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Träfflista för sökning "WFRF:(Dhillon P.) srt2:(1996-1999)"

Sökning: WFRF:(Dhillon P.) > (1996-1999)

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2.
  • Lindh, Magnus, 1960, et al. (författare)
  • Core promoter mutations and genotypes in relation to viral replication and liver damage in East Asian hepatitis B virus carriers.
  • 1999
  • Ingår i: The Journal of infectious diseases. - : Oxford University Press (OUP). - 0022-1899 .- 1537-6613. ; 179:4, s. 775-82
  • Tidskriftsartikel (refereegranskat)abstract
    • Virus load and liver damage, as measured by quantitative polymerase chain reaction and histology activity index, were related to genotype and core promoter mutations in 43 chronic hepatitis B virus (HBV) carriers of East Asian origin. T-1762 mutants were more frequent in genotype C strains and were associated with more inflammation (P=.0036) and fibrosis (P=.0088) of the liver but not with hepatitis B e antigen (HBeAg) status or virus load. Conversely, precore mutations were associated with less liver inflammation (P=. 08), which was linked to HBeAg negativity and lower viral replication. Carriers with genotype C were more often HBeAg positive (P=.03) with precore wild type strains and more-severe liver inflammation (P=.009) than were those with genotype B. These findings suggest that pathogenic differences between genotypes may exist and that the T-1762 mutation may be useful as a marker for progressive liver damage but seem to contradict that down-regulation of HBeAg production is the major effect of this mutation.
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3.
  • Shev, S, et al. (författare)
  • The importance of cofactors in the histologic progression of minimal and mild chronic hepatitis C
  • 1997
  • Ingår i: Liver. - 0106-9543. ; 17:5, s. 215-223
  • Tidskriftsartikel (refereegranskat)abstract
    • A follow-up liver biopsy was done 9-16 years (mean 12 years) after initial biopsy in 20 untreated Swedish patients infected with hepatitis C (8 men, 12 women; mean age 30 years at initial biopsy) in whom first biopsy had been classified as chronic persistent hepatitis. A significant progression of liver damage was found when using Histology Activity Index (HAI) scoring according to Knodell (p=0.006 for total HAI score; p=0.03 for grading, i.e., sum of HAI components 1, 2, and 3; p=0.01 for staging, i.e., HAI component 4, fibrosis). Fourteen of 20 (70%) patients had increased while 6 had decreased or unchanged HAI scores on follow-up biopsy. Occasional heavy alcohol drinkers (n=6) had an increased follow-up HAI score as compared with nondrinkers (p<0.05). Eight of 14 who deteriorated on follow-up versus 0 of 6 with improved or unchanged liver histology were anti-HBc positive (p=0.04). There was no significant correlation between HCV genotype and prognosis; however, the only two patients with liver cirrhosis on follow-up had genotype 1b. In conclusion, most patients with minimal or mild chronic hepatitis C in the present study had histologic progression on the latest biopsy. Cofactors such as alcohol abuse and exposure to hepatitis B may have a greater influence than HCV alone in determining the rate of deterioration of liver disease.
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