No abstract

A randomized, double-blind, multicenter study in 181 afebrile cancer patients with ANC levels < 500/microL receiving myelosuppressive chemotherapy was undertaken to compare sargramostim (yeast-derived recombinant human granulocyte-macrophage colony-stimulating factor, RhuGM-CSF) and filgrastim (bacteria-derived recombinant human granulocyte colony-stimulating factor, RhuG-CSF) in the treatment of chemotherapy-induced myelosuppression. Patients received daily subcutaneous (SC) injections of either agent until ANC levels reached at least 1500/microL. There was no statistical difference between treatment groups in the mean number of days to reach an ANC of 500/microL, but the mean number of days to reach ANC levels of 1000/microL and 1500/microL was approximately one day less in patients receiving filgrastim. Fewer patients in the sargramostim arm were hospitalized, and they had a shorter mean length of hospitalization, mean duration of fever, and mean duration of i.v. antibiotic therapy compared with patients who received filgrastim. Both growth factors were well tolerated. No patient was readmitted to the hospital after growth factor was discontinued. Sargramostim and filgrastim have comparable efficacy and tolerability in the treatment of standard-dose chemotherapy-induced myelosuppression in community practice.

A prospective, randomized, double-blind, multicenter study in cancer patients receiving myelosuppressive chemotherapy was undertaken to evaluate and compare the tolerability of sargramostim (yeast-derived recombinant human granulocyte-macrophage colony-stimulating factor, RhuGM-CSF) and filgrastim (bacteria-derived recombinant human granulocyte colony-stimulating factor, RhuG-CSF) in the prophylaxis or treatment of chemotherapy-induced neutropenia. In all, 137 evaluable patients received sargramostim (300 micrograms; 193 mg/m2) or filgrastim (481 mg; 7 mg/kg) once daily by self-administered s.c. injection, usually beginning within 48 h after completion of chemotherapy. With the exception of a slightly higher incidence of grade 1 fever (< 38.1 degrees C) with sargramostim, there were no statistically significant differences in the incidence or severity of local or systemic adverse events possibly related to the growth factors. Although the study was not designed to evaluate efficacy directly, there also were no statistically significant differences between treatment groups in total days of growth factor therapy, days of hospitalization, or days of i.v. antibiotic therapy during the treatment period. Both sargramostim and filgrastim were comparably well tolerated when given by s.c. injection in this group of patients, and no clinically significant differences between the growth factors were demonstrated.

A patient with acute myelomonocytic leukemia and multiple myeloma occurring simultaneously prior to initiation of chemotherapy is described. Possible mechanisms for this occurrence are discussed.Cancer 41:1381-1386, 1978. EVERAL INVESTIGATORS HAVE DESCRIBED T H ES development of acute myelomonocytic leukemia in patients with multiple myeloma.8~9~'0~'9 I n general, these have been patients w h o have undergone long-term chemotherapy with alkylating agents prior t o t h e development of t h e leukemia. It h a s been postulated i n these cases that chemotherapy h a d a leukemogenic effect or acted a s an immunosuppressant allowing t h e establishment of a malignant clone of cells. R a r e cases of t h e simultaneous occurrence of t h e two diseases have been reported. 1 6 3 2 0~2 3 W e describe a patient in w h o m well-documented acute myelomonocytic leukemia a n d multiple myeloma were simultaneously present prior t o the initiation of Chemotherapy. Included are electron microscopic and chromosomal findings. Postulated mechanisms of this simultaneous occurrence are discussed. CASE REPORTMSL, a 64-year-old white male first seen in May 1976, related a one-month history of increasing fatigue, low-grade fever, and anorexia, but no adenopathy or bleeding. Five years previously he had a partial gastrectomy for peptic ulcer disease. O n examination, there was no lymphadenopathy or hepatosplenomegaly. tion was evident on the peripheral smear. The platelet count was 208,000. Examination of the bone marrow smear showed a marked increase in cellularity with slight decrease in megakaryocytes. There was myeloid and myelomonocytoid hyperplasia with 25 percent blast forms. There was an increase in plasma cells of five to ten percent, some of which were primitive, multinucleated and in clusters (Figs. 1, 2). A diagnosis of myelomonocytic leukemia was made. Because the platelet and peripheral granulocyte counts were adequate, no treatment was initiated.Ten weeks later, with increasing symptomatology, increasing white-cell count to 105,000, and a decreasing platelet count of 46,000, the patient was admitted for initiation of chemotherapy with cystosine-arabinside by continuous infusion for seven days and daunomycin iv push for three days. The only positive physical finding at that time was a liver palpable two centimeters below the right costal margin. The serum muramidase was 117 mg/ml (normal 7-15 mg/ml), and the urine muramidase was 31 mg/ml (normal less than 2 mg/ml). Serum protein electrophoresis revealed the following: total protein 6.6, albumin 2.95, alpha-1 globulin 0.25, alpha-2 globulin 0.61, beta globulin 2.15, and gamma globulin 0.63, with a monoclonal spike in the beta region. Quantitative immunoglobulin levels showed IgG 720, IgA 2,550, IgM 22. There was an abnormal preciptin arc for IgA kappa paraprotein in both serum and urine. The urine was negative for Bence Jones protein. A bone marrow smear one week following chemotherapy showed normal cellularity with a marked decrease in megakaryocyte and erythroid activity. ...