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Biomedical subjects

G Realdi

Publications and source records attributed to G Realdi.

At least 127 records · Page 7Linked to original sources
PubMed1982

Virologic features of chronic hepatitis B virus infection in childhood.

Hepatitis B virus markers were studied in serum and liver of 24 children with chronic hepatitis. All patients had evidence of active virus replication, as shown by hepatitis B core antigen in the liver cell nuclei, independently of the severity of histologic lesions. Furthermore, 19 of 24 patients had hepatitis B e antigen in serum, and most patients showed a diffuse pattern of HBcAg distribution in the liver. In all 24 children, the presence of immunoglobin G bound to the liver cell surface paralleled the activity of virus replication, but it did not correlate with the severity of liver lesions. During a follow-up period of two to four years, the virus replication persisted in all eight patients receiving immunosuppressive therapy, whereas in 5 of 16 untreated patients we observed a seroconversion to antibody to HBeAg, which is currently regarded as a favorable event for the prognosis of the disease.

Child↗
PubMed1982

Long-term follow-up of acute and chronic non-A, non-B post-transfusion hepatitis: evidence of progression to liver cirrhosis.

The long-term outcome of non-A, non-B post-transfusion hepatitis was evaluated in 21 patients who developed the illness after open-heart surgery and could be followed thereafter up to five years. Histological chronic sequelae were documented in 13 patients, and consisted of chronic persistent hepatitis in one case, chronic lobular hepatitis in two and chronic active hepatitis in 10, five of whom also developed superimposed cirrhosis. Progression to these chronic states was in most cases symptomless, independently of the severity of liver lesions; one patient, however, died of gastrointestinal bleeding due to cirrhosis of the liver. During follow-up the biochemical pattern of chronic non-A, non-B hepatitis was unique, while striking fluctuations of transaminase levels. Liver histology proved essential to identify the severity of chronic liver lesions, as clinical and biochemical features were uniform and not indicative of it. Our results suggest that cirrhosis may develop, often with an asymptomatic course, in a significant number of patients who do not recover after acute post-transfusion non-A, non-B hepatitis.

Acute Disease↗
PubMed1982

Virological changes in chronic hepatitis type B treated with levamisole.

8 children, known to have been hepatitis B surface antigen (HBsAg) and hepatitis B e antigen (HBeAg) positive for more than 6 months and with chronic active hepatitis on biopsy, received 2.5 mg levamisole/kg/day, 2 days a week for 6-18 months. In 6 of the 8 children transaminases normalized within 4-18 months of therapy, with seroconversion to antibody to HBeAg (anti-HBe) and disappearance of HBV-DNA polymerase from serum and of hepatitis B core antigen (HBcAg) from liver. In these cases liver biopsies taken after treatment showed histological regression to chronic persistent hepatitis. Two distinct patterns of response to levamisole were noted: patients having higher pretreatment transaminase levels and lower expression of HBcAg in the liver showed an early transaminase normalization and anti-HBe seroconversion with therapy, while in patients with less active disease and more diffuse HBcAg positivity in pretreatment liver biopsies, longer treatment periods were necessary to achieve these effects. Our results suggest that long-term levamisole therapy may be beneficial in HBeAg-positive chronic hepatitis type B.

Adolescent↗
PubMed1982

Epidemiological aspects on acute viral hepatitis in northern Italy.

Incidence and epidemiological features of acute hepatitis types A, B and non-A non-B have been evaluated in 332 consecutive patients hospitalized in Padova, Italy. Hepatitis B was diagnosed in 59% of cases and was frequently related to drug addition, health care work and household contact with HBsAg-positive subjects. Hepatitis A represented 22% of cases and its peak incidence occurred in the second decade. Non-A non-B hepatitis affected 15% of patients including not only transfusion or drug related forms, but also sporadic cases that prevailed among elderly women.

Adolescent↗
PubMed1982

Core antigen-specific immunoglobulin G bound to the liver cell membrane in chronic hepatitis B.

The antibody specificity of immunoglobulin G bound to the liver cell membrane during hepatitis B virus infection and chronic liver disease has been studied in 8 patients after antibody elution with high molar urea. Eluted immunoglobulin G showed antibody specificity for hepatitis B core antigen by radioimmunoassay and by indirect immunofluorescence on positive liver tissue. On the contrary, no reaction could be detected against other viral antigens (i.e., hepatitis B surface antigen and hepatitis B e antigen) or against liver-specific proteins. Furthermore, in 5 selected cases, after urea removal of cytophilic antibody, hepatitis B core antigen could be demonstrated by direct immunofluorescence in a granular pattern on the liver cell surface, thus suggesting a masking effect of immunoglobulin G on membranous hepatitis B core antigen in patients with persistent virus replication in the liver.

Antibody Specificity↗
PubMed1981

Ultrastructural changes in the liver of patients with chronic non-A, non-B hepatitis.

Electron microscopy examination of liver biopsies from 8 patients with chronic non-A, non-B hepatitis revealed ultrastructural changes similar to those previously described in chimpanzees with experimentally induced acute non-A, non-B hepatitis. These changes consisted of intranuclear clusters of electron-dense, 15-27-nm particles that were detected in five out of the eight patients and of circular cytoplasmic structures that were present in seven cases. Other cytoplasmic abnormalities found in our patients related to the presence of curved membranes apparently developing from apposition of two cisternae of endoplasmic reticulum. In contrast with what has been reported in infected chimpanzees, the nuclear and cytoplasmic changes were not mutually exclusive in our patients, but coexisted in four of them.

Adult↗
PubMed1981

Changes in hepatitis B virus DNA-polymerase activity in patients with chronic infection.

Levels of serum hepatitis B virus DNA-polymerase (HBV-DNAP) were studied longitudinally over variable periods of time in 16 HBV chronic carriers using a modified assay procedure developed to increase reproducibility. Ten patients were tested on a short-term basis at 3- to 6-hr intervals for 48 hr or at 24- to 48-hr intervals for 15 consecutive days, and all showed marked vacillations in enzyme levels although hospitalized and untreated. Patients with chronic active hepatitis on liver biopsy had larger fluctuations compared to cases of chronic persistent hepatitis. Six patients were longitudinally tested over a period of 12-32 months and those three receiving immunosuppressive drugs showed a progressive increase in DNAP levels during therapy, but two returned to pretreatment levels after therapy was withdrawn and one even cleared permanently the complete virus with seroconversion to anti-HBe. Such outcome was also observed in one patient with chronic active hepatitis who remained untreated.

Chronic Disease↗
PubMed1981

Radioimmunoassay for hepatitis B 'e' antigen and antibody: correlations with viral replication and prognostic value.

The presence of hepatitis B 'e' antigen (HBeAg) and its antibody (anti-HBe was evaluated by radioimmunoassay (RIA) in various groups of HBsAg-positive patients. HBeAg was present in the majority of the sera from patients with acute viral hepatitis at onset of clinical symptoms and disappeared after 1 year. Almost all hemodialysis patients had HBeAg in their sera. 40% of the patients who had chronic active hepatitis and 50% with chronic persistent hepatitis had HBeAg with no relationship to the inflammatory activity of the disease evaluated by the presence of mononuclear infiltration in liver biopsy. The comparison between the presence of HBeAg and Dane particle-associated DNA-polymerase activity showed that HBeAg was consistently found in almost all the sera which presented DNA-polymerase activity. HBeAg, as determined by RIA, may therefore be useful in the screening of highly infective patients with elevated viral replication.

Antibodies, Viral↗
PubMed1981

Detection by immunofluorescence of an antigen-antibody system in patients with acute and chronic non-A, non-B hepatitis.

An antigen-antibody system has been identified by immunofluorescence in patients with non-A, non-B hepatitis. The non-A, non-B antigen was localized in the hepatocyte nuclei of liver biopsies from patients with acute post-transfusion or sporadic non-A, non-B hepatitis and in those from patients with chronic post-transfusion non-A, non-B hepatitis, the percentage of positive cells being most prominent in patients receiving immunosuppressive treatment. Absence of the antigen in normal livers and in livers from patients with type B hepatitis infection indicated its specific association with non-A, non-B infection. Antibody reacting with the nuclear antigen became detectable in serum during post-transfusion acute non-A, non-B hepatitis in 11 out of 15 cases; it was absent before transfusion. Six out of 12 cases of sporadic acute non-A, non-B hepatitis were also found to produce the antibody, which was repeatedly found to be absent during the acute phase in five patients with type A and in eight with type B hepatitis. The non-A, non-B antibody, mainly an IgM antibody, persisted in serum for prolonged periods of time after onset, both in patients showing biochemical resolution of their illness and in those who continued to have liver damage after the acute phase. Accordingly, eight out of nine patients with chronic non-A, non-B hepatitis were found positive for the antibody in serum, seven at the time the non-A, non-B antigen was detected in their liver. Thus this non-A, non-B associated antigen-antibody system shares remarkable similarities of behaviour with the "core" system of the hepatitis B virus.

Antibodies, Viral↗
PubMed1981

Chronic hepatitis type B in childhood: longitudinal study of 35 cases.

Clinical, virological, and histological features of hepatitis B virus infection have been examined in 35 children, aged 1 to 11 years, known to be hepatitis B surface antigen (HBsAg) carriers for at least six months when entering the study. Only 10 patients had a history of acute unresolved hepatitis: in the remaining cases the detection of HBsAg had been an occasional finding. Although 77% of the patients were asymptomatic, all had evidence of hepatic involvement and liver history showed the features of chronic persistent hepatitis in 18 cases and of chronic active hepatitis in 16 cases, with associated cirrhosis in two of them. One patient had only minimal histological changes. A high percentage of children with both chronic persistent and chronic active hepatitis had evidence of active virus replication throughout the observation period. During the follow-up study of one to eight years (mean 3.1 +/- 1.7 years), transaminase levels became consistently normal in five patients with chronic persistent hepatitis, and inflammatory infiltrates disappeared in three of them. However, only one of these children cleared HBsAg from serum. Eleven of 16 patients with chronic active hepatitis received immunosuppressive treatment but only one of them achieved a complete and protracted remission, although active viral replication persisted. On the other hand, two of five untreated patients reached complete remission after two and three years of follow-up respectively and one of them cleared HBsAg three years later. These results would suggest the possibility of a spontaneous complete remission of HBsAg positive chronic active hepatitis in children but also raise doubts about the usefulness of immunosuppressive therapy in such patients.

Carrier State↗
PubMed1981

Antibodies against human liver-specific protein (LSP) in acute and chronic viral hepatitis types A, B and non-A, non-B.

Sera from 42 patients with acute viral hepatitis (AVH), 97 patients with chronic active liver disease (CALD) and 89 controls were tested by radioimmunoprecipitation for the presence of antibodies against human liver-specific protein (LSP). Anti-LSP were found in all but one patient with AVH type A (93%) and in a smaller percentage of AVH type B (55%). In non-A, non-B cases, anti-LSP were found in low percentages: 27% in acute cases, 10% in chronic cases. Furthermore, in CALD, a significant difference was found between HBsAg-positive CAH and 'autoimmune' CAH, a significant difference was found between HBsAg-positive CAH and 'autoimmune' CAH, both in anti-LSP prevalence (21%, 67%; P less than 0.005) and in anti-LSP titre (1:154 +/- 170, 1:316 +/- 186; P less than 0.005). In HBsAg-negative/anti-HBc-positive CAH, three of 15 patients were anti-LSP positive. Anti-LSP were found only in three of 57 patients with various non-hepatic diseases with autoimmune features. None of the 12 healthy HBsAg carriers was positive. Hence there is evidence for a considerable heterogeneity in anti-LSP response in acute and in chronic inflammatory HBsAg-negative liver diseases. These data suggest that anti-LSP antibodies do not play a prominent role in the process of transition to chronicity of acute viral hepatitis particularly in non-A, non-B cases, whereas these antibodies may be important in the mechanism of ongoing liver cell injury in patients with 'autoimmune' CAH, and can represent a useful diagnostic marker of this type of hepatitis.

Acute Disease↗
PubMed1980

Suppressor cell activity in viral and non-viral chronic active hepatitis.

Suppressor cell function was studied in twenty-nine patients with chronic active hepatitis (CAH) in relation to possible aetiological causes and activity of liver disease. All fifteen patients with evidence of viral aetiology (ten HBsAg-positive CAH and five non-A, non-B CAH) showed normal suppressor cell function independently of severity of liver damage. In contrast, fourteen patients with HBsAg-negative CAH, including four cases with circulating antibodies to the hepatitis B virus, demonstrated a significant reduction in supprpessor cell activity compared to control subjects. No significant difference was found in this group between cases with and without circulating autoantibodies. In four out of five HBsAg-negative patients tested serially suppressor cell defect correlated with disease activity suggesting an abnormality in the regulation rather than a depletion of suppressor cells. These results suggest that different mechanisms are responsible for autoimmunity to the liver in virus and non-virus-related CAH.

Adolescent↗
PubMed1979

Relationship between membrane-bound immunoglobulin and viral antigens in liver cells from patients with hepatitis B virus infection.

In an attempt to define further the significance of immunoglobulin G (IgG) fixed in vivo to the hepatocyte membrane in hepatitis B virus (HBV) infection, we have studied the relationship between presence of membrane-bound IgG and that of intracellular hepatitis B surface (HBsAg) and core (HBcAg) antigens in hepatocytes from 25 HBsAg chronic carriers. For this purpose, we have used a double immunofluorescence technique that is able to detect IgG and viral antigens within the same liver cell. In 15 patients with HBsAg-positive chronic active hepatitis, we found a statistically significant association between detection of membrane-bound IgG and that of intranuclear HBcAg within the same liver cells. On the contrary HGsAg containing hepatocytes generally did not show IgG fixed on their surface. IgG was not detected on the liver cell surface in 10 other HBsAg carriers without active disease and with large amounts of HBsAg containing hepatocytes. These results suggest that in HBsAg-positive chronic active hepatitis membrane-bound IgG is directed against viral antigens or virus-induced neoantigens that appear on the surface of infected cells at the time of active virus replication. Modulation of virus expression by this IgG could play a role in the pathogenesis of the disease.

Carrier State↗