Search PubMed⌕ Search

Biomedical subjects

A Alberti

Publications and source records attributed to A Alberti.

At least 289 records · Page 16Linked to original sources
PubMed1987

Detection of hepatitis B virus DNA sequences in bone marrow of children with leukemia.

To investigate the possibility that hemopoietic cells may become infected with hepatitis B virus (HBV), viral DNA was studied by molecular hybridization in bone marrow aspirates of 51 children with leukemia. HBV-DNA was found in the bone marrow of eight children (15%) and Southern blot analysis revealed the presence of free, monomeric viral sequences. Only one of the eight children with HBV-DNA in bone marrow cells was HBsAg-positive in serum, whereas two additional patients were transiently HBsAg-positive in serum during follow-up, but were negative at the time HBV-DNA was found in bone marrow. Four other cases developed antibodies to HBV. Cases of myeloid leukemia were more frequently positive for HBV-DNA in bone marrow (55%), compared with cases of lymphoid leukemia (7%). These results indicate that hemopoietic cells are susceptible to infection with hepatitis B virus and stimulate new interest into the relation of HBV infection to the development of some forms of leukemia, as four of eight cases of myeloid leukemia were HBV-DNA positive in bone marrow aspirates at diagnosis, prior to receiving any transfusion therapy.

Adolescent↗
PubMed1987

Hepatitis B virus (HBV)-DNA-positive hepatocellular carcinoma following hepatitis B virus infection in a child.

Integrated hepatitis B virus (HBV) DNA sequences were found in neoplastic liver tissue of a hepatitis B surface antigen (HBsAg)-negative child who had previously suffered from HBsAg-positive chronic active hepatitis and was anti-HBs and anti-hepatitis B core (HBc) positive at the time of tumor development. Reintegration pattern was consistent with the presence of a single integration site of the HBV genome into cellular DNA, and clonal proliferation of such infected cells. A normal liver, tested in the same experiment with the same amount of total DNA, was negative for viral DNA sequences. These findings support the possible oncogenic role of HBV in the development of liver cancer, not only in adults, but also in children, even in patients who are negative for HBsAg at the time of tumor diagnosis.

Carcinoma, Hepatocellular↗
PubMed1987

IgM antibody to hepatitis B core antigen in children with chronic type B hepatitis.

IgM antibody to hepatitis B core antigen (anti-HBc IgM) was investigated by an antibody-capture radioimmunoassay (serum dilution 1:4000) in serum samples from 31 untreated children with chronic hepatitis B who were followed prospectively for 1-7 years. At the start, all patients were positive for hepatitis B e antigen (HBeAg), and anti-HBc IgM was detected in 23 cases, including 15 out of 16 with chronic active hepatitis and 7 out of 14 with chronic persistent hepatitis. A significant positive correlation was found between anti-HBc IgM levels and severity of liver damage (P less than 0.05), while an inverse relationship was found between anti-HBc IgM levels and distribution of hepatitis B core (HBcAg) antigen in the liver as detected by immunofluorescence. In fact 75% of anti-HBc IgM positive patients showed a focal HBcAg pattern (less than 40% positive nuclei), whereas 87% of antibody negative cases exhibited a diffuse HBcAg expression (more than 60% stained nuclei). During follow-up, seroconversion from HBeAg to anti-HBe with subsequent remission of liver disease occurred in 82% of patients presenting with detectable levels of anti-HBc, including three out of seven cases with chronic persistent hepatitis, but in none of the cases that were initially negative (P less than 0.01). These results indicate that during the natural course of chronic hepatitis B in children, anti-HBc IgM levels in serum reflect the degree of host immune response to infected hepatocytes. The close correlation between anti-HBc IgM seropositivity and seroconversion from HBeAg to anti-HBe suggests that anti HBc IgM may have a prognostic value during the follow-up of children with chronic HBeAg positive hepatitis B.

Adolescent↗
PubMed1987

Cell-mediated immunity to HBcAg in chronic HBV infection.

The role of hepatitis B core antigen (HBcAg) as a possible target of cell-mediated immune response in chronic hepatitis B virus (HBV) infection has been recently emphasized. Peripheral blood leukocytes (PBLs) from 35 chronic carriers of hepatitis B surface antigen (HBsAg) were studied in vitro for their immune response to a purified preparation of HBcAg isolated from circulating Dane particles. PBLs from all the studied HBsAg-positive patients yielded a stimulation index above 3, with values ranging from 3.1 to 38.1. None of the healthy seronegative subjects, taken as control group, had a stimulation index above 2, with a mean value +/- SD of 1.28 +/- 0.35. Levels of PBL stimulation correlated with the histologic activity of liver disease, and the differences reached statistical significance. These results indicate that lymphocyte response to HBcAg may be relevant in determining liver cell damage.

Adult↗
PubMed1987

Influence of hepatitis delta virus infection on progression to cirrhosis in chronic hepatitis type B.

Serological markers of hepatitis delta virus (HDV) infection were found in 18 (12%) of 146 consecutive patients with chronic hepatitis B, and the characteristics of patients who had antibody to HDV (anti-HDV-positive) were analyzed. During one to 15 years of follow-up, histological deterioration was documented in 77% of anti-HDV-positive patients; however, in hepatitis B surface antigen (HBsAg) carriers without HDV infection, histology deteriorated in 30% but improved or remained unchanged in the majority of patients (P less than .01). In seven (70%) of the 10 anti-HDV-positive patients who showed transition from chronic active hepatitis to cirrhosis, this event was observed within the first two years of follow-up. The probability of evolution to cirrhosis was significantly higher in anti-HDV-positive patients than in patients without antibody to HDV (P less than .001). These findings indicate that HDV infection in patients with chronic hepatitis B is associated with a more-rapid progression to cirrhosis compared with HBsAg carriers with chronic hepatitis and no evidence of HDV infection.

Adolescent↗
PubMed1987

HBV-DNA sequences are rarely detected in the liver of patients with HBsAg-negative chronic active liver disease and with hepatocellular carcinoma in Italy.

Hepatitis B virus sequences were studied by molecular hybridization in liver biopsies from patients with HBsAg-negative chronic liver disease or hepatocellular carcinoma, collected in Italy. Among the 42 patients with chronic liver disease who had no history of drug addiction, alcohol abuse nor evidence of metabolic and autoimmune disorders, only two (5%) had HBV-DNA sequences in the liver, although 23 of them (57%) were positive for antibodies to HBV in serum. HBV-DNA was also demonstrated in integrated form in the tumorous tissue of one out of eight cases with HBsAg-negative hepatocellular carcinoma. These incidences of HBV-DNA positivity in the liver are lower than those reported from other Mediterranean areas and similar to those of North Europe, United States and Japan, suggesting that etiologic factors other than HBV are responsible for the majority of HBsAg-negative chronic liver diseases in our region.

Base Sequence↗
PubMed1987

Prognosis in chronic lymphocytic leukemia: a retrospective multicentric study from the GIMEMA group.

Clinical and biological data were evaluated using Desu univariate analyses or Cox multivariate analyses in a series of 1,777 chronic lymphocytic leukemia (CLL) patients from an Italian Cooperative Group. In univariate analyses, age and sex of patients, presence of bone marrow (BM; greater than or equal to 50%), and peripheral blood (PB; greater than or equal to 60,000/microL) lymphocytosis, anemia (hemoglobin [Hb] less than 11 g/dL), thrombocytopenia (less than 100,000/microL), direct Coombs' test positivity, hepatomegaly, splenomegaly, and extent of lymph node involvement were shown to be of significant prognostic value. Multivariate analyses, through a stepwise procedure, showed that the most important prognostic variables are Hb, hepatomegaly, lymph node involvement, PB lymphocytosis, and age and sex of patients. Further covariates would produce an improvement having a nonsignificant P value. Based on the results of multivariate analyses, a four-step staging using the significant variables of the Cox model is proposed.

Adult↗
PubMed1987

[Delta agent infection and immunoglobulin G in acute HBsAg-positive hepatitis with chronic course].

In 18 patients with clinical evidence of acute hepatitis, positive for HBsAg, and evolution to chronic infection, we detected the presence of antibodies to the delta agent (anti-HDV), in relation to the immunoglobulin serum level. The IgG were significantly higher during the beginning of the acute phase in the 6 positive cases for anti-HDV than in the patients who were anti-HDV negative. In the group positive for anti-HDV, the IgG remained high also during the following months, with a more severe clinical evolution. Among patients positive for anti-HDV there were no significant differences between the initial level of IgG and the presence or not of IgM anti-HBc during the acute phase of the disease (respectively patients with co-infection or super-infection). These results show that the presence of high levels of IgG during the acute phase of HBsAg positive hepatitis suggests the co-existence of delta infection.

Acute Disease↗
PubMed1987

Definition of hepatitis B virus (HBV)-specific target antigens recognized by cytotoxic T cells in acute HBV infection.

We have investigated the specificity of cell-mediated cytotoxicity for autologous liver cells in 10 patients with acute hepatitis B in relation to the expression of hepatitis B virus (HBV) antigens and IgG on the surface of hepatocytes. Hepatitis B core antigen (HBcAg) was expressed on hepatocytes from six patients and hepatitis B surface antigen (HBcAG) from four, though always in association with HBcAg. Peripheral blood mononuclear cells (PBMC) were significantly cytotoxic in eight of the patients, and fractionation experiments revealed that the cytotoxic effect was equally mediated by T and non-T cells. Monoclonal antibody blocking experiments showed that HBcAg was the major target antigen recognized by T cells, although some inhibition of cytotoxicity was observed after pretreatment of target cells with monoclonal anti-HBs in patients with liver cell surface HBsAg. In contrast, non-T cells were not consistently inhibited by either monoclonal anti-HBc or anti-HBs. These findings further suggest that the HBV nucleoprotein serves as a target for recognition by cytotoxic T cells.

Acute Disease↗
PubMed1986

Prognostic value of "total tumor mass score" (TTM): a retrospective analysis of 130 patients with chronic lymphocytic leukemia.

The validity of the clinical staging of Jaksic and Vitale for chronic lymphocytic leukemia (CLL), designated total tumor mass score (TTM), was tested in 130 consecutive and previously untreated patients followed at our institution over a 15-year period. The analysis, extended to the whole population, confirmed the prognostic value of the TTM score. Patients with a high TTM (greater than 9.0) had an expected median survival (EMS) of 30 months; those with a low TTM (less than 8.9) had an EMS of 129 months (P less than 0.001). The prognostic value of TTM remained even after adjustment was made for age, sex, lymphocyte count, TTM distribution pattern, bone marrow failure, and response to therapy. Taking into account the value of the TTM score, patients of the intermediate risk group (stage II of Rai et al.) could be divided into two subgroups with a different prognosis (EMS 200 vs. 32 months; P less than 0.005). When used as a continuous quantitative parameter the TTM score may help to define response to therapy. In this study TTM response to therapy was significant for prognosis (P less than 0.001), and there seems to be relationship between the degree of response and survival probability.

Aged↗
PubMed1986

Monoclonal radioimmunoassay for hepatitis B surface antigen in sera of children with acute leukemia.

Hepatitis B surface antigen (HBsAg) was detected by a monoclonal antibody radioimmunoassay in sera from five of 43 children (11.6%) with acute leukemia, who were negative by conventional assay. None of the nine positive sera had evidence of reactivity for HBV-DNA or DNA-polymerase activity. No correlation was found between the presence of HBsAg in serum by monoclonal RIA and the behaviour of anti-viral antibodies. Twenty-two children could be studied for liver HBsAg by immunofluorescence, and nine of them (40.9%) were positive, including three patients having HBsAg reactivity in serum. These data indicate that monoclonal antibodies increase the sensitivity of RIA for the detection of serum HBsAg in children with acute leukemia, who previously have frequently been found to have an atypical hepatitis B virus (HBV) serology.

Acute Disease↗
PubMed1986

Levamisole therapy in chronic type B hepatitis. Results of a double-blind randomized trial.

A double-blind, randomized, controlled trial has been undertaken to evaluate treatment of chronic hepatitis type B with levamisole. Ten patients received levamisole (150 mg/day, 3 days/wk) and 10 received placebo until seroconversion to antibody to hepatitis B e antigen eventually occurred, or for a maximum of 18 mo. Final evaluation at 24 mo after starting treatment revealed that 60% of the patients in the levamisole group had become hepatitis B e antigen negative, 90% were hepatitis B virus-deoxyribonucleic acid negative in serum, and 8 of 9 (89%) patients had cleared hepatitis B core antigen from the liver. On the other hand, in the placebo group only 4 of the 10 subjects (40%) were hepatitis B e antigen and hepatitis B virus-deoxyribonucleic acid negative in serum and 3 of 8 (37.5%) of them became hepatitis B core antigen free in the liver. Moreover, in 8 patients of the treated group and in 4 of the control cases aminotransferase activities fell into the normal range. A liver biopsy specimen was obtained after treatment in 17 patients and 7 of 9 levamisole recipients showed marked improvement in hepatic histology, compared with 3 of 8 placebo recipients. These data show that patients treated with long-term levamisole therapy have a tendency toward normalization of aminotransferase activities and suppression of hepatitis B virus replication, suggesting that the drug may be of benefit in chronic hepatitis B e antigen-positive hepatitis.

Adolescent↗
PubMed1986

In vitro effect of lymphoblastoid alpha-interferon on subpopulations of effector cells mediating cytotoxicity for autologous hepatocytes in hepatitis B and non-A, non-B.

Controlled clinical trials are currently under way to assess the efficacy of interferon (IFN) in hepatitis B virus (HBV) infection. In the present study, T-enriched and non-T-enriched lymphocytes from six patients with acute and six patients with chronic HBV infection were cocultured with autologous liver cells with and without alpha-IFN (lymphoblastoid) at a concentration of 1000 U/ml of culture medium, in an 18 h cytotoxicity assay. IFN produced a significant enhancement of non-T-cell cytotoxicity in patients with acute and chronic HBV infection, from 34.3 +/- 19.6% to 60.0 +/- 11.2%, P less than 0.03, and from 41.2 +/- 17.2% to 65.5 +/- 9.8%, P less than 0.01, respectively. In contrast, no significant effect was observed on T cell-mediated cytotoxicity in either group of patients. The in vitro effect of alpha-IFN was also evaluated in four patients who developed chronic non-A, non-B hepatitis following blood transfusion, but no significant stimulatory effect was noted on either T- or non-T cell cytotoxicity. Similarly, no significant increase was observed in control subjects. The significant enhancement of non-T cell cytotoxicity, but not of T-cell cytotoxicity, for autologous hepatocytes in HBV infection suggests that alpha-IFN produces a selective stimulatory effect on non-T cells. The absence of a similar effect in patients with chronic non-A, non-B hepatitis and control subjects suggests that HBV infection alters the susceptibility of hepatocytes to IFN-stimulated non-T cell damage.

Adolescent↗