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Immunosuppression-related lymphomas and cancers in IBD: how can they be prevented?
1Department of Gastroenterology, AP-HP, Hôpital Saint-Antoine, Paris, France. laurent.beaugerie@sat.aphp.fr
Most of the immunosuppressive therapy-associated excess lymphomas in IBD are due to a loss of control of Epstein-Barr virus (EBV) infection. Systemic EBV viral-load monitoring and preemptive treatments are extensively used in the posttransplant setting, but these methods have not yet been evaluated in IBD patients and cannot therefore be recommended in this context. However, the systemic EBV viral load should be measured in cases of unexplained fever, lymphadenopathy or hemophagocytic syndrome, in order to optimize the diagnostics of early EBV-related lymphoproliferations. The risk of hepatosplenic T cell lymphoma can, theoretically, be limited by avoiding prolonged combination therapy with thiopurines and anti-tumor necrosis factor (anti-TNF) beyond 2 years in young males. Young males seronegative for EBV are at risk for fatal forms of primary EBV infection, with postmononucleosis lymphoproliferation. This incidence could be limited by considering avoiding treatment with thiopurines in this subgroup of patients. There is a marked excess risk of nonmelanoma skin cancer in IBD patients currently or previously treated with thiopurines, which justifies lifelong sun protection and dermatological screening in these patients. The level of risk is still unclear for monotherapies with anti-TNF. An excess of human papilloma virus (HPV)-related uterine cervix dysplasia and cancer has been reported in various populations of women with IBD, but the proper role of immunosuppressive therapy remains to be quantified. However, yearly screening for uterine cervix abnormalities is recommended for all female IBD patients, along with HPV vaccination in young girls.
Most of the immunosuppressive therapy-associated excess lymphomas in IBD are due to a loss of control of Epstein-Barr virus (EBV) infection. Systemic EBV viral-load monitoring and preemptive treatments are extensively used in the posttransplant setting, but these methods have not yet been evaluated in IBD patients and cannot therefore be recommended in this context. However, the systemic EBV viral load should be measured in cases of unexplained fever, lymphadenopathy or hemophagocytic syndrome, in order to optimize the diagnostics of early EBV-related lymphoproliferations. The risk of hepatosplenic T cell lymphoma can, theoretically, be limited by avoiding prolonged combination therapy with thiopurines and anti-tumor necrosis factor (anti-TNF) beyond 2 years in young males. Young males seronegative for EBV are at risk for fatal forms of primary EBV infection, with postmononucleosis lymphoproliferation. This incidence could be limited by considering avoiding treatment with thiopurines in this subgroup of patients. There is a marked excess risk of nonmelanoma skin cancer in IBD patients currently or previously treated with thiopurines, which justifies lifelong sun protection and dermatological screening in these patients. The level of risk is still unclear for monotherapies with anti-TNF. An excess of human papilloma virus (HPV)-related uterine cervix dysplasia and cancer has been reported in various populations of women with IBD, but the proper role of immunosuppressive therapy remains to be quantified. However, yearly screening for uterine cervix abnormalities is recommended for all female IBD patients, along with HPV vaccination in young girls.
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