Biomedical subjects

G Rodinò

Publications and source records attributed to G Rodinò.

10 recordsLinked to original sources

PubMed1995

Chronic hepatitis in patients with active hepatitis B virus and hepatitis C virus combined infections: a histological study.

OBJECTIVES: To evaluate whether peculiar histological changes are present in liver tissue of patients with chronic hepatitis by hepatitis B and hepatitis C (HBV and HCV) virus combined infections. METHODS: We studied liver biopsy specimens from 14 HB surface antigen/anti-HCV-positive patients consecutively admitted to hospital because of chronic liver disease from 1987 to 1992. Alcohol abusers, drug addicts, hepatitis delta virus- and HIV-infected subjects were excluded from the study. All of them were positive for serum HBV-DNA and/or intrahepatic HB core antigen and for serum HCV-RNA. Histological examination showed mild or moderate chronic hepatitis in nine cases and severe chronic hepatitis with cirrhosis in five cases. Two additional sets of liver biopsy specimens were also included in the study, consisting of liver samples from 14 patients with chronic liver disease due to active HBV infection alone (group B) and from 14 patients with active HCV infection alone (group C). Cases from group B and C matched for age, sex, and histological diagnosis with those from group B + C. Histological patterns of all the liver specimens of the three groups were re-examined by two authors who scored the found features using a scale from 0 to 3. RESULTS: No peculiar histological pattern was revealed in group B + C, and most of the detected microscopic features were similarly present in all three groups. Bile duct lesions and well defined lymphoid follicles were found only in liver samples of patients from groups C and B + C. Ground-glass hepatocytes were observed only in cases from the groups B and B + C. CONCLUSIONS: Histological examination of liver tissue from patients with chronic HBV and HCV combined infection does not show either typical patterns or evidence that this subgroup of chronic viral hepatitis is a more severe form of liver disease than that caused by a single virus infection. The observation in liver samples of peculiar lesions by HBV or HCV infection does not exclude a combined infection by both viruses.

Adult↗

PubMed1994

Persistence of "wild-type" and "e-minus" hepatitis B virus infection in chronic healthy HBsAg/anti-HBe positive carriers.

We examined nine chronic healthy hepatitis B surface antigen/antibody to hepatitis Be carriers with consistently normal liver chemistries and negative serum hepatitis B virus-DNA. Liver biopsy, performed twice, 10-11 years apart in all patients, showed normal histology and negative hepatitis B core antigen. DNA extracted from the second liver biopsy specimen, from 1 ml of serum from each patient and from an additional serum sample of 6 ml from two patients, was tested for pre-C/C and pre-S regions of hepatitis B virus-DNA by polymerase chain reaction amplification. Viral sequences were found in six of nine liver DNA extracts. In four cases both pre-C/C and pre-S regions were amplified, while the pre-C/C alone and the pre-S alone were detected in one case each. Direct sequencing of the amplified DNAs revealed no significant genomic changes in the pre-S and Core regions, while analysis of the pre-Core demonstrated the presence of a double viral population (wild-type and "e-defective") in four cases, and only "e-defective" hepatitis B virus in one case. No hepatitis B virus genomes were revealed in the serum sample when DNA was extracted from 1 ml of serum, while viral sequences were detected in both extracts of 6 ml of serum, indicating the presence of very low levels of viremia. These data suggest that episomal hepatitis B virus-DNA may persist for years in the liver of chronic healthy carriers in a latent state which may involve both wild-type and HBeAg-defective hepatitis B virus.

Carrier State↗

PubMed1994

Inapparent "wild-type" and "e-minus variant" HBV infection in patients with HCV-related chronic hepatitis.

We analysed DNA extracted from liver biopsy specimens and serum samples from 42 HCV-RNA-positive/HBsAg-negative subjects with chronic hepatitis. Twenty-eight of them were anti-HBs/anti-HBc-positive (group A), while 14 were negative for all HBV markers (group B). HBV sequences were found in hepatic DNA of 12 cases (11 of group A, one of group B), but in the serum of only two cases of group A. Sequencing analysis of pre-core region of HBV-DNA showed the presence of wild-type HBV in three cases, HBeAg-defective HBV in three cases, and the coexistence of both viral populations in six cases. These results indicate that HBV and HCV infection may coexist in HBsAg-negative chronic hepatitis, particularly in anti-HBs/anti-HBc-positive patients. However, HBV replication appears suppressed in these cases, and this state of latency may involve both wild and HBeAg-defective HBV types.

Adult↗

PubMed1993

Is the course of perinatal hepatitis B virus infection influenced by genetic heterogeneity of the virus?

We studied the relations between genetic heterogeneity of pre-C region of hepatitis B virus (HBV) DNA and outcome of HBV infection in 5 infants with perinatal infection, 3 born to anti-hepatitis B e antigen (HBeAg), and 2 to HBeAg positive mothers. HBV infection developed in the babies at 3-4 months of age, but it resolved with seroconversion to anti-HBs in infants born to anti-HBe positive mothers, while the infection became chronic in the 2 babies born to HBeAg positive mothers. HBV-DNA extracted from the first hepatitis B surface antigen (HBsAg) positive serum sample of each baby was amplified and directly sequenced for the pre-core region. HBV-DNA sequences from 3 babies born to anti-HBe positive mothers showed at position 1896 the contemporary presence of 2 nucleotides (G+A), indicating a mixture of wild-type and "e minus" variant HBV. These findings suggest a possible co-transmission of the 2 viruses from anti-HBe positive mothers to newborns. HBV-DNA from babies born to HBeAg positive mothers showed wild-type sequences only. The results of this study suggest that the outcome of HBV infection in newborns depends not only on the host's immunocompetence and on viremia level in maternal blood, but also on heterogeneity of HBV. Transmission of mixed HBV populations appears associated with an early immunoelimination of the virus, while infection with wild-type HBV alone contributes to induction of chronicity.

Base Sequence↗

PubMed1992

Histological behaviour of chronic hepatitis in patients treated with alpha interferon.

To evaluate the histological effects of alpha Interferon (IFN) therapy, serial liver biopsy specimens from 30 patients with chronic hepatitis were studied. The biopsies were examined using a scoring system. After 12 mths of IFN therapy responders were 8 out of 11 HBV infected patients, 10 out of 12 HCV infected patients and only 1 out of 7 patients with cryptogenetic hepatitis. As spontaneous improvement of hepatic changes is infrequent, our data indicate that in terms of histological patterns interferon therapy is effective in chronic viral hepatitis.

Hepatitis B↗

PubMed1991

Hepatitis B virus variant, with a deletion in the preS2 and two translational stop codons in the precore regions, in a patient with hepatocellular carcinoma.

We analyzed hepatitis B virus (HBV) genomes obtained from serum samples and liver biopsy specimen of a chronic HBsAg/anti-HBe carrier with hepatocellular carcinoma (HCC). Before the liver biopsy, performed at the time of HCC diagnosis, the patient had been followed for 2 years; the serum samples collected in that period resulted negative for HBV-DNA dot blot hybridization. The hepatic DNA was at first examined by Southern blot, but no HBV sequence was detected. Polymerase chain reaction (PCR) amplification revealed the presence of HBV genomes in DNA extracted from the liver tissue and from two serum samples collected, respectively, 1 and 2 years before the biopsy. Direct sequence of the amplified preC/C and preS regions showed that the viral populations present in serum and liver were identical and that they had a 34 nucleotide deletion in the preS2 region, while the preC region presented two mutations each introducing a translational stop codon, one at the carboxy terminal end and the other at the second codon of the region, both able to prevent HBeAg expression. These results identify a new HBV variant which was selected during a chronic infection, and had very low levels of replication as shown by its detection only after PCR amplification.

Base Sequence↗

PubMed1991

HBe antibody unrelated to 'e minus' hepatitis B virus variant infection in patients with chronic type D hepatitis.

The presence of HBV-DNA sequences was evaluated in DNA extracted from serum samples, peripheral blood lymphocytes and liver biopsy specimens of five HBsAg/anti-HBe-positive carriers with chronic HDV infection. DNAs were tested by polymerase chain reaction (PCR) amplification technique using two pairs of oligonucleotide primers specific for the preC/C and S regions of the HBV; viral sequences were found exclusively in liver extracts and only in three out of the five cases. The direct sequencing of the amplified preC/C regions showed wild-type sequences in two cases, while in the third case a combination of 'wild' and 'e minus variant' viral populations was observed. Moreover, liver DNA of one positive case was electrophoresed through a low melting agarose gel and the following amplification, performed on DNA re-extracted from three different fragments of the gel, showed the presence of free HBV genomes but the absence of replicative intermediate forms. These results show that anti-HBe positivity is not constantly related to precore mutant HBV infection and suggest that HDV inhibits HBeAg production. Moreover, as it was observed in 'e minus' HBV variants, also during a chronic HBV wild-type infection, the viral replication might be suppressed to undetectable levels.

Base Sequence↗

PubMed1991

Histological features in liver biopsy specimens of patients with acute reactivation of chronic type B hepatitis.

The histological features in liver biopsy specimens from seven patients with acute exacerbation of chronic type B hepatitis were analysed. In all the cases typical changes of acute hepatitis were superimposed on signs of chronicity, namely peripheral piecemeal necrosis, plasma cell infiltration and porto-portal bridges, which in three cases contained elastic fibres. Reactivation of silent hepatitis B virus chronic infection should be considered as a possible diagnosis in any patient with histological findings of acute and chronic hepatitis.

Biopsy↗

PubMed1990

Hepatitis B virus (HBV) markers and HBV-DNA in serum and liver tissue of patients with acute exacerbation of chronic type B hepatitis.

We analysed the serum samples and the liver biopsies of six consecutive chronic HBsAg/anti-HBe carriers admitted to hospital because of an episode of acute hepatitis. The six patients became positive for IgM anti-HBc and negative for HBeAg, hepatitis Delta virus (HDV) markers, IgM anti-hepatitis A virus (HAV), anti-cytomegalovirus (CMV) and anti-Epstein-Barr virus (EBV). Two patients showed positivity for hepatitis B virus (HBV)-DNA in serum obtained on admission, with no positivity in the subsequent weeks; the results of the other four patients were always negative for seric HBV-DNA. The Southern-blot analysis of the DNA extracted from the liver tissue of four subjects showed the presence of HBV-DNA in the form of replicative intermediates; focal positivity of HBcAg was detected in the liver of only one. The liver biopsies of the last two patients were negative for HBV-DNA and for HBcAg. The analysis of HBV-DNA in the liver extracts and the demonstration of an increase of the IgM anti-HBc titre at the time of the abrupt elevation of the aminotransferase levels seem to be the most useful tools in revealing HBV activation as a cause of acute hepatitis in chronic HBsAg carriers, overall when the phase of viremia is transient.

Antigens, Viral↗

PubMedDate not supplied

Polyphasic type A hepatitis: histological features.

The histology of polyphasic type A hepatitis was analyzed in liver biopsy specimens of two patients. The microscopic examination showed, together with changes of acute viral hepatitis, portal plasma cell infiltration, limiting plate erosion and porto-portal bridging necrosis. These features, although sometimes described in classical HAV hepatitis, appear to be similar to those commonly observed in severe and evolving forms of acute hepatitis due to other hepatotropic viruses. Only careful serological analyses can lead to a correct diagnosis and prognosis in case of polyphasic type A hepatitis.

Adult↗