Antineoplastics
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Reactions 1273 - 10 Oct 2009 S Antineoplastics Fatal reactivation of hepatitis B virus infection in a HBsAg-negative and anti-HBc-positive patient: case report A 52-year-old woman, who was hepatitis B virus core antibody (anti-HBc) positive and hepatitis B surface antigen (HBsAg) negative, developed fatal reactivation of hepatitis B virus infection during treatment with rituximab, cyclophosphamide, liposomal doxorubicin [Lipodox], vincristine and prednisolone. In August 2007, the woman was diagnosed with diffuse large B-cell lymphoma involving her duodenum and intraperitoneal and retroperitoneal lymph nodes; she was previously a hepatitis B virus carrier and, at the age of 44 years, she had become negative for both HBsAg and antibody to HBs and positive for anti-HBc. On 27 August 2007, she started receiving a combination therapy with rituximab, cyclophosphamide, liposomal doxorubicin, vincristine and prednisolone [dosages not stated]. The therapy was completed on 9 January 2008 after six cycles. Four weeks after her last cycle, she developed generalised malaise and poor appetite. Laboratory investigations revealed increased serum levels of ALT (654 U/L), AST (546 U/L) and total bilirubin (1.93 mg/dL). Acute hepatitis was considered and she was hospitalised on 25 February 2008. After admission, her ALT, AST and total bilirubin levels progressively increased. Investigations for hepatitis markers revealed that she was weakly positive for HBsAg and anti-HBs antibody, positive for anti-HBc IgG, and negative for anti-HCV and anti-HAV IgM. The woman started receiving lamivudine. She had a very high hepatitis B viral load (> 1 × 10 8 copies/mL). Over the next 2 weeks, her AST and ALT levels decreased from 859 to 267 U/L and from 765 to 413 U/L, respectively, but her total bilirubin level increased to 19.4 mg/dL. She also developed signs of hepatic decompensation, profound coagulopathy and hypoalbuminaemia. Entecavir was added to her treatment regimen. On 14 March 2008, her hepatitis B virus DNA level was 69 276 336 copies/mL. She received fresh frozen plasma. However, her clinical condition deteriorated and, on 15 March, she developed impaired consciousness due to hepatic encephalopathy. On 17 March, she started receiving molecular adsorbents recirculation system therapy. Her consciousness level and biochemical profiles showed a transient improvement but, due to a rapid deterioration of her general condition, a liver transplantation could not be performed. She subsequently died of liver failure on 19 March 2008. Wu JM, et al. Fatal reactivation of hepatitis B virus in a patient who was hepatitis B surface antigen negative and core antibody positive before receiving chemotherapy for non-Hodgkin lymphoma. Journal of Clinical Gastroenterology 43: 496-498, No. 5, May-Jun 2009 - Taiwan 801150909 1 Reactions 10 Oct 2009 No. 1273 0114-9954/10/1273-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
Transcript of Antineoplastics
Reactions 1273 - 10 Oct 2009
SAntineoplastics
Fatal reactivation of hepatitis B virus infection ina HBsAg-negative and anti-HBc-positive patient:case report
A 52-year-old woman, who was hepatitis B virus coreantibody (anti-HBc) positive and hepatitis B surface antigen(HBsAg) negative, developed fatal reactivation ofhepatitis B virus infection during treatment with rituximab,cyclophosphamide, liposomal doxorubicin [Lipodox],vincristine and prednisolone.
In August 2007, the woman was diagnosed with diffuselarge B-cell lymphoma involving her duodenum andintraperitoneal and retroperitoneal lymph nodes; she waspreviously a hepatitis B virus carrier and, at the age of44 years, she had become negative for both HBsAg andantibody to HBs and positive for anti-HBc. On 27 August2007, she started receiving a combination therapy withrituximab, cyclophosphamide, liposomal doxorubicin,vincristine and prednisolone [dosages not stated]. Thetherapy was completed on 9 January 2008 after six cycles.Four weeks after her last cycle, she developed generalisedmalaise and poor appetite. Laboratory investigationsrevealed increased serum levels of ALT (654 U/L), AST(546 U/L) and total bilirubin (1.93 mg/dL). Acute hepatitiswas considered and she was hospitalised on 25 February2008. After admission, her ALT, AST and total bilirubinlevels progressively increased. Investigations for hepatitismarkers revealed that she was weakly positive for HBsAgand anti-HBs antibody, positive for anti-HBc IgG, andnegative for anti-HCV and anti-HAV IgM.
The woman started receiving lamivudine. She had a veryhigh hepatitis B viral load (> 1 × 108 copies/mL). Over thenext 2 weeks, her AST and ALT levels decreased from859 to 267 U/L and from 765 to 413 U/L, respectively, buther total bilirubin level increased to 19.4 mg/dL. She alsodeveloped signs of hepatic decompensation, profoundcoagulopathy and hypoalbuminaemia. Entecavir was addedto her treatment regimen. On 14 March 2008, herhepatitis B virus DNA level was 69 276 336 copies/mL. Shereceived fresh frozen plasma. However, her clinicalcondition deteriorated and, on 15 March, she developedimpaired consciousness due to hepatic encephalopathy.On 17 March, she started receiving molecular adsorbentsrecirculation system therapy. Her consciousness level andbiochemical profiles showed a transient improvement but,due to a rapid deterioration of her general condition, a livertransplantation could not be performed. She subsequentlydied of liver failure on 19 March 2008.Wu JM, et al. Fatal reactivation of hepatitis B virus in a patient who was hepatitisB surface antigen negative and core antibody positive before receivingchemotherapy for non-Hodgkin lymphoma. Journal of Clinical Gastroenterology43: 496-498, No. 5, May-Jun 2009 - Taiwan 801150909
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Reactions 10 Oct 2009 No. 12730114-9954/10/1273-0001/$14.95 © 2010 Adis Data Information BV. All rights reserved
