An outbreak of fulminant hepatitis B in immunocompromised hemodialysis patients.
BACKGROUND
We aimed to clarify the pathogenesis of an outbreak of fulminant hepatitis B in hemodialysis (HD) patients whose compromised cell-mediated immunity in turn contributed to chronic hepatitis B virus (HBV) carriage.


METHODS
Five consecutive adult HD patients with acute hepatitis B were evaluated. Viral genotype, mutations, and HBV-DNA levels were studied in relation to viral clearance, liver disease severity, and liver histology by immunostaining.


RESULTS
All five patients had hepatitis B surface antigen (HBsAg) genotype C, a G-to-A stop codon mutation at nucleotide (nt) 1896 in the precore region, an A-to-T mutation at nt 1762 and an G-to-A mutation at nt 1764 in the basal core promoter. The possible index patient, who suffered from liver cirrhosis, had HBsAg genotype C, anti-hepatitis B envelope (HBe), and these mutations. The level of HBV-DNA declined by about 10 percent per week and no difference in viral kinetics between the patients who died and the survivor was found, irrespective of therapies. The amount of liver cell apoptosis, as assessed by single-stranded DNA, was scarce. The risk of fulminant hepatic failure did not correlate with the preexistent liver histopathological changes. Acute HBV superinfection was associated with hepatitis C virus (HCV) elimination and increased mortality.


CONCLUSIONS
This outbreak of fulminant hepatitis B suggests that HD patients can foster highly virulent HBV strains (possibly owing to their compromised immune responses), which may place others at risk of severe, life-threatening acute liver damage and at increased risk of mortality if chronic carriers of HCV should be infected. We aimed to clarify the pathogenesis of an outbreak of fulminant hepatitis B in hemodialysis (HD) patients whose compromised cell-mediated immunity in turn contributed to chronic hepatitis B virus (HBV) carriage.
Igaki
Naoya
N
Department of Internal Medicine, Takasago Municipal Hospital, 33-1 Kamimachi, Arai-cho, 676-8585, Takasago, Japan.
Nakaji
Miyuki
M
Moriguchi
Rintarou
R
Akiyama
Hiroyuki
H
Tamada
Fumihiko
F
Oimomi
Munetada
M
Goto
Takeo
T
D000368:Aged; D015415:Biomarkers / Q000032:analysis; D002353:Carrier State / Q000276:immunology; D018388:Codon, Terminator / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D004279:DNA, Viral / Q000235:genetics / Q000378:metabolism; D004196:Disease Outbreaks; D004801:Eosine Yellowish-(YS); D005260:Female; D005456:Fluorescent Dyes; D005838:Genotype; D006416:Hematoxylin; D016174:Hepacivirus / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D006510:Hepatitis B Antibodies / Q000276:immunology / Q000378:metabolism; D006514:Hepatitis B Surface Antigens / Q000276:immunology / Q000378:metabolism; D006513:Hepatitis B e Antigens / Q000276:immunology / Q000378:metabolism; D006515:Hepatitis B virus / Q000235:genetics / Q000276:immunology / Q000378:metabolism; D019694:Hepatitis B, Chronic / Q000175:diagnosis / Q000453:epidemiology* / Q000276:immunology*; D022781:Hepatocytes / Q000473:pathology; D006801:Humans; D016867:Immunocompromised Host / Q000276:immunology*; D007075:Immunoglobulin M / Q000276:immunology / Q000378:metabolism; D007150:Immunohistochemistry; D007564:Japan / Q000453:epidemiology; D008099:Liver / Q000166:cytology / Q000378:metabolism / Q000473:pathology; D017093:Liver Failure / Q000175:diagnosis / Q000453:epidemiology* / Q000276:immunology*; D008297:Male; D008875:Middle Aged; D009336:Necrosis; D017354:Point Mutation / Q000276:immunology; D012367:RNA, Viral / Q000235:genetics / Q000378:metabolism; D006435:Renal Dialysis; D012720:Severity of Illness Index; D013223:Statistics as Topic; D017211:Treatment Failure; D019562:Viral Load
D015415:Biomarkers; D018388:Codon, Terminator; D004279:DNA, Viral; D005456:Fluorescent Dyes; D006510:Hepatitis B Antibodies; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens; D007075:Immunoglobulin M; D012367:RNA, Viral; D004801:Eosine Yellowish-(YS); D006416:Hematoxylin