Patrice Cacoub, MD; Philippe Halfon, MD; Lucile Musset, PhD
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Cacoub P., Halfon P., Musset L.; Transfusion-Transmitted Virus and Mixed Cryoglobulinemia. Ann Intern Med. 1999;130:451-452. doi: 10.7326/0003-4819-130-5-199903020-00021
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Published: Ann Intern Med. 1999;130(5):451-452.
TO THE EDITOR:
A newly discovered DNA virus, transfusion-transmitted virus (TTV), has been implicated in fulminant non-A, B, or C hepatitis and chronic liver disease of unknown cause (1, 2). This virus shares several characteristics with parvoviruses, such as a high buoyant density. A high prevalence of TTV in blood donors (1.9%) and blood products (factor VIII and factor IX concentrates) (44% to 56%) from the United Kingdom was recently reported (3).
Mixed cryoglobulinemia is characterized by purpura, arthralgia, and asthenia associated with cryoglobulins composed of various immunoglobulins. Widespread vasculitis usually involves small and medium-sized vessels, particularly in the nervous system and the skin (4). Mixed cryoglobulinemia has been associated with autoimmune, infectious, or malignant hematologic disorders but may also occur in their absence; in that case, it is called essential mixed cryoglobulinemia. Mixed cryoglobulinemia is frequently associated with clinical and biological evidence of liver disease. Recently, it was shown that 55% to 85% of patients with essential mixed cryoglobulinemia have serologic evidence of hepatitis C virus (HCV) infection; this suggests a causative role of HCV (5). The underlying mechanisms of this production of mixed cryoglobulin are unknown, although a long duration of HCV infection, older age, and presence of cirrhosis seem to be predictive factors. Co-infection with parvovirus B19 or hepatitis G virus does not seem to play a role (5).
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