P.10.1 REACTIVATION OF HEPATITIS B VIRUS IN CANCER PATIENTS TREATED WITH CHEMOTHERAPY FOR SOLID TUMORS. IS THE PROPHYLAXIS REALLY REQUIRED?

P.10.1 REACTIVATION OF HEPATITIS B VIRUS IN CANCER PATIENTS TREATED WITH CHEMOTHERAPY FOR SOLID TUMORS. IS THE PROPHYLAXIS REALLY REQUIRED?

Abstracts of the 22nd National Congress of Digestive Diseases / Digestive and Liver Disease 48S2 (2016) e67–e231 still unknown. To explore the co...

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Abstracts of the 22nd National Congress of Digestive Diseases / Digestive and Liver Disease 48S2 (2016) e67–e231

still unknown. To explore the correlation between gut microbiota modulation and symptoms improvement in patients undergoing rifaximn treatment. Material and methods: Rifaximin 1200 mg/daily was administered for 10 days to patients with ulcerative colitis (UC), Crohn’s disease (CD), irritable bowel syndrome (IBS), diverticular disease (DD) and hepatic encephalopathy (HE). Inclusion criteria were: no exposure to antibiotics, pre-/pro-biotics and bowel colonoscopy preparation for at least one month, and omnivore normocaloric diet for at least one year. Fecal samples were collected and symptoms were assessed at baseline and at the end of treatment. Clinical improvement was evaluated by Mayo score for UC, CDAI for CD, IBS-SSS for IBS, GSS for DD, and West Haven classification for HE. Fecal microbiota composition was assessed by a metagenomic gene-targeted approach (16S rRNA) using the Roche 454 GS Junior ad Qiime pipeline. Biostatistic analysis was performed using R-statistics packages. Results: Twenty-five patients were included in the study. Clinical improvement was observed in 10 (40%) patients after rifaximin treatment. Nonmetric multidimensional scaling (NMDS) ordination on Bray Curtis distance highlighted a significant clustering of patients who experienced clinical improvement compared to those who did not (p=0.047; PERMANOVA). Differential abundance analysis revealed an increased abundance of Faecalbacterium prausnitzii in case of symptoms amelioration after rifaximin treatment (improved post vs pre: logFC =1.96; p=0.05; not improved post vs pre: logFC=-0.37; p=0.810 Figure 1 and 2). The post-treatment between-groups comparison confirmed a significantly higher abundance of Faecalbacterium prausnitzii in those patients whose symptoms improved after rifaximin (logFC =4; p=<0.0001). Clinical improvement was also paralleled by a significant increase in bacterial alpha-diversity (p=0.024).

Conclusions: Beneficial bacteria abundance is increased in patients with gastrointestinal diseases and hepatic encephalopathy who achieve clinical improvement after rifaximin treatment. This mechanism may mediate rifaximin efficacy in different pathologic settings.

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P.10 Liver 2

P.10.1 REACTIVATION OF HEPATITIS B VIRUS IN CANCER PATIENTS TREATED WITH CHEMOTHERAPY FOR SOLID TUMORS. IS THE PROPHYLAXIS REALLY REQUIRED? Federico A.1, Dallio M.*1, Brancaccio G.2, Iodice P.3, Fabozzi A.4, Del Prete S.3, Ciardiello F.4, Gaeta G.B.2, Loguercio C.1 Division of Hepatogastroenterology, Second University of Naples, Naples, Italy, 2Division of Infectious Diseases, Second University of Naples, Naples, Italy, 3Division of Oncology, S. Giovanni di Dio Hospital, Frattamaggiore (NA), Italy, 4Division of Oncology, Second University of Naples, Naples, Italy

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Background and aim: Reactivation of hepatitis B virus (HBV) during cancer chemotherapy has become an emerging clinical challenge. High rates of HBV reactivation, 38% to 54%, are now recognized in HBV-positive patients undergoing hematopoietic stem-cell transplantation and treatment for hematological malignancy, especially malignant lymphoma. Less clear is the magnitude of risk for clinically significant HBV reactivation with chemotherapy for non-hematological tumors. Aim of this study is to evaluate the risk of HBV reactivation in carriers and occult carriers of HBV cancer patients treated with chemotherapy for solid tumors. Material and methods: Two hundred sixty-seven patients with solid tumors were consecutively enrolled, between March 2013 and February 2014 at two Oncological Division in the Campania Region in Southern Italy. Before beginning the study, as a screening procedure, all patients underwent viral marker status (HBsAg/HBsAb, HBcAb, anti-HCV), liver function test with alanine amonitransferases (ALT), and liver ultrasonography. In HBsAg positive patients we evaluated hepatitis B e-antigen/ antibody (HBeAg/HBeAb), HBV-DNA (with real-time fluorescent PCR). HBV carriers were followed every 3 months by ALT, HBV DNA; occult carriers of HBV were followed every 3 months by ALT and HBsAg. Patients with hypertransaminasemia and HBV-DNA positivity were treated with tenofovir (245 mg/day). Results: Out of the 267 patients, 13 (4.8%) were HBsAg positive, of whom 6 were documented inactive carrier and 7 had chronic liver disease (1 compensated cirrhosis). Thirty-two patients (12%) were HBsAg negative/HBcAb positive and were classified as potential occult carriers of HBV. Among patients with HBsAg positive, 12/13 were anti-HBe positive and 1 patient was HBeAg positive. All patients with chronic liver disease had an HBV-DNA level >2000 IU/mL and carried genotype D of HBV. Six occult carrier and one inactive carrier patients were also anti-HCV positive. None of the patients undergo therapy with one of the following drugs: corticosteroids at high dose (>10 mg/day) for long time, cyclophosphamide, methotrexate. None of the patients had a reactivation of HBV over 18 months (range 2-24) of observation. The patient who was HBeAg positive at the enrolment seroconverted to anti-HBe during the course of treatment with tenofovir after 6 months. The antiviral agents were well tolerated and were not associated with any unexpected or additional toxicities to chemotherapy. Conclusions: Our study showed that none of the patients presented an HBV reactivation. Thus, it appears reasonable to avoid HBsAg and anti-HBc screening in these patients since anti-HBc result is not relevant to clinical decision. Clearly, screening strategy should be revised periodically, according to survey results on HBsAg prevalence in cancer patients.