THE ROLE OF GRANULOCYTE-COLONY-STIMULATING FACTOR (FILGRASTIM) IN MAINTAINING DOSE INTENSITY DURING CONVENTIONAL-DOSE CHEMOTHERAPY WITH ABVD IN HODGKINS-DISEASE

Background: The aim of the study was to evaluate the role and potentia l benefit of granulocyte colony-stimulating factor (G-CSF, Filgrastim) , administered following cytotoxic chemotherapy with the ABVD regimen in Hodgkin's disease, in maintaining cycle schedule and dose intensity and in decreasing neutropenia and number of infections. Patients and Methods: Twenty-two patients affected by high-risk Hodgkin's disease ( 14 localized and 8 diffuse), aged 15 to 69 years (median, 34), were gi ven ABVD chemotherapy for a total of 6 courses (for the purpose of thi s study, each single course of chemotherapy was considered as two 15-d ay periods). No patient was given G-CSF after the first cycle. After e ach cycle, G-CSF was administered only for: 1) absolute neutrophil cou nt < 1 x 10(9)/L between cycles; 2) delay in cycle schedule due to an absolute neutrophil count < 1 x 10(9)/L on the planned day of treatmen t; or 3) fever or a documented infection, regardless the absolute neut rophil count. Once administered, G-CSF was maintained in the subsequen t cycles. Results: Seventeen of 22 patients (77%) required the adminis tration of G-CSF (5 mu g/kg b.w.; a median of 5 doses/cycle); most of them (13/17) before the 5th dose of chemotherapy, The main reason for introducing G-CSF into therapy was neutropenia during the interval bet ween courses (n = 4) or on the planned day of treatment (n = 11). Comp aring 112 courses where G-CSF was not administered with 124 where it w as, in the latter group we observed: 1) a significantly tower (P = 0.0 002) incidence of cycle delays (0 vs 13), with a median delay of 7 day s (5 to 11). The main reason for cycle delay was neutropenia (n = 13); 2) a greater dose intensity delivered to the patients while on G-CSF (100% vs 95.2 +/- 8.8%; P = 0.0001); 3) an absolute neutrophil count s ignificantly higher at day 8 (P < 0.0001) and day 15 (P < 0.0001); 4) a significantly lower (P = 0.0003) incidence of neutropenia (2 vs. 17) . No difference in the incidence of infections was observed between th e two groups of cycles (P = 0.5889), but the duration and severity of the same were greater during chemotherapy without G-CSF, requiring ant ibiotic therapy and causing cycle delay. Conclusions: In conclusion, o ur data suggest the use of Filgrastim in Hodgkin's disease also during conventional-dose chemotherapy with ABVD. It is not required from the first dose of therapy, but as soon as neutropenia appears between cyc les or on the planned day of treatment. Then, its use allows maintenan ce of the chemotherapy schedule and dose intensity. It also decreases frequency, duration and severity of neutropenia and its sequelae.