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M Buti

Publications and source records attributed to M Buti.

106 records · Page 6Linked to original sources
PubMed1986

Diagnostic usefulness of anti-HBc-IgM and anti-HD antibodies in acute viral hepatitis.

To evaluate diagnostic improvement achieved with the determination of antibody to hepatitis core antigen of IgM type (anti-HBc-IgM) and antibody to delta antigen (anti-HD) in acute type B hepatitis, 155 patients (of whom 100 were drug addicts) were studied, using these markers in association with the classical markers of viral hepatitis (anti-HBc, anti-HBs, anti-HAV-IgM and anti-cytomegalovirus antibodies). With classical diagnostic criteria, 121 patients would have been diagnosed as having B hepatitis (HBs Ag and/or anti-HBc antibody positive without anti-HBs antibody), 33 non A non-B hepatitis (all markers negative or anti-HBc and anti-HBs positive) and 3 A hepatitis (anti-HAV-IgM antibody positive). With the current markers, 89 were B hepatitis (anti-HBc-IgM antibody positive), 18 were simultaneous B and D infections (anti-HBc-IgM and anti-HD antibodies positive), 6 were D hepatitis (anti-HBc-IgM antibody negative and anti-HD antibody positive), 39 non-A non-B hepatitis (anti-HBc-IgM, anti-HD, HAV-IgM and anti-cytomegalovirus antibodies negative) and 3 hepatitis A. Of the 121 cases initially diagnosed as B hepatitis, only 79 were actually B hepatitis, 16 were simultaneous B and D infections, 6 D hepatitis, 18 non-A non-B hepatitis and 2 A hepatitis. Of the 33 cases considered to be non A non-B hepatitis, only 21 were really non-A non-B hepatitis; 10 were B hepatitis and 2 B and D hepatitis. When anti-HBc-IgM and anti-HD antibodies were determined, the initial diagnosis was modified in 54 of 155 cases (35 p. 100).(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMedDate not supplied

Hepatitis B virus replication in acute hepatitis B, acute hepatitis B virus-hepatitis delta virus coinfection and acute hepatitis delta superinfection.

To evaluate the effect of hepatitis delta virus on the level of replication of hepatitis B virus and to assess the clinical significance that such an effect might have on the final outcome of the infection, the serological profile of hepatitis B virus DNA was investigated in 153 patients with acute or chronic hepatitis B virus infection with or without associated delta infection. Serum hepatitis B virus DNA was detected in 57% of patients with acute hepatitis B, 67% of those with acute hepatitis B virus-hepatitis delta virus coinfection and 25% of HBsAg carriers with hepatitis delta virus superinfection during the first week after the onset of symptoms. Patients with acute hepatitis B and those with acute hepatitis B virus-hepatitis delta virus coinfection did not differ significantly with respect to the serological profile of hepatitis B virus DNA and final clinical outcome. Within the group of HBsAg carriers with hepatitis delta virus superinfection, all patients who were initially negative for hepatitis B virus DNA developed chronic hepatitis delta virus infection, whereas 3 of the 4 patients with active hepatitis B virus infection at the time of superinfection showed transient inhibition of hepatitis B virus replication followed by termination of hepatitis delta virus infection in two patients. Therefore, although delta virus may inhibit the replication of hepatitis B virus among chronic HBsAg carriers, this effect is not readily apparent among patients with hepatitis B virus-hepatitis delta virus coinfection.

Acute Disease↗
PubMedDate not supplied

Hepatitis D virus RNA in acute delta infection: serological profile and correlation with other markers of hepatitis D virus infection.

To evaluate the profile of hepatitis D virus replication and the corresponding immunoresponse after acute hepatitis D virus infection, sera from 50 patients with acute hepatitis D (36 with acute hepatitis B virus-hepatitis D virus coinfection and 14 HBsAg carriers with hepatitis D virus superinfection) were investigated for the presence of hepatitis D virus RNA and other serological hepatitis D virus markers. During the first week after onset of symptoms, hepatitis D virus RNA was detected by spot hybridization with a similar frequency among patients with coinfection (64%) and those with superinfection (71%). The presence of hepatitis D virus RNA in the first serum sample correlated with that of circulating hepatitis D antigen in both groups of patients. The presence of hepatitis D virus RNA was transient and its clearance paralleled that of serum hepatitis D antigen among patients with coinfection, so that 1 month after the onset of symptoms serum hepatitis D virus RNA was no longer detectable in any of these patients. Conversely, serum hepatitis D virus RNA was still present in 78% of those with superinfection, all of whom developed chronic liver disease, thus suggesting that the persistence of hepatitis D virus RNA in the serum for more than 4 weeks might indicate progression to chronicity. In nine of the 14 patients (64%) with hepatitis D virus superinfection progressing to chronicity, hepatitis D virus RNA was persistently detected throughout the follow-up, whereas in five patients it was detected occasionally. In four superinfected patients hepatitis D virus RNA and hepatitis B virus DNA were detected simultaneously in serial samples, thus suggesting that, at least during early stages of chronic hepatitis D virus infection, both viruses may replicate at the same time.

Acute Disease↗
PubMedDate not supplied

What to do when standard therapy fails.

An important group of patients with chronic hepatitis C do not respond to interferon (IFN) therapy. Compared with untreated patients with chronic hepatitis C, non-responders have a higher percentage of cirrhosis, are more frequently infected by genotype 1 and usually have a viral load above 2 x 106 copies/ml. Also, patients with cirrhosis have lower life expectancy and higher risk of clinical complications, and therefore, are most in need of effective treatment strategies. There is no evidence that the re-treatment of non-responders with a standard regimen of IFN or more prolonged IFN therapy achieves a sustained biochemical or virological response. Between 20% and 40% of non-responder patients treated with IFN therapy for more than two years had an hepatic improvement in liver histology associated with a decrease in hepatitis C virus-ribonucleic acid levels. In contrast, combination therapy with IFN and ribavirin for six months now results in sustained response rates between 6% and 29% depending on the viral genotype and the presence or absence of cirrhosis. Patients infected with genotype 2 and 3 have a higher probability of achieving a sustained virological response than those infected by genotype 1. Currently, different studies are underway to determine whether high-dose IFN and/or induction therapy combined with ribavirin for more prolonged periods of time could increase the sustained response rate in non-responders. No other drugs appear to be efficacious in these patients, except the combination of IFN, ribavirin and amantadine which has shown interesting results in a preliminary trial but they need to be confirmed in further studies. These findings suggest that combination therapy is beneficial and can be recommended for some non-responder patients until other new therapies are available.

Amantadine↗
PubMedDate not supplied

[Quantitative determination of HBV-DNA in chronic hepatitis B: comparison of three methods].

The aim of this study was to evaluate a technique of quantitative determination of DNA-HBV in serum, bDNA Quantiplex, in a series of 90 patients with chronic HBV infection: 75 with chronic hepatitis B (24 HBeAg positive and 51 with anti-HBe) and 15 asymptomatic carriers of HBV (anti-HBe positive). The results were related to DNA-HBV determination by hydridation techniques in dot-blot and PCR. DNA-HBV was detected by the Quantiplex bDNA technique in 61 (81%) of the 75 patients with chronic hepatitis B, in 24 (100%) of the 24 HBeAg positive patients and in 37 (72%) of the 51 anti-HBe positive (p < 0.05) patients and in none of the asymptomatic HBV carriers. The median of DNA-HBV concentration was 4,000 pg/ml in the hepatitis HBeAg and 71 pg/ml in the ati-HBe positive (p < 0.05). A significant relation was observed between the ALT value and the DNA-HBV concentration (p < 0.05). DNA-HBV by dot-blot was positive in 22 (29%) of the chronic hepatitis B and in none of the asymptomatic HBV carriers. DNA-HBV was not observed by dot-blot in 39 patients positive for DNA-HBV by the Quantiplex bDNA technique. DNA-HBV by PCR was identified in 65 (87%) of the chronic hepatitis B and in one of the asymptomatic HBV carriers. The sensitivity of the Quantiplex bDNA technique (98% versus the PCR technique) is much greater than that observed with dot-blot. In conclusion, the determination of DNA-HBV by the Quantiplex bDNA technique may be considered a good method for evaluating the viremia and degree of viral replication in patients with chronic hepatitis B.

DNA, Viral↗