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Relation between GB virus C/hepatitis G virus and fulminant hepatic failure may be secondary to treatment with contaminated blood and/or blood products

Halasz, R (författare)
Barkholt, L (författare)
Lara, C (författare)
visa fler...
Hultgren, C (författare)
Karolinska Institutet
Ando, Y (författare)
Broome, U (författare)
Fischler, B (författare)
Karolinska Institutet
Nemeth, A (författare)
Karolinska Institutet
Ericzon, BG (författare)
Karolinska Institutet
Sonnerborg, A (författare)
Karolinska Institutet
Sallberg, M (författare)
Karolinska Institutet
visa färre...
 (creator_code:org_t)
1999-02-01
1999
Engelska.
Ingår i: Gut. - : BMJ. - 0017-5749 .- 1468-3288. ; 44:2, s. 274-278
  • Tidskriftsartikel (refereegranskat)
Abstract Ämnesord
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  • The role of the recently discovered GB virus C (GBV-C)/hepatitis G virus in fulminant hepatic failure (FHF) has been debated. Although GBV-C RNA has been detected in many cases of FHF, recent data suggest that the relation between GBV-C and FHF may be accidental.AimsTo retrospectively investigate the possible relation between the presence of GBV-C markers (RNA or antibodies to the GBV-C envelope 2 (E2) glycoprotein) and FHF.MethodsThe presence of GBV-C RNA was determined in serum samples from 58 patients diagnosed with FHF using a reverse transcriptase polymerase chain reaction. Amplified genetic fragments were directly sequenced by the dideoxy chain termination method. Antibodies to GBV-C in serum samples were detected by enzyme immunoassay based on a recombinant GBV-C E2 protein.ResultsNine (16%) patients with FHF had GBV-C RNA and 14 (24%) had GBV-C E2 antibodies, which are higher frequencies than in healthy subjects (p<0.01 and p<0.05 respectively). Seven of ten patients with GBV-C markers during FHF tested negative for these markers before therapy with blood and/or blood products. Sequence analysis of the GBV-C NS3 region fragments of six FHF patients showed no common sequence pattern or motif.ConclusionsThe frequencies of both GBV-C RNA and antibodies are higher in patients with FHF than in healthy subjects. However, these increased frequencies may in many cases be explained by the use of contaminated blood and/or blood products given as therapy.

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