Correlation of hepatitis B virus, hepatitis D virus and human immunodeficiency virus type I infection markers in hepatitis B surface antigen positive haemophiliacs and patients without haemophilia with clinical and histopathological outcome of hepatitis.
The hepatitis D virus (HDV) infection plays a major role in severe liver damage caused by hepatitis. To establish the prevalence of HDV infection in haemophilic patients and patients without haemophilia, 87 patients with chronic hepatitis B virus (HBV) infection were examined for serological evidence of delta hepatitis. In addition HBV, HDV and human immunodeficiency virus type 1 (HIV) infection markers were compared to clinical and histopathological outcome of hepatitis. Out of 46 haemophiliacs 30 (65%) were anti-HD-seropositive; 10 out of 30 anti-HD-positive patients (33%) had pathological liver function tests compared to 2 out of 16 anti-HD-negative haemophiliacs (13%). The rate of HIV infection did not differ between the HDV infected and the non-HDV infected individuals with haemophilia (17/27 anti-HD-positive patients versus 12/16 anti-HD-negative patients). Two haemophilic anti-HD-positive patients underwent liver biopsy, in both cases hepatitis D antigen (HDAg) was detected in the biopsies. Only 2 out of 41 patients without haemophilia were anti-HD-positive. Both had pathological liver function tests; chronic active hepatitis and cirrhosis, respectively, were diagnosed and HDAg was found in the liver biopsies. Out of 39 anti-HD-seronegative patients without haemophilia, 26 (67%) were hepatitis B e antigen positive; in the sera of 20 patients (51%) HBV-DNA was demonstrated, but only 6 patients (15%) had pathological liver function tests. In conclusion a high seroprevalence of HDV infection was found in haemophilic patients treated with non-pasteurized commercial clotting factor concentrates. An endemic spreading of HDV infection in patients without haemophilia with chronic HBV infection could not be detected.(ABSTRACT TRUNCATED AT 250 WORDS)
Wagner
N
N
Department of Paediatrics, University of Bonn, Berlin, Federal Republic of Germany.
Rotthauwe
H W
HW
Becker
M
M
Dienes
H P
HP
Mertens
T
T
Födisch
H J
HJ
Brackmann
H H
HH
D000163:Acquired Immunodeficiency Syndrome / Q000150:complications*; D000293:Adolescent; D000328:Adult; D000956:Antigens, Viral / Q000032:analysis; D001706:Biopsy; D002648:Child; D002675:Child, Preschool; D004279:DNA, Viral / Q000032:analysis; D006467:Hemophilia A / Q000150:complications*; D006508:Hepatitis Antibodies / Q000032:analysis; D006509:Hepatitis B / Q000150:complications*; D006514:Hepatitis B Surface Antigens / Q000032:analysis; D006513:Hepatitis B e Antigens / Q000032:analysis; D006515:Hepatitis B virus / Q000235:genetics; D003699:Hepatitis D / Q000150:complications*; D003698:Hepatitis Delta Virus / Q000276:immunology; D006521:Hepatitis, Chronic / Q000276:immunology; D006801:Humans; D008099:Liver / Q000276:immunology; D008297:Male; D008875:Middle Aged; D011863:Radioimmunoassay
D000956:Antigens, Viral; D004279:DNA, Viral; D006508:Hepatitis Antibodies; D006514:Hepatitis B Surface Antigens; D006513:Hepatitis B e Antigens