Antineoplastics

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Reactions 1039 - 19 Feb 2005 S Antineoplastics Fatal hepatitis B reactivation: case report A 34-year-old man who was a hepatitis B virus (HBV) carrier, developed a reactivation of HBV and died following treatment with cyclophosphamide, doxorubicin, vincristine, prednisone (CHOP) and rituximab for stage IV non-Hodgkin’s lymphoma. The man, who had a hepatitis B viral load of 3600 copies/mL, received four cycles of CHOP/rituximab [dosages not stated ] at 3-week intervals. His fifth cycle of CHOP/rituximab was withheld because of elevated liver enzymes and, 3 days later, he presented with nausea and vomiting and was hospitalised. Examination revealed he had tenderness in his right upper abdominal quadrant and was jaundiced, notably in his sclera. Laboratory investigations showed he had AST and ALT levels of 1090 IU/L and 1013 IU/L, respectively, a total bilirubin level of 5.9 mg%, a prothrombin time of 36.7 seconds (normal 12–16), an INR of 3.67, an activated partial thromboplastin time of 52 seconds (26–38), and a blood HBV viral load of > 200 × 10 9 copies/mL. DNA sequence analysis revealed a precore 1896 mutant of HBV. Lymphocytes were detected, although his CD20+ lymphocytes were completely depleted. A diagnosis of acute liver failure from a reactivation of his HBV infection was considered. The man received lamivudine; on hospital day 6, adefovir was added as his total bilirubin level continued to rise. Although he continued to receive antivirals and supportive care, his total bilirubin level reached 48 mg% and his liver enzymes increased. On hospital day 30, he developed haematemesis followed by respiratory insufficiency and he required ventilatory support. He subsequently died on hospital day 39. Author comment: "The lack of circulating CD20+ lymphocytes supports the hypothesis that rituximab-induced immunosuppression contributed to hepatitis B reactivation, but does not exclude the role of CHOP, since this regimen has also been implicated." Zell JA, et al. Precore mutant hepatitis B reactivation after treatment with CHOP- rituximab. Anti-Cancer Drugs 16: 83-85, No. 1, Jan 2005 - USA 801001286 1 Reactions 19 Feb 2005 No. 1039 0114-9954/10/1039-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved

Transcript of Antineoplastics

Page 1: Antineoplastics

Reactions 1039 - 19 Feb 2005

SAntineoplastics

Fatal hepatitis B reactivation: case reportA 34-year-old man who was a hepatitis B virus (HBV) carrier,

developed a reactivation of HBV and died following treatmentwith cyclophosphamide, doxorubicin, vincristine, prednisone(CHOP) and rituximab for stage IV non-Hodgkin’s lymphoma.

The man, who had a hepatitis B viral load of 3600 copies/mL,received four cycles of CHOP/rituximab [dosages not stated ]at 3-week intervals. His fifth cycle of CHOP/rituximab waswithheld because of elevated liver enzymes and, 3 days later,he presented with nausea and vomiting and was hospitalised.Examination revealed he had tenderness in his right upperabdominal quadrant and was jaundiced, notably in his sclera.Laboratory investigations showed he had AST and ALT levels of1090 IU/L and 1013 IU/L, respectively, a total bilirubin level of5.9 mg%, a prothrombin time of 36.7 seconds (normal 12–16),an INR of 3.67, an activated partial thromboplastin time of52 seconds (26–38), and a blood HBV viral load of > 200 × 109

copies/mL. DNA sequence analysis revealed a precore 1896mutant of HBV. Lymphocytes were detected, although hisCD20+ lymphocytes were completely depleted. A diagnosisof acute liver failure from a reactivation of his HBV infectionwas considered.

The man received lamivudine; on hospital day 6, adefovirwas added as his total bilirubin level continued to rise.Although he continued to receive antivirals and supportivecare, his total bilirubin level reached 48 mg% and his liverenzymes increased. On hospital day 30, he developedhaematemesis followed by respiratory insufficiency and herequired ventilatory support. He subsequently died on hospitalday 39.

Author comment: "The lack of circulating CD20+lymphocytes supports the hypothesis that rituximab-inducedimmunosuppression contributed to hepatitis B reactivation,but does not exclude the role of CHOP, since this regimenhas also been implicated."Zell JA, et al. Precore mutant hepatitis B reactivation after treatment with CHOP-rituximab. Anti-Cancer Drugs 16: 83-85, No. 1, Jan 2005 - USA 801001286

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Reactions 19 Feb 2005 No. 10390114-9954/10/1039-0001/$14.95 Adis © 2010 Springer International Publishing AG. All rights reserved