The advent of specific antiviral therapy for chronic hepatitis C has increased the importance of establishing the correct etiology of chronic hepatitis in patients, especially because interferon alfa (IFN-a) has been reported to exacerbate autoimmune hepatitis (AIH), whereas corticosteroids increase
Serologic markers of viral hepatitis A, B, C, and D in patients with hemophilia
✍ Scribed by Ashir Kumar; Roshni Kulkarni; Dennis L. Murray; Renuka Gera; Ajovi B. Scott-Emuakpor; Kathy Bosma; John A. Penner
- Publisher
- John Wiley and Sons
- Year
- 1993
- Tongue
- English
- Weight
- 557 KB
- Volume
- 41
- Category
- Article
- ISSN
- 0146-6615
No coin nor oath required. For personal study only.
✦ Synopsis
Abstract
Forty‐one patients with hemophilia A were studied for the prevalence of serological markers for hepatitis A, hepatitis B, hepatitis C (non‐A and non‐B hepatitis), and delta hepatitis (hepatitis D). Ten of 41 (24.4%) patients demonstrated hepatitis A antibody and 31 of 41 (75.6%) patients had a serologic marker for previous hepatitis B infection; four of these 31 patients (13%) also demonstrated antibody to delta agent (hepatitis D). Thirty‐seven of 41 (90.2%) patients demonstrated antibody for hepatitis C. Nine of 31 (29%) patients with a hepatitis B marker (no hepatitis B vaccinees) were negative for anti‐HBc but positive for anti‐HBs; all of these nine patients were HIV antibody positive, although they had no overt immunodeficiency. Twenty‐six of 41 (63.5%) patients were HIV antibody positive. Of HIV antibody positive patients, 27%, 88%, and 100% demonstrated evidence of a previous hepatitis A, hepatitis B, or hepatitis C, respectively. Of HIV antibody negative patients; 20%, 53%, and 73% of the patients demonstrated evidence of a previous hepatitis A, hepatitis B, or hepatitis C infections, respectively. The difference between HIV antibody positive and HIV antibody negative groups was not significant for hepatitis A but was significant for hepatitis B (P < 0.001) and hepatitis C (P < .001). Of the 31 patients with a hepatitis B serologic marker, all had antibody to hepatitis C. Of 10 patients, without a hepatitis B serologic marker, only 6 (60%) had antibody to hepatitis C. Clinically, none of our patients demonstrated any evidence of liver disease; however, 10 patients reported a previous history of hepatitis. These data suggest that patients with hemophilia in the United States, particularly those with HIV antibody, have high prevalence of hepatitis B and C infections.
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