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Saudi Journal of Kidney Diseases and Transplantation
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REVIEW ARTICLE Table of Contents   
Year : 2010  |  Volume : 21  |  Issue : 4  |  Page : 621-627
Impact of immunosuppression and chemotherapy on reactivation of Viral hepatitis


1 Iran Research Center of Gastroenterology and Liver Disease, Firuzgar Hospital, Iran University of Medical Sciences, Tehran, Iran
2 Baqiyatallah Research Center for Gastroenterology and Liver Disease, Baqiyatallah University of Medical Sciences, Tehran, Iran
3 Prevention and Treatment of Rabies center, Department of vaccination, Pasteur Institute of Iran, Tehran, Iran

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Date of Web Publication26-Jun-2010
 

   Abstract 

Chemotherapy drugs, biological medications that are used to treat cancer, may cause hepatic side effects. Patients with pre-existing viral hepatitis may be more susceptible to exacer­bation of their underlying liver disease, and risk of drug-induced hepatotoxicity. We conducted a search on immunosuppression, and its impact on reactivation of viral hepatitis, using the electro­nic medical databases. Before starting chemotherapy, it is recommended to record the past history of liver disease and check for hepatitis B virus (HBV) and hepatitis C virus (HCV) serology. In immunosuppressed patients, radiation toxicity, graft versus host disease, hepatic veno-occlusive disease, acalculous cholecystitis, tumor infiltration, ischemia, other viruses such as CMV and her­pes virus, and systemic infection should also be considered. Transplant recipients with serologic evidence of previous infection with hepatitis B or C, or those who receive organs from a seropo­sitive donor, should have viral load levels monitored before and after transplantation and, may also require treatment. We believe that there is a role for prophylactic use of antiviral treatment in patients at risk for HBV reactivation.

How to cite this article:
Fallahian F, Alavian SM, Fallahian V, Zamani F. Impact of immunosuppression and chemotherapy on reactivation of Viral hepatitis. Saudi J Kidney Dis Transpl 2010;21:621-7

How to cite this URL:
Fallahian F, Alavian SM, Fallahian V, Zamani F. Impact of immunosuppression and chemotherapy on reactivation of Viral hepatitis. Saudi J Kidney Dis Transpl [serial online] 2010 [cited 2020 Oct 24];21:621-7. Available from: https://www.sjkdt.org/text.asp?2010/21/4/621/64616

   Introduction Top


Chemotherapeutic agents such as interferon, interleukin and monoclonal antibodies that are used to treat cancer, may cause hepatic side effects. Patients with pre-existing liver disease may be more susceptible to exacerbation of their underlying liver disease, as well as to an increased risk of drug-induced hepatotoxicity. Such patients should undergo a full diagnostic workup prior to chemotherapy to elucidate the cause and severity of the liver disease. Identi­fication of patients at risk for viral hepatitis is very important when evaluating and treating hematological malignancies. Viral hepatitis is the third major cause of liver dysfunction in al­lergenic transplant recipients. We performed a search using the electronic database Medline (1987 to 2008), Embase, Ovid, Google (for Lo­cal websites and medical journals), Websites of Iranian universities and Iran medex in English and Persian language on immunosuppression, hepatitis, reactivation, and the impact of immu­nosuppression on reactivation of viral hepati­tis. Serologic screening for all patients should include testing for anti-hepatitis C virus (HCV) antibody, hepatitis B surface antigen (HBs Ag), hepatitis B surface antibody (anti-HBs), and he­patitis B core antibody (anti-HBc). To prevent reactivation of hepatitis B virus (HBV) virus, prophylaxis with nucleoside analogues should be initiated for all HBs Ag-positive patients. HCV infection appears to have little impact on short-term survival after bone marrow trans­plantation (BMT), but can impact long-term survival due to progression of liver disease. [1] In this manuscript, we review the reactivation of viral hepatitis (HBV and HCV), their transmis­sion, HBV genetic diversity, and management in patients receiving chemotherapy.


   HBV Reactivation and Management Top


Patients with pre-existing liver disease may be more susceptible to exacerbation of their underlying liver disease, as well as to an in­creased risk of drug-induced hepatotoxicity. Such patients should undergo a full diagnostic work-up prior to chemotherapy to elucidate the cause and severity of the liver disease. Reacti­vation of hepatitis is indicated by an abrupt increase in aspartate aminotransferase (AST) and alanine aminotransferase (ALT) levels, with or without symptoms of hepatitis, in a patient with underlying chronic liver disease. Hepa­titis B virus reactivation is a well-described complication in cancer patients who receive cytotoxic chemotherapy and may result in va­rying degrees of liver damage. As chemothe­rapy is used increasingly in cancer patients, HBV reactivation during cytotoxic treatment may become a more common problem in future years. In lymphoma patients, the incidence of chronic HBV infection has been reported to be 26% of whom, 47% developed HBV reactiva­tion during chemotherapy. In a study, 78 pa­tients (12%) of 626 consecutive cancer pa­tients were found to be HBs Ag positive; 34 (44%) developed raised ALT levels during their course of chemotherapy. In these 34 patients, hepatitis was attributed to HBV reactivation in 15 patients (44%), chronic active HBV infec­tion and HCV infection in one patient each (3%), malignant hepatic infiltration in two pa­tients (6%), and the use of hepatotoxic chemo­therapeutic agents in 11 patients (32%). The cause of hepatitis was unknown in four pa­tients (12%). HBV reactivation was more likely to develop in patients who were male, of younger age, HBe Ag sero-positive, and those with lymphoma. In HBV endemic areas, pa­tients with risk factors for HBV reactivation should be identified prior to receiving cyto­toxic treatment and monitored closely. The po­tential benefit of lamivudine requires further confirmation. [2]

In a study involving 138 consecutive cancer patients who were HBV carriers and undergoing chemotherapy, 128 patients had sera available for real-time PCR HBV DNA measurement. Multivariate analysis revealed pre-chemotherapy HBV DNA level, the use of steroids and a diag­nosis of lymphoma or breast cancer to be sig­nificant factors. Based on real-time HBV DNA PCR assay, detectable baseline HBV DNA prior to the administration of cytotoxic chemothe­rapy, the use of steroids and a diagnosis of lymphoma or breast cancer are predictive fac­tors for the development of HBV reactivation. [3] In another study, 28 cancer patients (consis­ting of 14 consecutive patients who developed HBV reactivation and another 14 who had no reactivation during cytotoxic chemotherapy) were reported. In the majority of cases, the type of virus, i.e. wild/mutant that was detected during the reactivation was identical to that de­tected in the pre-treatment samples. With res­pect to the preC promoter region, the two com­monest mutations detected were at nt 1762 (A to T) and nt 1764 (G to A). When this region was translated into amino acid sequences, stop codons leading to truncated X protein at car­boxyl terminus were found in four patients, three of whom developed HBV reactivation. According to this study, chronic HBV carriers who are HBe Ag negative/anti-HBe positive with nt 1896 mutation (G to A) may be more likely to develop HBV reactivation during cy­totoxic chemotherapy than those with the wild type virus. Cytotoxic chemotherapy does not appear to select out mutant HBV, or to be consistently mutagenic in patients who deve­lop HBV reactivation. The occurrence of stop codons in the amino acid sequences of the X protein in three patients who developed HBV reactivation, including one who was detected only at the time of reactivation, is of particular interest, as such mutant viruses remain repli­cation competent. [4]

In a study, five patients with solid tumors de­veloped severe HBV-related liver disease du­ring treatment with cytotoxic agents (with de­xamethasone as anti-emetic). All had clinical and serological evidence of reactivation of the liver disease. Three patients developed icteric hepatitis; two recovered fully and one died from progressive metastatic disease while re­covering from the reactivation. The other two died from progressive liver failure. Direct se­quencing of the polymerase chain reaction (PCR) products of the pre-core (preC) and pre­core promoter region of the HBV-DNA was carried out on the patients' serum samples ta­ken during the episode of reactivation. In each case, similar mutations (G to A) in nucleotide 1896 of the preC region were found, together with additional mutations in the preC promo­ter. The present findings suggest that reactiva­tion involving a mutant hepatitis B virus may lead to liver failure, which is possibly more severe than that caused by wild type HBV, and can be triggered by cytotoxic chemotherapy, or the administration of corticosteroids. In Eastern Asia, the HBV carriage rate in adults is high. HBV reactivation and severe liver disease du­ring cytotoxic treatment may become a serious and common problem in this region as cyto­toxic chemotherapy is more widely used. Pa­tients should be screened routinely for HBs Ag in endemic areas of chronic HBV infection prior to receiving cytotoxic treatment. The pos­sibility of HBV reactivation should be consi­dered in patients developing liver dysfunction. Patients who are HBe Ag negative/anti-HBe positive and are suspected to be having HBV reactivation, should have HBV-DNA levels mea­sured for confirmation as they may carry a mu­tant HBV. [5]

Chronic carriers of the HBV usually show HBs Ag in their sera. In some individuals, how­ever, this antigen cannot be detected by routine serological assays despite the presence of virus in liver and peripheral blood. One reason for this lack of HBs Ag might be mutations in the part of the molecule recognized by specific an­tibodies. These findings suggest that at least some of the chronic low-level carriers of HBV, where surface antigen is not detected, could be infected by diagnostic escape mutants and/or by variants with impaired replication. [6]

In a study of 2431 patients with early breast cancer who received adjuvant chemotherapy, 111 were HBs Ag positive, 37 patients (33.3%) developed acute hepatitis, of whom, 23 (20.7%) were related to HBV reactivation. All 23 pa­tients who developed HBV reactivation received lamivudine as a therapeutic measure at the time of HBV reactivation. Despite the use of lamivudine, disruption in the chemotherapy protocol occurred in 18 patients (78.3%) and 14 of these patients had premature termination of their chemotherapy.

HBV reactivation occurred in a significant proportion of HBs Ag positive patients during adjuvant anthracycline-based chemotherapy. Once hepatitis developed, most patients could not finish the chemotherapy as planned, despite lamivudine treatment. Until the risk factors for reactivation are clearly identified, Hbs Ag-po­sitive patients should begin prophylactic anti­viral treatment before initiating chemothe­rapy. [7] HBV reactivation has been reported in kidney transplant recipients. In the absence of HBs Ag positivity, reactivation of HBV should be assessed using HBV viral loads. [8]

Vaccination against HBV in non-immune re­nal transplant candidates is essential. Compared with the immune response to immunization before transplantation, the efficacy of standard HBV vaccination is reduced when the vaccine is administered after transplant (with response rates of 5% to 15%). [9] In hemodialysis patients given intradermal vaccination, immunity waned more rapidly. [10] For immunocompromised persons, the Centers for Diseases Control reco­mmends Recombivax-HB or Engerix-B at a higher dose (40 ΅g) given at one site in a four­dose schedule at 0, 1, 2, and 6 months. [11] HBV transmission may occur during childhood, du­ring medical treatment overseas and due to heterosexual contact. For about a third of cases of acute HBV infection, no route of transmi­ssion is reported, but analysis of secular trends and age distribution suggest that many of these may be related to injectable drug abuse. End­emic transmission gives rise to only a small proportion of all new chronic infections, with the vast majority arising from immigration of established HBV carriers. The UK prevalence of HBV infection is dependant on global rather than national immunization policy. Endemic transmission may be reduced by improving immunization coverage among drug abusers, which is expected to also reduce the number of cases without a risk factor reported. In addition, immunization options that better suit the needs of ethnic minorities need to be explored. [12] Multiple reports have suggested a benefit from prophylactic use of antiviral treatments in pa­tients at risk for HBV reactivation. The grea­test experience has been with lamivudine. A meta-analysis of 14 studies involving a total of 275 patients receiving chemotherapy found that preventive lamivudine therapy reduced the risk of HBV reactivation and HBV-related hepa­titis by 80 to 100%. [13]

Based on these factors, we recommend that patients who have risk factors for HBV infec­tion should be tested for exposure to HBV prior to initiation of immunosuppressive the­rapy. This includes patients born in hyper-en­demic areas, homosexual men, those with his­tory of active injection drug abuse, patients on hemodialysis, HIV infected patients, as well as family, household, and sexual contacts of HBV­infected persons. Serologic testing should in­clude assessment of HBs Ag; further testing should include HBe Ag, anti-HBe, and HBV DNA level if the patient is HBs Ag positive. It is reasonable to initiate lamivudine (100 mg orally once daily) at least one to two weeks prior to starting chemotherapy in HBs Ag po­sitive patients who are scheduled to undergo chemotherapy or chemoradiation therapy (inclu­ding patients undergoing intra-arterial infusion chemotherapy), regardless of HBe Ag and HBV DNA status. Treatment should be maintained for at least six months after withdrawal of che­motherapy; longer duration of treatment may be necessary in patients who had high serum HBV DNA prior to treatment. Several reports have demonstrated clinical improvement with antiviral treatment in patients who developed re­activation of HBV. [14] Antiviral treatment should be initiated as soon as a flare is determined to be related to hepatitis B as the effects of an­tiviral therapy take time, and may not prevent progression to hepatic decompensation if treat­ment is delayed until the patient develops jaun­dice. Patients should be monitored closely with determination of liver biochemical tests and prothrombin time. Early referral to a trans­plant center should be considered in patients who appear to have a severe and progressive course, although transplant may not be feasible in patients with active malignancy.

Reactivation has also been described follo­wing therapy with other forms of immunosup­pression, particularly with infliximab therapy for Crohn's disease and rheumatoid arthritis, or long-term steroid therapy. Although there are no direct data from which to derive reco­mmendations, prophylaxis should be considered in HBsAg positive patients receiving anti-TNF therapy, and those who require long-term treat­ment with other potent immunosuppressive the­rapies.

The benefit of pre-emptive therapy in patients with serological markers of recovered HBV in­fection is less clear. It may be reasonable to mo­nitor such patients closely and to initiate treat­ment when serum HBV DNA level becomes de­tectable or when a hepatitis flare is diagnosed. [15]


   HCV Reactivation and Management Top


Although severe hepatitis from reactivation of HCV infection has been documented in case reports, the relationship between chemotherapy and HCV reactivation is less clear than that for HBV infection. [16] In three large series of pa­tients who had anti-HCV antibodies, treatment for hematologic malignancies was associated with mild abnormalities of the liver function tests in up to 18% of patients. [17] In another re­port of 33 patients, 32 had active disease as manifested by positivity for HCV RNA and elevation of the serum transaminases, noted in 55% of the subjects. However, only one pa­tient was characterized as having a severe re­activation of an underlying hepatitis. [18] Thus, although chemotherapy may be associated with abnormalities in liver function tests, this does not appear to be a major issue except possibly for patients with evidence of an active infec­tion. Infection with HCV does appear to in­crease the risk of developing veno-occlusive disease (VOD) in patients receiving high-dose chemotherapy and hematopoietic stem cell transplantation, although results have been in­consistent. [19] In a retrospective study on the impact of HCV infection on kidney transplant patients > 20-years old, HCV antibody carriers had a poorer survival rate (because of liver dysfunction) in the second decade compared with the non-infected group (63.9 versus 87.9% for 20-year survival; P < 0.05). [20] HCV infec­tion is diagnosed serologically, although some patients with active disease and positive HCV viral load remain antibody-negative. [21]

The reported prevalence of HCV among the hemodialysis (HD) population has varied greatly from 1.9 to 84.6% in different countries in re­cent years. The length of time on dialysis is generally believed to be associated with HCV acquisition in these subjects. Several recent re­ports failed to recognize any significant role of blood transfusion. Also, several phylogenetic analyses of viral isolates suggest nosocomial patient-to-patient transmission of HCV among HD patients for which, the main potential source is believed to be contaminated hands and articles. [22]

Hepatitis C-associated liver failure is the most common indication for liver transplan­tation. Approximately 10% of HCV-infected recipients will die or lose their allograft due to hepatitis C-associated allograft failure. Although the choice of calcineurin inhibitor, mycophe­nolate mofetil, or both has not been clearly shown to affect histologic recurrence of hepa­titis C, higher cumulative exposure to corti­costeroids is associated with increased morta­lity and more severe histologic recurrence. In contrast to treatment of non-HCV-infected re­cipients, treatment of HCV-infected transplant recipients for acute cellular rejection is asso­ciated with attenuated patient survival. Steroid­resistant rejection with or without the use of T­-cell-depleting therapies is associated with a greater than five-fold increased risk of mor­tality in HCV-infected liver transplant reci­pients. Pegylated interferon, with or without ribavirin, should be considered for treatment of recipients with histologically apparent re­currence of hepatitis C before total bilirubin exceeds 3 mg/dL.

The role of hepatitis C immunoglobulin and new immunosuppres-sive agents in the mana­gement of hepatitis C after transplant conti­nues to evolve. [23]

Allograft infection with HCV in immunosup­pressed adults results in decreased allograft and patient survival. Risk factors for accelerated progression of hepatitis C related to immuno­suppression include treated episodes of acute cellular rejection (ACR), pulse therapy with methyl-prednisolone, and use of OKT3. Both interferon alfa (IFN-alpha) and ribavirin (RVN) show antiviral actions against HCV and stimu­late innate and adaptive immunity to increase cytolysis and polarize T helper subtype 1 (T (H) 1) responses. In addition, IFN-alpha inhibits fib­rogenesis in the liver.

Both IFN-alpha and RVN have been studied in immunosuppressed liver transplant recipients as prophylaxis or treatment of established he­patitis C to reduce allograft failure and patient mortality. [24]

Recurrent hepatitis C after liver transplanta­tion is a progressive disease; in 20% of pa­tients it produces liver cirrhosis without treat­ment beside immunosuppression, within five years. The treatment of recurrent HCV infec­tion is the most important determinant of sur­vival in patients with transplantation.

The drug of choice of chronic hepatitis C after transplantation is the combined therapy with pegylated interferon and ribavirin. This therapy is able to assure virus-free stage in 20-50% of patients. [25]


   Conclusions Top


Before starting chemotherapy, biological me­dications or monoclonal antibodies to treat cancer, it is recommended to note the past history of liver disease and check for HBV and HCV serology. We suggest a benefit from pro­phylactic use of antiviral treatments in patients at risk for HBV reactivation. However, other causes of hepatic injury should also be sought, in particular, alcohol, drugs, and superinfec­tion with other hepatitis viruses such as A or D. In immunosuppressed patients, radiation to­xicity, graft versus host disease, hepatic veno­occlusive disease, acalculous cholecystitis, tu­mor infiltration, ischemia, other viruses such as CMV and herpes virus, and systemic infec­tion should also be considered. Transplant re­cipients with serologic evidence of previous infection with hepatitis B or C, or those who receive cells from a seropositive donor, should have viral load levels monitored before and after transplantation and also may require treat­ment. Agents with activity against the HBV include lamivudine, tenofovir, and entecavir. Hepatitis C is currently treated with pegylated interferon and ribavirin, with acceptable safety profiles and cure in up to 50% of patients. [26] Regarding hepatitis C, no evident correlation exists between hepatitis C genotype and type or severity of liver disease after transplanta­tion. [27] In many cases, side effects of chemo­therapy can be prevented or controlled.

 
   References Top

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2.Yeo W, Chan PK, Zhong S, et al. Frequency of hepatitis B virus reactivation in cancer patients undergoing cytotoxic chemotherapy: a pros­pective study of 626 patients with identifi­cation of risk factors. J Med Virol 2000;62: 299-307.  Back to cited text no. 2  [PUBMED]  [FULLTEXT]  
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5.Steinberg JL, Yeo W, Zhong S, et al. Hepatitis virus reactivation in patients undergoing cytotoxic chemotherapy for solid tumours: precore/core mutations may play an important role. J Med Virol 2000;60:249-55.  Back to cited text no. 5  [PUBMED]  [FULLTEXT]  
6.Weinberger KM, Bauer T, Bohm S, Jilg W. High genetic variability of the group-specific a-determinant of hepatitis B virus surface antigen (HBsAg) and the corresponding frag­ment of the viral polymerase in chronic virus carriers lacking detectable HBsAg in serum. J Gen Virol 2000;81:1165-74.  Back to cited text no. 6      
7.Kim MK, Ahn JH, Kim SB, et al. Hepatitis B reactivation during adjuvant anthraxcycline­based chemotherapy in patients with breast cancer: a single institution's experience. Korean J Intern Med 2007;22:237-43.  Back to cited text no. 7  [PUBMED]  [FULLTEXT]  
8.Rostaing L, Henry S, Cisterne JM, Duffaut M, Icart J, Durand D. Efficacy and safety of lamivudine on replication of recurrent hepatitis after cadaveric renal transplantation. Trans­plantation 1997;64:1624-7.  Back to cited text no. 8      
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12.Hahne S, Ramsay M, Balogun K, Edmunds WJ, Mortimer P. Incidence and routes of transmi­ssion of hepatitis B virus in England and Wales, 1995-2000: implications for immuni­zation policy. J Clin Virol 2004;29:211-20.  Back to cited text no. 12      
13.Loomba R, Rowley A, Wesley R, et al. Syste­matic review: the effect of preventive lami­vudine on hepatitis B reactivation during che­motherapy. Ann Intern Med 2008;148:519.  Back to cited text no. 13  [PUBMED]  [FULLTEXT]  
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22.Rahnavardi M, Hosseini Moghaddam SM, Alavian SM. Hepatitis C in Hemodialysis patients: Current global magnitude, natural history, diagnostic difficulties, and preventive measures. Am J Nephrol 2008;28:628-40.  Back to cited text no. 22  [PUBMED]  [FULLTEXT]  
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Correspondence Address:
Farahnaz Fallahian
Gastroenterintestinal and Liver Disease Research Center, Iran University of Medical Sciences, Firuzgar Hospital, Vali asr Square, Aban St., Tehran
Iran
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