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Hepatitis C virus infection and autoimmune thrombocytopenic purpura
J M Pawlotsky1, M Bouvier, P Fromont
1Department of Bacteriology and Virology, Hôpital Henri Mondor, Créteil, France.
Insights
Hepatitis C virus (HCV) infection is linked to autoimmune disorders. While not the primary cause of autoimmune thrombocytopenic purpura (ATP), HCV transmission can complicate ATP treatment via blood products.
Area of Science:
- Immunology
- Hepatology
- Virology
Background:
- Chronic hepatitis C virus (HCV) infections are associated with extra-hepatic immunological manifestations and autoimmune disorders.
- Autoimmune thrombocytopenic purpura (ATP) is one such disorder where an association with HCV is investigated.
Purpose of the Study:
- To determine the prevalence of HCV markers in patients diagnosed with ATP.
- To investigate a potential relationship between ATP and HCV infection.
Main Methods:
- Studied 139 patients with ATP (45 men, 94 women; mean age 42).
- Tested cryopreserved sera for anti-HCV antibodies and HCV-RNA.
- Monitored seroconversion and potential transmission routes.
Main Results:
- 10% (14/139) of ATP patients had anti-HCV antibodies.
- Four cases showed transient seropositivity due to immunoglobulin infusion.
- Seven patients had concurrent chronic hepatitis C; in five, HCV infection preceded ATP, suggesting a potential role.
Conclusions:
- HCV is not the primary cause of ATP but a potential etiological factor in some cases.
- HCV transmission can occur during ATP treatment involving blood product infusions.
Background/Aims:
Chronic hepatitis C virus infections are often associated with extra-hepatic immunological manifestations, including various autoimmune disorders. The aims of this study were: (i) to determine the prevalence of hepatitis C virus markers in patients with autoimmune thrombocytopenic purpura, and (ii) to determine whether a relationship could exist between autoimmune thrombocytopenic purpura and hepatitis C virus infections.
Methods:
One hundred and thirty-nine patients with autoimmune thrombocytopenic purpura (45 men, 94 women, mean age 42 years, range 16-90) were studied.
Results:
Anti-HCV antibodies were sought in their first and last available cryopreserved sera. In case of seropositivity, all their available cryopreserved sera were tested for anti-HCV antibodies and for HCV-RNA. Anti-HCV antibodies were detected in 14 of the 139 patients (10%). Four patients had transient anti-HCV seropositivity due to passive transfer of anti-HCV antibodies secondary to the infusion of intravenous immunoglobulin concentrates. Three patients seroconverted during follow up, due to intravenous drug use in one case, transfusion of non-HCV-screened blood units in one case, and infusion of intravenous immunoglobulins in one case. Seven patients had chronic hepatitis C discovered at the same time as autoimmune thrombocytopenic purpura. In two of them, hepatitis C virus transmission was the consequence of autoimmune thrombocytopenic purpura treatment but, in five cases, hepatitis C virus infection predated autoimmune thrombocytopenic purpura, so that the role of hepatitis C virus in autoimmune thrombocytopenic purpura could be suggested.
Conclusions:
Whereas hepatitis C virus does not appear to be the main etiological agent of autoimmune thrombocytopenic purpura can be envisaged. On the other hand, treatment of autoimmune thrombocytopenic purpura or autoimmune thrombocytopenic purpura-related symptoms by blood product infusion can be complicated by hepatitis C virus transmission.