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| |  Hepatitis C-Positive Patients Treated With Rituximab Are at Increased Risk of Liver Toxicities: Presented at IM By Crina Frincu-Mallos, PhD WASHINGTON, DC -- May 19, 2008 -- The use of rituximab, a monoclonal antibody used for the treatment of Non-Hodgkin's Lymphoma (NHL), resulted in major liver toxicity in Hepatitis C-positive patients, according to research reported here at the 2008 Internal Medicine Annual Scientific Meeting (IM). Rituximab is an effective therapy in patients with NHL, other B-cell malignancies, and autoimmune diseases, such as immune thrombocytopenic purpura (ITP). However, its use has been associated with Hepatitis B reactivation resulting in hepatic failure, as well as with fatal viral infections with varicella zoster, herpes simplex virus, cytomegalovirus, or parvovirus B19. "Data on the effects of rituximab on patients with Hepatitis C [are] limited," explained lead author Mustapha Ali Khalife, MD, Associate Internist, Henry Ford Hospital, Detroit, Michigan, in a poster presentation here on May 15. Dr. Khalife and colleagues performed a retrospective analysis, looking at the hospital records of 635 patients treated with rituximab between 1998 and 2006. After eliminating records where the patient's Hepatitis C serology status was unavailable or negative, the investigators were left with 23 patients. Of the total 23 patients, 12 patients with positive Hepatitis C serology received rituximab as a single agent, while 11 patients were treated with rituximab in combination with chemotherapy. Patients received treatment with rituximab, either single agent or in combination for NHL (n = 17), ITP (n = 2), thrombotic thrombocytopenic purpura (TTP) (n = 2), chronic lymphocytic leukemia (CLL) (n = 1), and Felty's syndrome (n = 1). "Hepatic events were defined as increases of transaminases more than twice the upper limit of normal range, increases in the Hepatitis C viral load, and deaths due to liver failure and attributed to rituximab," said Dr. Khalife. Out of the 23 patients with hepatitis C viral load, 11 patients experienced increases in transaminases. Of these 11 patients, 18% (n = 2) had transaminitis (pancreatitis, liver metastasis) while 45% (n = 5) were chemotherapy-related. "No specific etiology was determined for the rest [n = 4]," said Dr. Khalife. The mean time to elevation of transaminases in the 11 patients was 6.8 +- 5.3 months. Investigators used computer tomography (CT) scans, taken at baseline and at various timepoints during treatment, to assess worsening signs of cirrhosis. Two patients with normal liver CT scans, prior to receiving the first dose of rituximab, developed signs of liver cirrhosis, according to CT scans taken at 12 and 48 months. There were 2 deaths attributed to liver failure, a hepato-renal syndrome and a hepatic encephalopathy, occurring respectively at 53 and 9 months after the start of the treatment, noted the investigators. Dr. Khalife and his colleagues concluded that the high incidence of liver events in hepatitis C-positive patients receiving rituximab demands a close follow-up of viral loads and transaminase levels. Further randomised studies are needed to assess the contributions of the hepatitis C virus itself, rituximab alone, and chemotherapy for the development of liver toxicities, added the investigators.
[Presentation title: High Incidence of Hepatic Events in Patients With Hepatitis-C Treated With Rituximab. Abstract RPF#33]
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