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Biomedical subjects

G Fattovich

Publications and source records attributed to G Fattovich.

90 records · Page 5Linked to original sources
PubMed1978

Antibody dependent cellular cytotoxicity (ADCC) in acute hepatitis B and in chronic active hepatitis.

Antibody-dependent cellular cytotoxicity (ADCC) of peripheral blood lymphocytes against chicken red blood cells (ChRBC) in the presence of specific antiserum has been studied in normal subjects and in patients with acute hepatitis B and with chronic active hepatitis (CAH). ADCC was significantly reduced in patients with acute hepatitis B studied three weeks after the onset of jaundice and in patients with CAH showing clinical, biochemical and histological features of activity. On the other hand, lymphocytes from patients with CAH in histological remission or in clinical and biochemical resolution, showed a significantly increased cytotoxicity. The effect of serum factors on ADCC of normal lymphocytes was investigated using serial serum samples from five patients with acute hepatitis B and five with CAH. Our data suggest that serum factors may be responsible for the impairment of ADCC in our patients, although other mechanisms may also be implied. Sera obtained at the time when ADCC of patients' lymphocytes was reduced, significantly inhibited ADCC of normal lymphocytes when compared with sera obtained at the time when ADCC of patients' lymphocytes was normal or increased. In all cases with CAH, the disappearance or reduction of inhibiting activity correlated with histological remission. In patients with CAH the study of serum factors inhibiting ADCC of normal lymphocytes may be a useful parameter in assessing disease activity.

Acute Disease↗
PubMed1976

[Infection due to hepatitis B virus and host immune response].

Cell-mediated immunity (CMI) to hepatitis B surface antigen (HBsAg) was investigated in patients who recovered from acute hepatitis B and in chronic carriers of the antigen, either with or without liver disease. The study was performed using leucocyte migration inhibition test and purified HBsAg. In antigen-negative post-hepatitis patients the frequency of cellular immunity to HBsAg (63.6%) showed a significant difference to controls. On the other hand, only one out of 5 antigen-positive post-hepatitis patients showed sensitisation to HBsAg; four out of these cases had chronic hepatitis at liver biopsy. In HBsAg-chronic carriers, with or without liver disease, the frequency of CMI to HBsAg was not significant to controls. A significant correlation was noted between inflammatory activity and inhibition of migration. Our results suggest that a normal cellular immune response to HBsAg is necessary for the recovery from acute hepatitis B and for the clearance of the virus. In HBsAg-chronic carriers this response seems to be absent or inadequate, leading to the state of healthy chronic carriers or to the evolution to HBsAg-chronic hepatitis, respectively. The high frequency of CMI in HBsAg-negative chronic active hepatitis, suggests that hepatitis B virus infection may play a role in the ethiology of the disease.

Antibodies, Viral↗
PubMedDate not supplied

Clinical, virologic and histologic outcome following seroconversion from HBeAg to anti-HBe in chronic hepatitis type B.

Seventy consecutive HBsAg- and HBeAg-positive patients with biopsy-proven chronic hepatitis were followed prospectively with serial determinations of SGPT levels and hepatitis B virus serum markers including HBsAg, HBeAg, anti-HBe and hepatitis B virus DNA. During a period of 1 to 11 years (mean +/- S.D.: 5.0 +/- 2.3 years), 28 patients remained persistently HBeAg positive, most with continuing biochemical and histologic activity, while 41 cases seroconverted to anti-HBe. One patient became HBeAg and anti-HBe negative. After seroconversion, 87.8% of the cases showed sustained normalization of SGPT, and clearance of hepatitis B virus DNA from serum and histologic improvement was documented in 79% of the cases who had a control liver biopsy, while 15.8% developed cirrhosis. In two patients (4.9%), the disease remained active despite seroconversion, and both cases had evidence of continuing hepatitis B virus replication. Finally, reactivation of liver damage and of hepatitis B virus replication was observed in three additional patients (7.3%) who had transiently normalized SGPT after seroconversion. All 70 patients were analyzed for hepatitis delta virus markers, and only two persistently HBeAg-positive cases were found positive for antibody to hepatitis delta virus in serum, one also having hepatitis delta antigen in the liver. These findings indicate that, in chronic hepatitis type B, termination of virus replication is associated in most patients with biochemical and histologic regression of inflammatory activity. After anti-HBe seroconversion has occurred, virus replication and liver disease may persist or reactivate in a small proportion of patients thus giving origin to the well-recognized group of anti-HBe positive, hepatitis B virus DNA-positive chronic hepatitis type B.

Adolescent↗
PubMedDate not supplied

Long-term follow-up of anti-HBe-positive chronic active hepatitis B.

Twenty-eight patients with chronic active hepatitis without cirrhosis who were positive for hepatitis B surface antigen and antibody to hepatitis B e antigen were followed for 1 to 15 years (mean 6.6 years) and underwent follow-up biopsy. At presentation, 12 of the 28 patients (43%) had hepatitis B virus DNA in serum, 10 (36%) had serologic evidence of hepatitis delta virus infection and 6 (21%) had no serologic markers of either hepatitis B virus replication or hepatitis delta virus infection. During follow-up, 15 (54%) patients developed active cirrhosis, including eight patients with hepatitis delta virus infection and five with hepatitis B virus DNA in serum. In seven (47%) of the 15 patients, cirrhosis developed within the first 2 years; all seven patients had bridging necrosis in the first liver biopsy, and five of these were infected with hepatitis delta virus. The remaining 13 (46%) patients did not develop cirrhosis during follow-up and showed either unchanged features of chronic active hepatitis (seven cases) or histologic improvement to chronic persistent hepatitis (five cases) or to normal liver (one case). In conclusion, the prognosis of anti-HBe-positive patients with chronic hepatitis B is poor, as 54% of the cases developed cirrhosis during a mean histologic follow-up period of 4.5 years, mainly in association with hepatitis delta virus infection or continuing hepatitis B virus replication.

Adolescent↗
PubMedDate not supplied

Polymerase-chain-reaction-based semi-quantification of hepatitis D viraemia in patients treated with high doses of alpha 2b interferon.

To study the antiviral efficacy of high doses of alpha 2b interferon (alpha 2b-IFN) for chronic hepatitis D treatment, we used polymerase-chain-reaction(PCR)-based semi-quantitative detection of HDV RNA. The semi-quantification method used was based on the appearance of a positive amplification signal as a function of the number of PCR cycles. By amplifying dilutions (10(-1)-10(-8)) of an HDV-positive woodchuck liver RNA, we confirmed that exponential amplification efficacy occurred at between 20 and 30 cycles. Positive signals were observed from dilution 10(-2) (gel electrophoresis after 20 cycles of PCR) to dilution 10(-7) (hybridization after 30 cycles of PCR). To characterize the HDV RNA level in sera of 8 patients treated with alpha 2b-IFN (10 MU/3 times a week) for 1 year, we extracted RNA from serum samples taken every 6 months. All samples were amplified in parallel for 20 and 30 PCR cycles. Analysis of HDV cDNA after ethidium bromide/agarose gel electrophoresis and after molecular hybridization (100 times more sensitive than gel analysis), enabled us to grade the signals observed from negative to positive as 1+, 2+, 3+ and 4+, with all results being positive. Three types of evolution of HDV viraemia were evidenced among the 8 treated patients. HDV replication continued to occur at a high level at the 6th and 12th month in 2 patient sera. For 2 other patients, an HDV RNA decrease or disappearance was evidenced in the serum at the 6th month; however, viral replication recurred at a higher level at the 12th month.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMedDate not supplied

Clinical evolution of HCV-related chronic hepatitis.

Evolution of HCV positive chronic hepatitis to cirrhosis has been reported to occur in about 30% of patients after five years of follow-up. In contrast, evolution of cirrhosis to decompensation and liver failure is slow, with a survival rate at 5 and 10 years of 91% and 79%, respectively. These findings support the hypothesis that histologic cirrhosis and clinical cirrhosis are different facets of the same disease, the latter developing after a long period of time and being related not only to liver disease per se, but also to other factors only partially identified. During this long-term evolution, extrahepatic manifestations may occur due to the formation of antigen-antibody immunocomplexes, which may eventually lead to death due to renal or cardiac complications.

Chronic Disease↗