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J I Esteban

Publications and source records attributed to J I Esteban.

At least 73 records · Page 4Linked to original sources
PubMed1987

Anti-HD IgM as a marker of chronic delta infection.

The value of anti-HD IgM as a marker of chronic delta infection was evaluated by correlating its presence in serum with that of HD-Ag in liver cells and with the degree of inflammatory activity. Thirty-six patients with HBsAg-positive chronic hepatitis and anti-HD at high titers were studied. Overall, the liver cells of 26 patients contained HD-Ag and 27 were positive for IgM anti-HD. The correlation between both markers was excellent: 25 cases were positive for both serum anti-HD IgM and intrahepatic HD-Ag and 8 were negative for both markers. There was only 1 HD-Ag-positive patient, who was anti-HD IgM-negative. Two patients were anti-HD IgM-positive and HD-Ag-negative. Histological damage was more severe in anti-HD IgM-positive cases than in those negative for this marker (Knodell's index 13.5 vs 11.9, P less than 0.01). We conclude that anti-HD IgM is a good marker of chronic active delta infection.

Adolescent↗
PubMed1986

Serological diagnosis of acute delta hepatitis.

Sixty-three intravenous drug addicts with HBsAg positive hepatitis were studied to evaluate the diagnostic usefulness of hepatitis delta virus (HDV) markers for diagnosis of acute HDV infection. Patients were tested for HBsAg, anti-HBc-IgM, and anti-HD-IgM by radioimmunoassay (RIA), and for hepatitis delta antigen (HD-Ag) by a commercial enzyme-linked immunoassay (ELISA). At least two serum samples at a mean interval of 4 wk were examined from each patient. HDV markers were found in 41 cases. In the first serum sample (obtained within 1-5 wk after onset of illness) HD-Ag was found in 32 cases and was the only HDV marker in 22; in the remaining 10 cases, HD-Ag was found along with total anti-HD, and in 6 of them anti-HD-IgM was also detected. Five additional patients were only positive for total anti-HD, and anti-HD of the IgM class was the only marker in one patient. HD-Ag was found more often in the patients studied during the first 2 wk of illness. In the second serum sample, HD-Ag was never the only marker detected, seven patients were still positive, and in all of them anti-HD was also present. Thirty patients were only positive for anti-HD. Seroconversion from HD-Ag to anti-HD occurred in 20 of 22 (91%) patients. The results suggest that HD-Ag determination by ELISA in the initial serum sample, during the first 2 wk of illness, may be the most sensitive test for the diagnosis of acute delta infection, and that seroconversion to anti-HD usually occurs after the sixth week of illness.

Acute Disease↗
PubMed1986

Immunoprophylaxis of perinatal transmission of the hepatitis B virus: efficacy of hepatitis B immune globulin and hepatitis B vaccine in a low-prevalence area.

One hundred eleven newborn infants born of Spanish hepatitis B surface antigen (HBsAg) carrier mothers were consecutively assigned to one of three treatment groups. Group A was treated with three or four doses of hepatitis B immune globulin (HBIG) in one of three different schedules. Group B received one dose of hepatitis B vaccine (Hevac-B, Pasteur) at birth and at 1, 2 and 12 months. Group C was treated with the same vaccination schedule as group B and in addition received a single dose of HBIG at birth. Comparisons were made in the 85 babies who had strictly completed the immunization schedule and had been followed for at least 12 months. The three immunization protocols were equally effective, since none of the children became a chronic HBsAg carrier or developed acute symptomatic infection. There were five transient and subclinical infections among children who received only HBIG (group A), one transient infection in group B, and one in group C. There seems to be some correlation between anti-HBs levels and degree of protection, since all transient infections in group A occurred in the subgroups who did not maintain protective antibodies during the first 6 months. Although the percentage of responders in the two vaccinated groups did not differ significantly, children who received only vaccine reached higher antibody levels than those who also received HBIG. Our results suggest that any immunization schedule able to maintain anti-HBs levels during the first 6 months of life would be useful to prevent mother-to-infant transmission of the hepatitis B virus in areas where most of the carrier women are expected to be anti-HBe positive and hence relatively less infectious.

Carrier State↗
PubMed1986

Prolonged inhibition of hepatitis B virus replication with vidarabine monophosphate in chronic active type B hepatitis.

Eight patients with chronic (mean 52 months) type B hepatitis (chronic active hepatitis and active cirrhosis) and markers of active viral replication (presence of HBeAg and HBV-DNA in serum) were treated with Ara-AMP for 7-12 weeks. The mean follow-up time was 18.3 months. All but one patient responded to treatment. In seven patients, HBeAg and HBV-DNA became negative and developed anti-HBe. One patient lost HBsAg as well as HBeAg and HBV-DNA. HBcAg in liver tissue became undetectable or greatly reduced in the seven patients in whom it was strongly positive. Aminotransferase and immunoglobulin levels reverted to normal in the seven responders and remained normal through the entire follow-up period. A second liver biopsy, performed after completion of therapy, showed improvement in six of eight cases, with disappearance of lobular activity. Two patients treated for 12 weeks developed a severe polyneuropathy lasting for 6 months. A 7-week course of Ara-AMP seems to induce long-lasting inhibition of viral replication, along with an improvement in liver function tests and liver histology, without significant side effects. On the other hand, a 12-week course was associated with the development of a severe and prolonged polyneuropathy.

Adult↗
PubMed1985

Importance of western blot analysis in predicting infectivity of anti-HTLV-III/LAV positive blood.

Stored donor and recipient sera from prospective studies of post-transfusion hepatitis were analysed for the presence of human T-cell lymphotropic virus type-III/lymphadenopathy associated virus (HTLV-III/LAV) antibodies as determined by enzyme-linked immunosorbent assays (ELISA). Of 3961 donor samples given to 461 patients, only 2 (0.05%) contained specific HTLV-III/LAV antibodies as determined by an avidin-biotin-enhanced western blot tech nique. Anti-HTLV-III/LAV was measured before and 3 and 6 months after transfusion in 295 recipients of anti-HTLV-III-negative blood, 7 recipients of ELISA-positive blood which was western blot negative, and 2 recipients of ELISA-positive blood confirmed as specific by western blot. Only the last 2 recipients became infected with HTLV-III/LAV, as assessed by antibody seroconversion (p less than 0.0001). Serocon version occurred early (6 and 8 weeks after transfusion) and was characterised first by antibody to p24 and later by antibody to p41. AIDS has not developed in either patient, but one has a T4/T8 ratio of 0.4 and impaired mitogen responses; the second patient has no evidence of immune dysfunction 4 years after exposure. This study confirms that HTLV-III/LAV infection can be transmitted by blood transfusion and supports the advisability of anti-HTLV-III/LAV testing of all blood donors. It also confirms the validity of western blot testing for HTLV-III/LAV specificity and suggests that ELISA-positive, western-blot-negative blood may not be infectious.

Acquired Immunodeficiency Syndrome↗
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↗