|
|
 Previous Article | Table of Contents | Next Article 
A multicenter study of viral hepatitis in a United States hemophilic
population
CL Troisi, FB Hollinger, WK Hoots, C Contant, J Gill, M Ragni, R Parmley, C Sexauer, E Gomperts and G Buchanan
Baylor College of Medicine, Houston, TX 77030.
Hemophilia A and B patients seen at nine US regional treatment centers were
tested for serologic markers of hepatitis B virus (HBV), hepatitis C virus
(HCV), and hepatitis delta virus (HDV) during 1987 and 1988. Because human
immunodeficiency virus (HIV) infection, a potentially confounding variable,
was present in 53% of the group, the population was divided by HIV status
for analysis purposes. In the HIV-positive group (N = 382), less than 1%
had not been infected with HBV, HCV, or HDV, whereas 75% had evidence of
infection with HBV and 98% with HCV. HBsAg, a marker of active HBV
infection, was present in 12% of subjects; 96% of these were HCV positive.
Anti-HDV was detected in 35 subjects (9.1%); all were anti-HBc positive.
Ten of the 35 (29%) also were positive for IgM anti-HDV, indicating current
infection. All 10 were HBsAg positive and 7 of the 9 tested were HDV RNA
positive. Severe/moderate hemophilia B patients were more likely to have
experienced an HBV infection and to be anti-HDV positive than were similar
hemophilia A patients (22% v 8%, P < .05). In the HIV-negative group (N
= 345), the subjects were younger and had less severe hemophilia than the
HIV-positive patients. No evidence of HBV, HCV, or HDV infection was found
in 18%, whereas 33% had experienced HBV infection and 79% were anti-HCV
positive. Within this group, 4% were HBsAg positive. All 13 subjects with
anti-HDV (4% of the HIV-negative group) also possessed anti-HBc. One (7.7%)
was IgM anti-HDV positive and the serum from another contained HDV RNA.
Both of these individuals were HBsAg positive. As in the HIV-positive
group, severe/moderate hemophilia B patients were more likely to be HBV and
HDV positive than were hemophilia A patients (9% v 3%, P < .05). A
prevalence study of viral hepatitis in a large US hemophilic population
showed that active infection with HCV is common, occurring in 89% of all
study patients regardless of HIV status. Evidence of active HBV infection
was found in 8%; 19% of these were actively infected with HDV. HDV was more
common in hemophilia B patients after controlling for disease severity.
Volume 81,
Issue 2,
pp. 412-418,
01/15/1993
Copyright © 1993 by The American Society of Hematology
 CiteULike  Connotea  Del.icio.us  Digg  Reddit  Technorati What's this?
This article has been cited by other articles:
|
|
|
|
 
S. F. De Meyer, H. Deckmyn, and K. Vanhoorelbeke
von Willebrand factor to the rescue
Blood,
May 21, 2009;
113(21):
5049 - 5057.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Zhang, P. S. Rosenberg, D. L. Brown, L. Preiss, B. A. Konkle, M. E. Eyster, J. J. Goedert, and for the Second Multicenter Hemophilia Cohort Study
Correlates of spontaneous clearance of hepatitis C virus among people with hemophilia
Blood,
February 1, 2006;
107(3):
892 - 897.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
R. C. James and C. A. Mustard
Geographic Location of Commercial Plasma Donation Clinics in the United States, 1980-1995
Am J Public Health,
July 1, 2004;
94(7):
1224 - 1229.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Winnock, D. Salmon-Ceron, F. Dabis, and G. Chene
Interaction between HIV-1 and HCV infections: towards a new entity?
J. Antimicrob. Chemother.,
June 1, 2004;
53(6):
936 - 946.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
A H Mohsen, P Easterbrook, C B Taylor, and S Norris
Hepatitis C and HIV-1 coinfection
Gut,
October 1, 2002;
51(4):
601 - 608.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. J. Goedert, M. E. Eyster, M. M. Lederman, T. Mandalaki, P. de Moerloose, G. C. White II, A. L. Angiolillo, N. L. C. Luban, K. E. Sherman, M. Manco-Johnson, et al.
End-stage liver disease in persons with hemophilia and transfusion-associated infections
Blood,
August 13, 2002;
100(5):
1584 - 1589.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
E. Santagostino, M. G. Rumi, M. Rivi, M. Colombo, and P. M. Mannucci
Sustained suppression of hepatitis C virus by interferon and ribavirin in hemophilic patients not responding to interferon monotherapy
Blood,
February 1, 2002;
99(3):
1089 - 1091.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
M. Franchini, G. Rossetti, A. Tagliaferri, F. Capra, E. de Maria, C. Pattacini, G. Lippi, G. Lo Cascio, M. de Gironcoli, and G. Gandini
The natural history of chronic hepatitis C in a cohort of HIV-negative Italian patients with hereditary bleeding disorders
Blood,
September 15, 2001;
98(6):
1836 - 1841.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
V. R. Arruda, J. N. Hagstrom, J. Deitch, T. Heiman-Patterson, R. M. Camire, K. Chu, P. A. Fields, R. W. Herzog, L. B. Couto, P. J. Larson, et al.
Posttranslational modifications of recombinant myotube-synthesized human factor IX
Blood,
January 1, 2001;
97(1):
130 - 138.
[Abstract]
[Full Text]
[PDF]
|
|
|
|
|
|
|
J. N. Lozier and K. M. Brinkhous
Gene Therapy and the Hemophilias
JAMA,
January 5, 1994;
271(1):
47 - 51.
[Abstract]
[PDF]
|
|
|
|
|
