more efficacious is the response to interferon. Future clinical trials should focus on higher doses for longer periods, repeated courses or on combination therapy with nucleoside analogs or immuno-stimulant drugs.

Chronic Disease↗
PubMed1991

Hemorheologic and coagulative pattern in hypercholesterolemic subjects treated with lipid-lowering drugs.

The effects on the coagulative and rheologic pattern of two lipid-lowering drugs, bezafibrate and simvastatin, were studied in 36 hypercholesterolemic subjects. Patients were randomly divided into two groups (18 subjects each) and received bezafibrate R 400 mg/day or simvatatin 10-40 mg/day over a twelve week period. Besides a decrease in plasma fibrinogen and fibrinopeptide A (p less than 0.001 both), bezafibrate induced a reduction of factor VIIc and VIIIc activity (p less than 0.001 both), while antithrombin 3 activity was increased (p less than 0.001) and the hemorheologic pattern was greatly improved (p less than 0.001). Simvastatin caused a slight decrease in factor VIIIc activity and a moderate reduction of beta-thromboglobulin. The efficacy of bezafibrate in reducing the activation of the coagulative cascade and improving the hemorheologic pattern has been confirmed; the peculiar triglycerides- and fibrinogen-lowering effect of the drug, not observed with simvastatin, could be responsible for these modifications.

Adult↗
PubMed1991

Pathobiology of chronic hepatitis virus infection and hepatocellular carcinoma (HCC).

Hepatitis viruses may cause liver cancer (HCC) through an indirect mechanism inducing inflammation and cirrhosis. Only hepatitis B virus (HBV) was shown to have a direct oncogenetic potential. Hepatitis D virus (HDV) infection, superimposed on the oncogenetic background provided by chronic HBV infection, appears to provide an additional risk for HCC. Patients with florid infections from both HBV and HDV and active liver inflammation develop HCC at a significantly younger age than those infected by HBV alone or infected by hepatitis C virus (about 10 years earlier). In patients positive for serum HBV-DNA/HDV-RNA and/or IgM anti-HBc/IgM anti-HD it is mandatory to program a more frequent (thrice a year) schedule of screenings (ultrasound scan, alpha-1-phetoprotein, etc.) for prophylaxis of HCC.

Animals↗
PubMed1991

Diagnostic advances in viral hepatitis: the discovery of hepatitis C virus and genetic heterogeneity of hepatitis B virus.

The discovery of hepatitis C virus (HCV) and its serological markers represents a new milestone in the history of viral hepatitis and allows a specific diagnosis of viral hepatitis in more than 90 percent of cases. In addition, testing for anti-HCV plays a crucial role in prevention of post-transfusion non-A, non-B hepatitis. The multifaceted spectrum of liver disease associated with hepatitis B virus (HBV) infection, spanning from a healthy carrier state to severe forms of chronic hepatitis, was traditionally attributed to variability of host's antiviral immune response. The finding that a peculiar natural course and response to interferon of chronic hepatitis B is associated with the infection of a defective HBV unable to secrete the "e" antigen (HBeAg-minus) emphasizes the clinical implications of the genetic heterogeneity of hepatitis viruses.

Biomarkers↗
PubMed1991

Hepatitis B virus replication modulates pathogenesis of hepatitis D virus in chronic hepatitis D.

Hepatitis D virus and hepatitis B virus nucleic acids were detected by Northern and Southern blot hybridization in the sera and livers of 85 chronic carriers of HBsAg and anti-hepatitis D followed up for a mean of 10 yr. We identified three subsets of patients: 13 with hepatitis D virus and hepatitis B virus viremia, 53 with serum hepatitis D virus RNA, but without hepatitis B virus DNA and 19 negative for both nucleic acids. Genomic and subgenomic forms of hepatitis D virus RNA were detected only in patients with hepatitis D virus and hepatitis B virus viremia. Histological findings and disease activity at admission were comparable in the three groups of patients, but the outcome was significantly worse in patients with active replication of both viruses; two of them died of terminal liver failure and hepatocellular carcinoma developed in two; the remaining patients had an uneventful course. These results suggest that active hepatitis B virus replication represents an important previously unrecognized determinant of severe liver damage in patients with chronic hepatitis D virus infection. Since hepatitis B virus provides the means for hepatitis D virus secretion and release from infected cells, active hepatitis B virus multiplication favoring the spread of hepatitis D virus from cell to cell may increase the pathogenetic potential of the defective agent.

Adolescent↗
PubMed1991

Diagnosis of Budd-Chiari syndrome by pulsed Doppler ultrasound.

Computed tomography and real-time ultrasonography may not be conclusive for the diagnosis of the Budd-Chiari syndrome; in many cases more information may be needed, especially on vascular alterations. Doppler ultrasonography provides qualitative data on flow direction and pattern, thereby contributing significantly to diagnosis. Eight cases in which hepatic vein patency was unclear and presence of intrahepatic vessels resembling hepatic veins raised problems of interpretation in real-time ultrasonography are described. In some cases, patency or occlusion of the upper portion of the inferior vena cava were difficult to identify with real-time ultrasonography. Doppler ultrasonographic investigation showed flow in the hepatic veins to be completely absent in two cases and reversed in another two. In the remaining four cases, a flat waveform was evident. Flow in the inferior vena cava was reversed in four cases and showed a flat waveform in three other cases. Portal vein thrombosis was detected in only one case, whereas the remaining seven patients showed slow hepatopetal flow. These findings demonstrate that absent or reversed flow in the hepatic veins and/or flat flow in the hepatic veins associated with reversed flow in the inferior vena cava may be considered diagnostic for the Budd-Chiari syndrome. For this series the sensitivity of Doppler ultrasonography was 87.5%.

Adult↗
PubMed1990

Detection of hepatitis C viral sequences in non-A, non-B hepatitis.

The role of hepatitis C virus (HCV) in post-transfusion non-A, non-B hepatitis (NANBH) was investigated by analysing clinical samples for both HCV RNA by cDNA/polymerase chain reaction and antibodies against C100-3 by radioimmunoassay. Of fifteen chronic NANBH patients and one patient with chronic cryptogenic liver disease, ten were positive for anti-C100-3 and seven of the ten had viral sequences in their livers. However, two patients negative for anti-C100-3 also had substantial levels of HCV RNA in their livers. In acute post-transfusion NANBH (one surgical patient and two experimentally infected chimpanzees), HCV RNA was detected in the absence of anti-C100-3. In addition, infectious plasma from a seronegative patient with acute post-transfusion NANBH and a seronegative pool of plasma from a chimpanzee with chronic post-transfusion NANBH had high levels of HCV. These findings show that anti-C100-3-positive patients with chronic post-transfusion NANBH are likely to be viraemic; confirm that antibodies to C100-3 are a marker for infectivity; and suggest that the prevalence of HCV infections may be underestimated from the frequency of antibodies to C100-3 alone.

Animals↗
PubMed1990

Riboprobe assay for HDV RNA: a sensitive method for the detection of the HDV genome in clinical serum samples.

We have used a new hybridization assay for the detection of the genome of hepatitis delta virus (HDV) in serum using a strand-specific RNA probe obtained by transcription of a recombinant riboprobe. This assay was tested on a panel of 30 sera from HBsAg carriers with hepatitis delta antigen (HDAg) in the liver. The riboprobe assay detected HDV RNA in the serum of 83% of the patients, while 63% were positive using the DNA hybridization assay. HDAg was detected in 73% of the same sera by immunoblotting. The riboprobe assay was also compared to other assays on serial samples from an experimentally infected chimpanzee. These results demonstrate that the Northern blot assay using the RNA probe is more sensitive than the homologous DNA probe for the detection of HDV in serum and is also more sensitive than the immunoblot assay for HDAg. The riboprobe assay is the most sensitive of currently available methods to measure HD viremia.

Adult↗
PubMed1990

A precore-defective mutant of hepatitis B virus associated with e antigen-negative chronic liver disease.

The pathogenesis of chronic liver disease (CLD) due to persistent hepatitis B virus (HBV) infection has not been defined, but the disease activity is believed to correlate with the presence of hepatitis B e-antigen (HBeAg) antigenemia and high viremia. The molecular characterization of an HBV mutant isolated from an HBeAg-negative patient with severe CLD required amplification of the circulating HBV DNA (2 pg/ml) by the polymerase chain reaction (PCR). Direct sequencing of the nucleotides from five independent amplifications of the conserved precore region consistently revealed a G to A mutation in each of the two terminal codons of the precore region. Codon 28 was mutated from tryptophan-encoding TGG to a translational stop codon, TAG; codon 29 preceding the core initiation codon was changed from GGC to GAC. For biologic evaluation of these mutations on HBV replication and expression of HBeAg in vitro, HepG2 cells were transfected with cloned, recircularized mutant HBV DNA. The transfected cells contained subviral core particles in the cytoplasm and secreted mature HBV, without HBeAg, into the medium. The findings present the first evidence that complete HBV genomes can be amplified by PCR and are replication-competent in vitro. The data also indicate that HBeAg is not necessary for replication of HBV and furthermore suggest that HBeAg is not required for the progression of HBV-induced CLD.

Adult↗