Cyclophosphamide anemia

Trastuzumab (Herceptin) [Antineeplastic/Monoover express the HERlIneu. protein breast CA adjuvant, w/ doxorubicin, cyclophosphamide, and paclitaxel if pt HER2/neu(+) Action MoAb binds human EGF receptor 2 protein HER2) mediates cellular cytotox Dose Per protocol, typical 2 mg/kg/IV/wk Caution [B, ] CV dysfxn, alla-gy/inf Rxns Contra Live vaccines Disp Inj SE Anemia, cardiomyopathy, nephrotic synd, pneumonitis Interactions t Risk of cardiac dysfxn W/ anthracycline, cyclophosphamide, doxorubicin, epirubicin EMS Cardiomyopathy, ventricular dysfxn and pulm tox have been reported monitor for Sxs of reduced cardiac Fxn OD Sxs unknown... 

Cyclophosphamide s major toxic effect is myelosuppression resulting in blood dyscrasias, such as leukopenia, anemia, thrombocytopenia, and hypoprothrom-binemia. 

Autoimmune hemolytic anemia Prednisone,1 cyclophosphamide, chlorambucil, mercaptopurine, azathioprine, high-dose gamma globulin Usually good... 

Drugs that cause damage to proliferating cells such as those in bone marrow, will cause a similar effect to benzene. Thus cyclophosphamide, the anticancer drug, inhibits the clonal expansion of T- and B-cell precursors in the bone marrow and causes anemia. 

Giebel S, Wojnar J, Krawczyk-Kulis M, Markiewicz M, et al. 2006. Treosulfan, cyclophosphamide and antithymocyte globulin for allogeneic hematopoietic cell transplantation in acquired severe aplastic anemia. Ann Transplant. 11 23-27. 

Cyclophosphamide Cytoxan, Neosar Acute and chronic lymphocytic leukemia acute and chronic myelocytic leukemia carcinoma of ovary, breast Hodgkin disease non-Hodgkin lymphomas multiple myeloma Blood disorders (anemia, leukopenia, thrombocytopenia] Gl distress (nausea, vomiting, loss of appetite] bladder irritation hair loss car-diotoxicity pulmonary toxicity... 

Total body irradiation, a routine preconditioning procedure for treatment of leukemia and aplastic anemia before bone marrow transplantation, decreased TAC of blood plasma by 36%, as estimated by cyclic voltammetry (C26). TAC was found to decrease by about 40% during chemotherapy of patients with various hematologic malignancies with busuflan, VP-16, and cyclophosphamide (D12). The controversial procedure of blood ozonation was reported to decrease blood plasma TAC by 20% (B17). Treatment of hypercholesterolemic patients with bezafibrate (600 mg/day) for 1 month decreased TAC of their blood serum (G16). Propofol anesthesia decreased TAC of blood plasma of patients by 9.5% this effect was caused by hemodilution because mean hemoglobin concentration of the blood decreased accordingly (S26). 

Leukopenia, and less commonly thrombocytopenia or anemia, due to cyclophosphamide are typically dose-related in the therapeutic range. Cyclophosphamide-induced anemia has led to retinopathy presenting as striated hemorrhage of the retina (12). 

Single cases of agranulocytosis and Coombs negative hemolytic anemia have been attributed to twice-weekly mterleukin-12 in 28 patients with renal cell cancer or melanoma (2). The patients responded only to cyclophosphamide and/or glucocorticoids, and the causative role of interleukin-12 was therefore inconclusive. 

A 26-year-old woman with a diffuse large B cell lymphoma received CHOP (cyclophosphamide, hydroxy-daunomycin, Oncovin, and prednisone), ritnximab, and radiotherapy (14). She developed a transfnsion-dependent anemia. Bone marrow biopsy confirmed pure red cell aplasia and parvovirus infection. She had no antibodies to parvovirus, suggesting that she never had a previous exposure. Intravenous immunoglobulin resulted in a reticulocytosis and recovery of her hemoglobin. 

Carboplatin and cyclophosphamide are indicated in the treatment of advanced ovarian carcinoma. Cisplatin and carboplatin produce predominantly interstrand DNA crosslinks rather than DNA-protein cross-links, and the effect is cell-cycle nonspecific. Carboplatin is not bound to plasma proteins, whereas platinum from carboplatin becomes bound to plasma protein and is eliminated slowly with a half-life of 5 days. The major route of elimination of carboplatin is the kidneys, and its doses should be reduced in renal impairment. Furthermore, the coadministration of aminoglycosides increases the chance of nephrotoxicity. Carboplatin causes anemia, neutropenia, leukopenia, and thrombocytopenia requiring transfusions. Cisplatin and, to a lesser extent, carboplatin cause emesis, which requires treatment with antiemetic agents. Alopecia, pain, and asthenia do occur (see also Figure 15). 

Clinical use Cyclophosphamide is effective in autoimmune diseases (including hemolytic anemia), antibody-induced red cell aplasia, bone marrow transplants, and possibly other organ transplant procedures. Cyclophosphamide does not prevent the graft-versus-host reaction in bone marrow transplantation. 

Brodsky RA, Chen AR, Dorr D, Fuchs EJ, Huff CA, Luznik L, Smith BD, Matsui WH, Goodman SN, Ambinder RF, Jones RJ. High-dose cyclophosphamide for severe aplastic anemia long-term foUow-up. Blood 2010 115(11) 2136-41. 

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