Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0022104 (irritable bowel syndrome)
 8,033 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

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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PMID:Immunosuppression-related lymphomas and cancers in IBD: how can they be prevented? 2279 8

The role of human cytomegalovirus (HCMV) and Epstein-Barr virus (EBV) in the exacerbation of inflammatory bowel disease (IBD) is still uncertain. We prospectively investigated the presence of EBV and HCMV infection in both epithelial and immune cells of colonic mucosa of IBD patients, both refractory and responders to standard therapies, in comparison with patients suffering from irritable bowel syndrome who were considered as controls, by using quantitative real-time polymerase chain reaction, immunohistochemistry and in situ hybridization, in an attempt to assess viral localization, DNA load, life cycle phase and possible correlation with disease activity indexes. We obtained clear evidence of the presence of high DNA loads of both viruses in either enterocytes or immune cells of refractory IBD patients, whereas we observed low levels in the responder group and an absence of detectable copies in all cell populations of controls. Remarkably, the values of EBV and HCMV DNA in inflamed mucosa were invariably higher than in non-inflamed areas in both IBD groups, and the EBV DNA loads in the cell populations of diseased mucosa of refractory IBD patients positively correlated with the severity of mucosal damage and clinical indexes of activity. Moreover, EBV infection resulted the most prevalent either alone or in combination with HCMV, while immunohistochemistry and in situ hybridization did not allow us to distinguish between the different phases of viral life cycle. Finally, as regards treatment, these novel findings could pave the way for the use of new antiviral molecules in the treatment of this condition.
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PMID:Differential cellular localization of Epstein-Barr virus and human cytomegalovirus in the colonic mucosa of patients with active or quiescent inflammatory bowel disease. 2665 90