Here, we report a case of de novo type B hepatitis in a patient with hepatitis B surface antigen (HBsAg) negative but positive for low titer of anti-HBc antibody (anti-HBc titer; dilution 200; negative). As the disease was anticipated in advance, the patient received nucleos(t)ide analogs, but de novo type B hepatitis was developed, because of discontinuation of antiviral drugs. A 59-year-old male with a history of T cell rich diffuse large Bcell lymphoma (DLBCL) and was treated with rituximab plus cyclophosphomide, doxorubicin, vincristine and prednisolone (R-CHOP). The patient responded to anticancer therapy and his complete responder status was confirmed by PET-CT on October 4, 2010. As the patient was expressing low levels of anti-HBc (anti-HBc titer; dilution 200-negative), he was given lamivudine to block HBV reactivation, but the drug was continued after 1 year due to apparent improvement. Stoppage of antiviral drug resulted in detectable HBV DNA and evidences of liver damages and he was referred to our department for specialized consultation about liver-related complications. He was given entecavir at a dose of 1 gm/day from May 2012. However, the parameters of liver function test showed anomaly indicating progressive liver damages. Subsequently, he was given steroid pulse therapy with 1,000 mg of prednisolone and tapered successively. The levels of HBV DNA decreased and parameters of liver function test were improved. A biopsy specimen taken in July 2012 showed the findings compatible with resolved acute hepatitis. To prevent de novo type B hepatitis, critical observation and timely management of the patients are necessary. The administration with nucleoside analogs at least 1 year after R-CHOP therapy is recommended in guideline of Japanese Society of Hepatology. However, we should reconsider the term of administration with nucleoside analogs after R-CHOP therapy.