Antineoplastics
1
Reactions 1307 - 26 Jun 2010 time/INR 3.1, HBsAg positive, HBeAg negative, anti-HBe positive, anti-HBc IgM negative, and HBV DNA S Antineoplastics > 7.5 × 10 7 IU/mL. He was diagnosed with acute liver failure and HBV infection. His synthetic liver function Hepatitis B virus reactivation: 4 case reports deteriorated further and encephalopathy developed. He Four patients developed hepatitis B virus (HBV) eventually underwent liver transplantation, and received reactivation during treatment with antineoplastics [dosages lamivudine and adefovir together with immunoglobulin not stated]. against hepatitis B for prophylaxis against HBV recurrence. Patient 1, a 56-year-old woman, had a history of acute At last follow-up, there had been no recurrence of HBV infection at the age of 25 years, with transition into hepatitis B, and his lymphoma was in remission with chronicity. She was diagnosed with non-Hodgkin’s rituximab maintenance therapy. lymphoma (NHL) in 1995, and received chemotherapy [details not stated] and achieved remission. However, she Frankova S, et al. Reactivation of hepatitis B as a complication during lymphoma developed a relapse and received CHOP therapy. Ceska a Slovenska Gastroenterologie a Hepatologie 63: 280-283, No. 6, 2009 [Czech; summarised from a translation] - Czech Republic 803022385 (cyclophosphamide, doxorubicin, vincristine and prednisone) in about 2000. In 2004, she had a second relapse and received R-ICE (rituximab, ifosfamide, carboplatin and etoposide) followed by rituximab monotherapy. For more that a year after the completion of chemotherapy in 2006, she had jaundice and elevated hepatic enzymes (ALT 4.0 µcat/L, bilirubin 100 µmol/L); ascites were already present on ultrasound, and gastroscopy showed oesophageal varices. Liver biopsy revealed fibrotising cholestatic hepatitis, and her haematologist started her on prednisone 60 mg/day. She was eventually hospitalised in March 2007 with acute liver failure. She had fatigue, lack of appetite, jaundice, stage II hepatic encephalopathy, lower limb oedema and ascites. Investigations showed kidney failure, and severe liver dysfunction due to a relapse of chronic hepatitis B (HBsAg positive, HBeAg negative, HBV DNA 4.16 × 10 7 IU/mL). Despite immediate commencement of lamivudine and adefovir, she died 2 days after admission in a hepatic coma. Patient 2, a 63-year-old woman with large B-cell lymphoma, received five cycles of R-CHOP from August to December 2007. In January 2008, she developed jaundice, and the following laboratory values were obtained: AST 18 µmol/L, ALT 11 µcat/L, bilirubin 219 µmol/L, albumin 28 g/L and prothrombin time/INR 1.37. There were also objective signs of hepatic cirrhosis. HBsAg positivity had already been detected in August 2007 prior to commencing chemotherapy. Her condition was assessed as reactivation of chronic HBV infection, with a HBV DNA level of > 1.1 × 10 7 IU/mL. She received lamivudine, and, after 6 months of treatment, HBV DNA was not detectable in her serum, and she had normal liver tests and synthetic liver function; she continued lamivudine. Her serum HBV DNA remained negative 1 year after starting treatment. Patient 3, a 42-year-old man, began R-CHOP in July 2007 for follicular NHL. In March 2008, after eight cycles, he was in complete remission; however, in April 2008, he was hospitalised with jaundice and liver failure (AST 107 µcat/L, ALT 39 µcat/L, prothrombin time/INR 3.0 and bilirubin 378 µmol/L). HBsAg was positive, HBeAg was negative, anti-HBe was positive and anti-HBc IgM was negative. He was diagnosed with hepatitis B. He had not been previously assessed for serum markers of viral hepatitis. His synthetic liver function deteriorated and hepatic encephalopathy progressed, prompting transfer and administration of lamivudine and adefovir; he then underwent orthotopic liver transplantation. As prophylaxis against Hepatitis B recurrence, lamivudine and adefovir were retained in the graft, together with immunoglobulin against hepatitis B. One year after transplantation, there had been no recurrence of hepatitis B. Patient 4, a 47-year-old man, was diagnosed with NHL. He received six cycles of R-CHOP from August to November 2008. He achieved remission but was hospitalised on 1 February 2009 with jaundice. Investigations revealed he following findings: total bilirubin 600 µmol/L, AST 25 µcat/L, ALT 50 µcat/L, prothrombin 1 Reactions 26 Jun 2010 No. 1307 0114-9954/10/1307-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
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Transcript of Antineoplastics
Reactions 1307 - 26 Jun 2010
time/INR 3.1, HBsAg positive, HBeAg negative, anti-HBepositive, anti-HBc IgM negative, and HBV DNA SAntineoplastics> 7.5 × 107 IU/mL. He was diagnosed with acute liverfailure and HBV infection. His synthetic liver functionHepatitis B virus reactivation: 4 case reportsdeteriorated further and encephalopathy developed. HeFour patients developed hepatitis B virus (HBV)eventually underwent liver transplantation, and receivedreactivation during treatment with antineoplastics [dosageslamivudine and adefovir together with immunoglobulinnot stated].against hepatitis B for prophylaxis against HBV recurrence.Patient 1, a 56-year-old woman, had a history of acuteAt last follow-up, there had been no recurrence ofHBV infection at the age of 25 years, with transition intohepatitis B, and his lymphoma was in remission withchronicity. She was diagnosed with non-Hodgkin’srituximab maintenance therapy.lymphoma (NHL) in 1995, and received chemotherapy
[details not stated] and achieved remission. However, she Frankova S, et al. Reactivation of hepatitis B as a complication during lymphomadeveloped a relapse and received CHOP therapy. Ceska a Slovenska Gastroenterologie a Hepatologie 63: 280-283, No. 6,
2009 [Czech; summarised from a translation] - Czech Republic 803022385(cyclophosphamide, doxorubicin, vincristine andprednisone) in about 2000. In 2004, she had a secondrelapse and received R-ICE (rituximab, ifosfamide,carboplatin and etoposide) followed by rituximabmonotherapy. For more that a year after the completion ofchemotherapy in 2006, she had jaundice and elevatedhepatic enzymes (ALT 4.0 µcat/L, bilirubin 100 µmol/L);ascites were already present on ultrasound, andgastroscopy showed oesophageal varices. Liver biopsyrevealed fibrotising cholestatic hepatitis, and herhaematologist started her on prednisone 60 mg/day. Shewas eventually hospitalised in March 2007 with acute liverfailure. She had fatigue, lack of appetite, jaundice, stage IIhepatic encephalopathy, lower limb oedema and ascites.Investigations showed kidney failure, and severe liverdysfunction due to a relapse of chronic hepatitis B (HBsAgpositive, HBeAg negative, HBV DNA 4.16 × 107 IU/mL).Despite immediate commencement of lamivudine andadefovir, she died 2 days after admission in a hepatic coma.
Patient 2, a 63-year-old woman with large B-celllymphoma, received five cycles of R-CHOP from August toDecember 2007. In January 2008, she developed jaundice,and the following laboratory values were obtained: AST18 µmol/L, ALT 11 µcat/L, bilirubin 219 µmol/L, albumin28 g/L and prothrombin time/INR 1.37. There were alsoobjective signs of hepatic cirrhosis. HBsAg positivity hadalready been detected in August 2007 prior to commencingchemotherapy. Her condition was assessed as reactivationof chronic HBV infection, with a HBV DNA level of> 1.1 × 107 IU/mL. She received lamivudine, and, after6 months of treatment, HBV DNA was not detectable in herserum, and she had normal liver tests and synthetic liverfunction; she continued lamivudine. Her serum HBV DNAremained negative 1 year after starting treatment.
Patient 3, a 42-year-old man, began R-CHOP in July 2007for follicular NHL. In March 2008, after eight cycles, he wasin complete remission; however, in April 2008, he washospitalised with jaundice and liver failure (AST 107 µcat/L,ALT 39 µcat/L, prothrombin time/INR 3.0 and bilirubin378 µmol/L). HBsAg was positive, HBeAg was negative,anti-HBe was positive and anti-HBc IgM was negative. Hewas diagnosed with hepatitis B. He had not been previouslyassessed for serum markers of viral hepatitis. His syntheticliver function deteriorated and hepatic encephalopathyprogressed, prompting transfer and administration oflamivudine and adefovir; he then underwent orthotopicliver transplantation. As prophylaxis against Hepatitis Brecurrence, lamivudine and adefovir were retained in thegraft, together with immunoglobulin against hepatitis B.One year after transplantation, there had been norecurrence of hepatitis B.
Patient 4, a 47-year-old man, was diagnosed with NHL.He received six cycles of R-CHOP from August toNovember 2008. He achieved remission but washospitalised on 1 February 2009 with jaundice.Investigations revealed he following findings: total bilirubin600 µmol/L, AST 25 µcat/L, ALT 50 µcat/L, prothrombin
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Reactions 26 Jun 2010 No. 13070114-9954/10/1307-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
