Classical Hodgkin lymphoma-like post-transplant lymphoproliferative disease after allogeneic stem cell transplantation for primary myelofibrosis is successfully treated with nivolumab: A case report.

INTRODUCTION: Post-transplant lymphoproliferative disease (PTLD), a lymphoid proliferation observed after the solid organ transplantation or allogeneic stem cell transplant, is an important and mortal complication that can occur during the post-transplant period. Classical Hodgkin lymphoma-like PTLD is the least form of PTLD. We are presenting an adult case of classical Hodgkin lymphoma-like PTLD which was successfully treated with nivolumab. CASE REPORT: A 31-year-old female was diagnosed with primary myelofibrosis and we performed allogeneic stem cell transplantation from her HLA fully matched brother in 2015. Two years after transplant, classical Hodgkin lymphoma-like PTLD was diagnosed. The patient was resistant to six cycles of ABVD chemotherapy and four cycles of brentuximab vedotin. MANAGEMENT AND OUTCOME: After the failure of ABVD and brentuximab vedotin, we started nivolumab therapy at a dose of 3 mg/kg every 2 weeks. After six cycles, we achieved a PET negative complete remission. After 10 cycles of nivolumab, the patient is still followed with a complete remission. Still, there is no evidence of acute or chronic GvHD, and therefore no need for immunosuppressive treatment. No auto-immune complication was observed. It is planned to give nivolumab treatment to the patient until the progression. DISCUSSION: Our case has depicted that the classical Hodgkin lymphoma type PTLD may be resistant to the conventional treatments and anti-CD30 brentuximab vedotine. In such cases, nivolumab may be an effective and worth assessing agent in terms of both activity and safety profile.

CD38 Expression and Variation as a Prognostic Factor Chronic Lymphocytic Leukemia.

BACKGROUND: In this study, we aimed to determine a cutoff level for CD38 that would aid us in identifying chronic lymphocytic leukemia patients in need of early therapy and predicting patients at sufficiently low risk who would likely exhibit a rapid improvement; we also aimed to find out if CD38 expression would show variability during disease course and determine the extent of CD38 expression. METHODS: 124 patients were diagnosed with CLL. CD38 and ZAP-70 expression levels were measured with four color flowcytometry. Time from diagnosis to initial therapy was calculated for all patients. CD38 expression was studied for a second time during follow-up in 50 patients. RESULTS: For cutoff levels of 7%, 20%, and 30%, CD38 expressions were 61.3%, 25%, and 24.2%, respectively. At all three cutoff levels there were significant correlations with all parameters except age between CD38+ vs. CD38- groups (p < 0.001). The comparative rates of starting therapy for cutoff levels of 7%, 20%, and 30% in CD38+ and CD38- groups were 77.5% vs. 6.25%; 100% vs. 30.7%, and 100% vs. 31.5%, respectively (p < 0.001). Multiple Cox Proportional Hazards Regression analysis: for a cutoff level of 7%, survival was affected by STAGE, ZAP70, and CD38. CONCLUSIONS: A CD38 cutoff level of 7% determined by standardized laboratory techniques is an important prognostic marker. However, the number and frequency of repeat measurements of CD38 expression, and cutoff level of CD38 expression that significantly predict disease prognosis should be further determined by future cohort studies.