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Non-Hodkin’s lymphomas (NHL) are a group of heterogenous malignant lymphoid disorders that associate anemia either from diagnosis or during the evolution of the disease. The anemic syndrome can be present at the moment of diagnosis or can develop during the evolution of non-Hodgkin’s lymphomas, with negative effects on the therapeutic regimen due to reduction of intensity and density of drug doses, overall survival and quality of life of these patients. Various pathophysiological mechanisms responsible for the development of anemia are depicted in literature: pro-inflammatory cytokines and hepcidin action on iron metabolism and erythropoiesis, bone marrow failure caused by infiltration of malignant lymphomatous cells, cytopenias secondary to chemotherapy, immune peripheral destruction of red blood cells, iron and folate deficiency due to chronic bleeding.

To evaluate the prevalence of anemic syndrome in patients with non-Hodgkin’s lymphomas and the pathophysiological mechanisms involved in the development of anemia.

A retrospective study was conducted on 85 patients (informed consent obtained) with non-Hodgkin’s lymphoma, who were admitted to the Clinic of Hematology, Filantropia City Hospital, Craiova, Romania, in between 2013 and 2015, in order to evaluate the prevalence and pathophysiological mechanisms involved in the development of anemia in this study group.

In our study group, the median age at diagnosis of non-Hodgkin’s lymphoma was 64 years, sex distribution was males:females = 1,3, and the rural to urban area index = 1,2. 85,88% of patients had B type NHL and 14,12% T type NHL. 20% of NHL were indolent lymphomas, aggressive lymphomas in 54% cases and very aggressive lymphomas in 26%. NHL repartition on stage of disease revealed: type I – 2.35%, type II – 18.81%, type III – 57.64%, and type IV – 21.16%. In our study group, 84% of patients enrolled had anemia, with the anemic syndrome affecting the 50-59 years and 70-79 years age groups. 59.73% of patients had anemia at diagnosis and 40.27% of patients developed anemia during the evolution of NHL. The pathophysiological mechanisms involved in the development of anemia were: perturbations of iron metabolism and erythropoiesis under pro-inflammatory cytokines and hepcidin actions (47.25%), bone marrow failure induced by lymphomatous infiltration (25%), anemia induced by chemotherapy (18.05%), and autoimmune hemolysis (9.7%). Five patients with anemia induced by chemotherapy and three patients with lymphomatous infiltration of the bone marrow also associated iron and/or folate deficiency.

In our study, anemia was present in 84% of NHL cases, more frequently found in patients that associated comorbidities and belonged to the 50-60 years and 70-80 years age groups. In half of the cases, anemia was moderately severe. 47.25 % of patients had simple chronic anemia due to perturbations of the iron metabolism and of erythropoiesis, and 25% of patients presented anemia due to bone marrow failure. Chemotherapy lead to an anemic syndrome in 18.05% of cases, whereas hemolysis of autoimmune cause was responsible for 9.7% of cases of anemia diagnosed. The management of anemia is extremely important in patients with NHL because it influences the administration of chemotherapy (dose intensity and density), prognosis and quality of life.