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Biomedical subjects

E Tabor

Publications and source records attributed to E Tabor.

171 records · Page 10Linked to original sources

Studies of donors who transmit posttransfusion hepatitis.

Sera and questionnaires were evaluated retrospectively from 128 volunteer blood donors whose blood had been implicated in cases of clinically recognized post-transfusion hepatitis in recipients of one- or two-unit blood transfusion between 1971 and 1977. Serologic markers of hepatitis B virus (HBV) infection were found in 23 percent, compared to 9.7 percent of 3,230 prospective blood donors. The prevalence of antibody to hepatitis A virus was similar among implicated donors (44%), prospective donors (58%), and among those implicated donors with (41%) and without (44%) HBV markers. Among implicated donors, none had a history at the time of donation of having had clinically recognizable hepatitis, 93 percent had no history of prior blood transfusion, and 80 percent had normal hepatic enzymes. Data from this study confirm that non-A, non-B hepatitis has been a common form of posttransfusion hepatitis in recent years, since 77 percent of these implicated donors had no HBV serologic markers. In addition, these donors could not be distinguished by age, race, sex, history of clinical hepatitis or of prior blood transfusion, or in most cases by hepatic enzyme levels.

Aging↗

Hepatitis B e antigen in volunteer and paid blood donors.

Sera from 200 volunteer donors and 200 paid blood donors, all positive for hepatitis B surface antigen (HBsAg), were tested for the presence of hepatitis B e antigen (HBeAg).HBeAg was detected in 31 HBsAg-positive paid donors (15%), and in 11 HBsAg-positive volunteer donors (5%) by agar gel diffusion. The presence of HBsAg was associated with higher titers of HBsAg. No significant difference was found in the prevalence of antibody to HBeAg (anti-HBe) in the two donor groups. Rheumatoid factor was not associated with the presence or absence of HBeAg or anti-HBe, indicating that HBeAg is probably not an anti-IgG. These data support the epidemiological evidence that paid blood donors appear to be more likely than volunteer donors to transmit hepatitis B virus infection to recipients of their blood.

Aging↗

Antibody to hepatitis B core antigen in blood donors with a history of hepatitis.

Sera and questionnaires from 3,230 prospective U.S. volunteer blood donors were obtained in an earlier study to determine the prevalence of serologic markers of hepatitis B virus (HBV) and hepatitis A virus (HAV) among prospective blood donors with or without a history of either hepatitis or blood transfusion. These sera were reevaluated using a radioimmunoassay for antibody to hepatitis B core antigen (anti-HBc). Anti-HBc in the absence of hepatitis B surface antigen (HBsAg) or its antibody (anti-HBs) was detected in 30 of 1,151 (2.6%) prospective donors with a history of hepatitis, compared to four of 1,086 (0.4%) with no history of hepatitis (p less than 0.001). Although end-point dilution titers of anti-HBc greater than or equal to 1:100 and the presence of IgM anti-HBc were more frequently detected among donors with a history of hepatitis than among donors with no history of hepatitis, the difference was not statistically significant. Unlike a history of hepatitis, a history of transfusion or a history of exposure to persons with hepatitis had no significant association with the detection of anti-HBc in the absence of other HBV serologic markers.

Antibodies↗

Additional evidence for more than one agent of human non-A, non-B hepatitis. Transmission and passage studies in chimpanzees.

Evidence supporting the existence of two agents of human non-A, non-B hepatitis was obtained by the inoculation of chimpanzees sequentially with serum from a chronically infected human (Inoculum I) and with fibrinogen prepared from pooled plasma (Inoculum IV), each of which had transmitted non-A, non-B hepatitis to humans. Passage inoculations of serum samples obtained during the acute stages of chimpanzee infections transmitted by either the agent in Inoculum I or IV also transmitted non-A, non-B hepatitis to additional chimpanzees. Transmission and passage of the agent in Inoculum IV were conducted in chimpanzees which previously had recovered from infection by the agent in Inoculum I. Cytoplasmic tubules in hepatocytes, which have been described during non-A, non-B hepatitis, were observed by electron microscopy in liver biopsies obtained during all infections transmitted by the agent in Inoculum I. These cytoplasmic tubules were not detected in liver biopsies from chimpanzees infected by Inoculum IV, except in one chimpanzee inoculated by Inoculum IV without prior exposure to the agent in Inoculum I. The cytoplasmic tubules observed in this study were found to be composed of transverse bands arranged with a periodicity of approximately 17 nm. These studies suggest that two different agents or distinct serotypes of human non-A, non-B hepatitis may have been present in these inocula, although reactivation of latent infection or reinfection could not be ruled out completely.

Animals↗

The epidemiology of virus transmission by plasma derivatives: clinical studies verifying the lack of transmission of hepatitis B and C viruses and HIV type 1.

During the past 50 years, most US-licensed plasma derivatives have maintained an impressive record of not transmitting HBV, HCV, or HIV Albumin (50-year history) has never transmitted these viruses. PPF (40-year history) transmitted HBV on only one occasion, which was associated with a design flaw in one manufacturing plant. IGIM has never transmitted any of these viruses since the requirement of sensitive serologic screening tests for HBV (24 years). IGIV (17-year history) transmitted HCV in only one outbreak involving the product of one manufacturer. Even AHF and FIX have not transmitted these viruses since effective virus-inactivation processes in manufacturing were developed. In summary, there has been no transmission of HBV, HCV, or HIV by US-licensed plasma derivatives since the introduction of effective virus-inactivation procedures. This means, essentially, that there has been no transmission of these viruses since the end of 1987; the sole exception is IGIV, by which there has been no transmission since 1994.

Female↗

The liver histology and frequency of clearance of the hepatitis B surface antigen (HBsAg) in chronic carriers.

Two hundred four volunteer blood donors with hepatitis B surface antigen found in their blood were followed for 3 to 44 months. The annual clearance rate of this antigen was 1.7%. Liver enzyme levels (aminotransferase) were elevated in 45 (22.1%) on at least one occasion, in 26 (12.7%) for one month or more, and in 13 for more than six months. Liver biopsies were performed on 17 chronic carriers with normal enzymes and nonspecific histologic abnormalities were found in 14 and mild diffuse hepatitis in three. Seventeen carriers with abnormal enzymes were biopsied, and specimens revealed chronic active hepatitis (CAH) in seven, including two with bridging necrosis and three with cirrhosis. CAH was found in 7 of 26 (26.9%) carriers with abnormal liver enzymes persisting for at least one month and 4 of 13 (30.8%) with abnormal liver enzymes for more than six months.

Biopsy↗

Correlation of immunohistochemical staining and mutations of p53 in human hepatocellular carcinoma.

Mutations of the p53 tumor suppressor gene are common in hepatocellular carcinomas (HCCs). Detection of mutations by sequencing provides more information than immunohistochemical staining, but the equipment needed and the time required make it less practical for use in large-scale studies or in studies in developing countries. The degree of correlation between results obtained with these two methods has been studied in various tumors but has not been well-established in human HCCs. Paraffin sections of HCCs of 28 patients from Qidong, China were immunohistochemically stained using monoclonal antibody to p53. In addition, exons 5-8 of the p53 gene were sequenced in these HCCs. Of the 28 HCCs, nine had 0-9% of nuclei stained for p53, and 19 had 50-95% stained. Mutations in p53 exons 5-8 were found in 17/28 (61%) HCCs, including 15 at codon 249 (exon 7), one at codon 198 (exon 6), and one at codon 175 (exon 5). Among these 17 cases with p53 mutations, 16 cases (94%) had 50-95% of nuclei stained. Among 11 HCCs with no mutations by sequencing, 8 were also negative by immunohistochemistry (0-9% of nuclei stained) (73%) (the five HCCs with no staining whatsoever all had wild-type p53). Immunohistochemical staining to detect p53 mutations in human HCCs detected most mutations that were detected by sequencing (94% sensitivity, 73% specificity), and this method is therefore suitable when sequencing cannot be performed.

Adult↗