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Background:
Chemotherapy induced neutropenia (CIN) was a challenge to physicians until the discovery of growth factors. Neutropenia predisposes the patient to infection with increased morbidity, mortality, and cost of hospitalization. Not only does CIN leads to a delay in chemotherapy but also a dose reduction, which results in decreased efficacy and impact on survival. Filgrastim is a granulocyte colony stimulating factor that leads to the proliferation, differentiation and function of neutrophils. With an increase in the neutrophil count and function, Filgrastim reduces the incidence of neutropenia and the complications associated with febrile neutropenia (FN), making it possible to deliver chemotherapy on time, without dose adjustment. ASCO guidelines recommend that Filgastrim be given at 5 mcg/kg/day starting from days 1–3 after chemotherapy for patients with the risk of FN greater than 20% until the absolute neutrophil count is near-normal. It was recently reported that two doses of Filgrastim were comparable to higher number doses to prevent the nadir. We hypothesized that only a single dose is sufficient to prevent the nadir and delay in treatment.
Patients and Methods:
A retrospective analysis of chart data from all patients treated at The Brooklyn Hospital Center ambulatory clinic was reviewed after the initiation of chemotherapy. Data collected included the white cell count, neutrophil count, dates of chemotherapy and Filgrastim administration. Patients who received one dose of Filgastrim within 2–3 days, but not less than 24 hours prior to receiving subsequent chemotherapy comprised the study population. Data was analyzed for each individual cycle of chemotherapy.
Results:
The study population consisted of 11 patients with a total of 33 cycles of chemotherapy. Of the 11 patients, 9 had breast cancer, 1 had embryonal cancer, and 1 had colon cancer. Chemotherapy varied from Etoposide and Cisplatin, FOLFOX with Bevacizumab, and Adriamycin with Cyclophosphamid (AC) followed by Paclitaxel where the AC was given as a dose dense regimen. All the cycles had adequate response in neutrophil count to a single dose of Filgrastim when it was delivered within 2–3 days, but not before 24 hours of receiving chemotherapy. The mean absolute neutrophil count prior to Filgrastim was 0.8 compared to 6.0 (p=0.0001) after a single dose. There was no delay in treatment noticed as a result of the single dose of Filgrastim in all the 33 cycles.
Conclusion:
Filgrastim as a single dose is sufficient to treat CIN and prevent delay in subsequent treatment.
Disclosures:
No relevant conflicts of interest to declare.
Introduction Immune thrombocytopenia is an autoimmune disorder associated with increased thrombocyte destruction and impaired production in the bone marrow. Proposed mechanisms include an antibody or autoreactive T-cell-associated autoimmunity and thrombopoietin deficiency among others. Clinical manifestations are predominantly mucocutaneous hemorrhages including petechiae, purpura, mucosal bleeding in the urinary or the gastrointestinal tracts, menorrhagia, and epistaxis. The purpose of the treatment is to prevent bleeding rather than normalizing the platelet counts. First-line treatments include corticosteroids ± intravenous immunoglobulin and Anti-D which mainly decrease antibody-mediated platelet destruction and increase the number of peripheral Tregs. Second-line and subsequent therapies include splenectomy, chimeric anti-CD20 antibody (rituximab), which eliminates B cells and act as an immunomodulatory agent, and Thrombopoietin receptor agonists (romiplostim), which promote platelet production. Case report We describe a 40-year-old male patient diagnosed with immune thrombocytopenia that was refractory to first-line corticosteroid and intravenous immunoglobulin and second-line romiplostim monotherapy treatments. Management and outcome: The patient was given the romiplostim and rituximab combination which not only successfully treated thrombocytopenia but also resulted in grade 3 bone pains and the patient’s subsequent refusal to continue therapy. Discussion Common adverse effects of rituximab are infusion reactions and prolonged immunosuppression; those of romiplostim include thrombosis, headaches, arthralgia–myalgia, and gastrointestinal symptoms. This case shows that romiplostim has not caused any discernible side effects when given alone, while combination with rituximab resulted in severe bone and joint pains. We hypothesize that this combination regimen shows a synergistic effect both in terms of efficacy and adverse-effect probability and/or severity.
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