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PubMed1997

[A case of pleural metastasis of invasive thymoma with pulmonary metastasis responding to chemotherapy with cyclophosphamide and prednisolone].

The patient, a 48-year old male, was seen with hoarseness in December 1990. A chest radiograph and chest CT scan showed an anterior mediastinal mass. Median sternotomy revealed epithelial thymoma with involved partial lung and pericardium. After surgery, he received external radiation to the mediastinum. One year later he was given another 40 Gy external radiation in the cervical and mediastinal recurrence region. In May 1994, a chest CT scan revealed an extrapleural and bilateral lung mass. Histological examination revealed recurrent epithelial thymoma in the left cervical muscle biopsy, so treatment with cyclophosphamide and prednisolone were begun. A dose of 100 mg/body/day of cyclophosphamide and a dose of 10 mg/body/day of prednisolone were administered every 2 week. Complete remission was induced with four cycles of this treatment of cyclophosphamide and prednisolone. The chemotherapy was thus continued for 20 cycles in 14 months. This chemotherapy with cyclophosphamide and prednisolone appeared to be useful and safe for recurrent thymoma at the outpatient clinic level.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1997

Treatment of cyclophosphamide induced hemorrhagic cystitis with neodymium:YAG laser in pediatric patients.

PURPOSE: Hemorrhagic cystitis is a significant and sometimes fatal complication of cyclophosphamide therapy. We report our recent experience using a neodymium (Nd):YAG laser to treat 3 pediatric patients with cyclophosphamide induced cystitis. MATERIALS AND METHODS: Between May 1994 and March 1995 we treated 3 pediatric patients 6 to 8 years old with an Nd:YAG laser for severe hemorrhagic cyclophosphamide induced cystitis. All patients presented with gross hematuria and conservative measures failed. The Nd:YAG laser (20 watts and 2-second pulse mode) was used to fulgurate bleeding endoscopically. All patients required 2 laser treatment sessions with a total energy range of 8,011 to 16,595 J. and strict parameters to avoid small bowel injury. RESULTS: All 3 patients had resolution of gross hematuria with Nd:YAG therapy. They were discharged home within 3 days after repeat laser treatment with grossly clear urine and stable hematocrit. At followup of 11 to 18 months the patients have grossly clear urine and they are free of symptoms. CONCLUSIONS: Our experience suggests that the Nd:YAG laser can be effective and safe for treating refractory cyclophosphamide induced hemorrhagic cystitis in pediatric patients.

Child↗
PubMed1997

Docetaxel and cyclophosphamide in patients with advanced solid tumors.

This trial was designed to determine the recommended maximum tolerated dose (MTD), toxicity, pharmacokinetics, and efficacy of docetaxel (Taxotere) and cyclophosphamide (Cytoxan, Neosar) for phase II studies. Both drugs were administered to 39 patients with advanced solid tumors, 26 of whom had breast cancer. Docetaxel doses ranged from 60 to 85 mg/m2 and cyclophosphamide doses ranged from 600 to 800 mg/m2. All patients received steroid prophylaxis. The MTDs for patients with a history of prior chemotherapy were 75 mg/m2 of docetaxel and 700 mg/m2 of cyclophosphamide. For patients with no prior chemotherapy, the MTDs were 75 mg/m2 of docetaxel and 800 mg/m2 of cyclophosphamide. The dose-limiting toxicity was neutropenic fever, observed in 41% of patients and 13% of cycles. Addition of granulocyte colony-stimulating factor (G-CSF, filgrastim [Neupogen]) did not permit further dose escalation, although it did result in briefer periods of neutropenia.

Antineoplastic Combined Chemotherapy Protocols↗
PubMedDate not supplied

The association of cyclophosphamide and dexamethasone in advanced refractory multiple myeloma patients.

VAD is the most active regimen in refractory myeloma patients; however, the role of vincristine and doxorubicin remains unclear. Relatively high doses of cyclophosphamide (3.6 g/sqm) increased the response rate and survival in resistant MM. Cyclophosphamide and dexamethasone were administered to 28 patients with advanced refractory myeloma. Thirteen patients received cyclophosphamide 1.2 g/sqm on days 1 and 3 and dexamethasone 40 mg/day from day 1 to day 4, every 4 weeks for 6 cycles (schedule A); 15 patients were treated with cyclophosphamide 0.5 g/sqm on days 1 and 3 and dexamethasone 40 mg/day from day 1 to day 4, every two weeks for 12 cycles (schedule B). Overall, 21 patients (75%) responded and 10 achieved an objective response (36%), while 11 reached a partial response. Twenty patients died (68%), most of them of disease progression, and 8 are still alive (32%). Median length of response and survival is 6 and 8 months, respectively. Therapy was easily applied and well tolerated. The overall response rate (75%) compares favorably with the best published results in this setting. The two schedules proved to be equally effective but patients treated with schedule B had more infections, which may have been related to the higher dosage of steroids.

Adult↗
PubMed1997

Dose-finding study of paclitaxel and cyclophosphamide in women with advanced breast cancer.

The primary aim of this study was to define the maximum tolerated doses of paclitaxel (Taxol; Bristol-Myers Squibb Company, Princeton, NJ) given by 3-hour infusion and cyclophosphamide given by intravenous bolus every 3 weeks in patients with breast cancer. Patients had received a maximum of one prior chemotherapy for advanced disease. The maximum tolerated dose of the combination was also determined with granulocyte colony-stimulating factor (G-CSF) support. The 80 women who took part in this study received 347 fully evaluable courses of therapy. Starting doses were paclitaxel 135 mg/m2 and cyclophosphamide 750 mg/m2; G-CSF support (5 microg/kg subcutaneously) was added at the subsequent cycle if specific dose-limiting toxicities had occurred during the previous cycle. Febrile neutropenia and severe thrombocytopenia defined the maximum tolerated doses as paclitaxel 200 mg/m2 and cyclophosphamide 2,000 mg/m2, with or without G-CSF support, in patients with or without a prior chemotherapy. Recommended doses were paclitaxel 200 mg/m2 and cyclophosphamide 1,750 mg/m2 in these two groups of patients. The overall response rate was 25% among patients who had received prior therapy for metastatic disease and 50% in patients who had not been previously treated. Complete remissions were reported in 9% of patients, but only among those who were previously untreated.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed1996

[A study on interval of intravenous cyclophosphamide pulse in the treatment of severe systemic lupus erythematosus].

The aim of this study was to compare the clinical efficacy and adverse effects of intravenous cyclophosphamide pulse therapy between 2-week and 4-week intervals in the treatment of severe systemic lupus erythematosus. 52 patients were involved in the study and were equally divided into two groups. The pulse intervals were 2 weeks for group I and 4 weeks for group II. Each pulse dose of cyclophosphamide was 15 mg/kg. Every patient took prednisone 1 mg/kg daily for first 8 weeks and then tapered. Most of disease indices recovered quicker in group I than in group II. The group with short interval was better than that of long one on total efficacy and remission rate. The cyclophosphamide cumulative doses were not different between two groups as disease activity index dropped 50%. The pulse interval had to be prolonged from 2 weeks to 4 weeks to six patients in group I (23.1%) because of leukopenia, and be shortened from 4 weeks to 2 weeks to five cases in group II (19.2%) because of inefficacy. There was no statistical difference in adverse effects between two groups. Intravenous cyclophosphamide pulse therapy with two-weeks interval is advantageous to recovery of severe systemic lupus erythematosus provided blood test prior to each pulse. We suggest that pulse interval should be individualized.

Adolescent↗
PubMed1997

Cyclophosphamide-induced structural and biochemical changes in testis and epididymidis of rats.

Effect of cyclophosphamide administration (100 mg/kg body weight, ip, for 5 consecutive days) was studied on albino rat testis and epididymidis after 3 and 6 weeks of treatment. Cyclophosphamide decreased testis and cauda epididymidal weights, sperm count, motile and viable spermatozoa and increased percentage of abnormal spermatozoa. The biochemical changes observed in the testis include increase in acid and alkaline phosphatase activities and decrease in proteins and activity of lactate dehydrogenase. The levels of lipids and total cholesterol were not affected. In the epididymidis cyclophosphamide caused decrease in the tubular diameter and increase in its epithelial height. It is concluded that cyclophosphamide brings about structural and biochemical changes in the testis and epididymidis.

Animals↗
PubMed1998

Apoptosis-like changes in the lungs induced by cyclophosphamide and papain. I. An ultrastructural study.

An ultrastructural study was made to analyze the structural and cellular features of the pulmonary lesions produced in Wistar rats by the administration of cyclophosphamide (CP) and/or papain (P). Combined administration of cyclophosphamide and papain caused severe damage to lung tissue including necrosis, particularly to alveolar epithelial and endothelial cells. Some of the damaged type II cells showed nuclear and cytoplasmic features that are considered indicative of apoptosis. Apoptosis-like changes were also observed in endothelial and mesenchymal cells in the interstitium of interalveolar septa. Phagocytosis of apoptotic bodies by macrophages was found too. Apoptosis-like changes were not revealed in those areas of lung tissue where fibroplasia processes prevailed. Nor were they observed in the animals receiving papain only. Occasionally apoptosis-like changes were found in type II cells and in endothelial cells in rats given cyclophosphamide only. The results obtained also suggest the possibility of active participation of type II alveolar epithelial cells in the fibroplasia process in the course of lung rebuilding in acute lung tissue damage induced with simultaneous administration of cyclophosphamide and papain.

Animals↗
PubMed1997

High-dose infusional doxorubicin and cyclophosphamide: a feasibility study of tandem high-dose chemotherapy cycles without stem cell support.

The purpose of this study was to determine the maximally tolerated dose of doxorubicin administered during two cycles of intensive chemotherapy with cyclophosphamide and doxorubicin without stem cell support in patients with advanced cancer and to assess the cumulative cardiac toxicity of the regimen by noninvasive radionuclide imaging and by pre-and postchemotherapy endomyocardial biopsies. Thirty-eight patients (thirty-six with high risk or metastatic breast cancer) were treated in a dose-escalation trial using a fixed dose of i.v. cyclophosphamide (4.2 g/m2) administered over 2 h on day 5 and escalating doses of doxorubicin (50-175 mg/m2) given as a 96-h continuous i.v. infusion on days 1-4, using Filgrastim (granulocyte colony-stimulating factor) for hematological support beginning on day 6. All patients underwent pretreatment, and 28 patients underwent postchemotherapy endomyocardial biopsies. Twenty-nine of 38 patients received two cycles of treatment (median number of days between cycles, 44; range, 34-62). Twenty-one patients had received doxorubicin previously at cumulative dose levels </=150 mg/m2; all patients had pretreatment endomyocardial biopsy scores less than 1. One patient treated at the highest dose level of doxorubicin (175 mg/m2) developed symptoms of mild congestive heart failure following two cycles of chemotherapy. Pre- and posttreatment radionuclide ejection fractions were 65 and 45%, respectively; this patient had a posttreatment endomyocardial biopsy score of 1 (damage to <5% of myocytes). One additional patient at this dose level had an asymptomatic biopsy score of 1, with a decrease in ejection fraction from 62 to 43%; this recovered to 58% 5 months after completion of chemotherapy. Six additional patients treated at lower dose levels had abnormal posttreatment endomyocardial biopsies without abnormal posttreatment ejection fractions. Nine patients received only one cycle of chemotherapy: five patients due to decreased cardiac ejection fraction following cycle 1 (two of these patients had normal endomyocardial biopsies, and two patients had biopsy scores of 1); one patient secondary to tumor progression following cycle one; one patient due to persistently detectable Clostridium difficile toxin in the stool; one patient refused cycle two; and one patient died following cycle one of complications related to sepsis. A single patient experienced a grand mal seizure associated with orthostatic hypotension, which was considered the dose-limiting toxicity. The median duration (over two cycles) of granulocytopenia (absolute granulocyte count <500/microliter) at the maximally tolerated dose level of 150 mg/m2 was 8.5 days (range, 5-13 days), and the median duration of thrombocytopenia (platelets <20,000/microliter) was 2.5 days (range, 0-9 days). The median duration of hospitalization including chemotherapy administration was 23 days (range, 19-36 days). Other toxicities included stomatitis, fever, diarrhea, and emesis. One patient developed acute leukemia 54 months posttreatment. We conclude that two courses of high-dose cyclophosphamide and doxorubicin using granulocyte colony-stimulating factor are feasible and safe with tolerable myocardial toxicity as evidenced by serial endomyocardial biopsies. The dose-limiting toxicity encountered was a grand mal seizure. The recommended Phase II dose is doxorubicin 150 mg/m2 administered as a 96-h infusion on days 1-4, with cyclophosphamide 4. 2 g/m2 on day 5 and G-CSF 5 microgram/kg/day started on day 6 and administered until the total WBC is above 10,000/microliter for three consecutive days.

Adult↗
PubMed1976

Comparative study of cyclophosphamide, 6-mercaptopurine, azathiopurine and methotrexate. Relative effects on the humoral and the cellular immune response in the mouse.

The effects of cyclophosphamide, methotrexate, azathioprine and 6-mercaptopurine on the concomitant development of the humoral and the cellular immune responses of mice to a single antigen, the El4 tumour cell, were investigated. The measurements of cellular and humoral immunity were carried out in the same animal using lymphocyte and antibody mediated lysis of the El4 cell, a measurement system independent of underlying anti-inflammatory effects. A regimen of daily cyclophosphamide had a more pronounced suppressive effect on the humoral response than on the cellular response, in agreement with other investigators. A single low dose of cyclophosphamide stimulated the cellular response and suppressed the humoral response. Single or multiple high doses of cyclophosphamide maximally suppressed both the cellular and humoral response. Azathioprine and 6-mercaptopurine, in contrast to the results of other investigations, caused equivalent inhibition of both the humoral and cellular responses and thus lacked selectivity. Methotrexate also provided equivalent inhibition of both the humoral and cellular responses at all dose levels investigated.

Animals↗
PubMed1998

Type II alveolar epithelial cells and cyclophosphamide-induced lung fibrosis.

The aim of the study was to evaluate the quantitative and morphological changes in type II alveolar epithelial cells in the course of cyclophosphamide-induced lung damage. The experiments used 40 Wistar rats, of 170 g body weight. The animals were divided into two experimental groups. Group I animals were given cyclophosphamide (Endoxan-ASTA) in a single intraperitoneal dose of 150 mg/1kg b.w./1 ml PBS. Group II (control) received 1 ml PBS. All the animals were sacrificed after 1, 7, 14 and 28 days following intraperitoneal cyclophosphamide or PBS administration. Morphological examinations of pulmonary tissue were based on ultrastructural analysis in the transmission electron microscope. Quantitative studies of type II cells were performed basing on sections stained for alkaline phosphatase. The results of the quantitative analysis showed statistically significant alterations in the number of type II alveolar epithelial cells after 14 and 28 days following cyclophosphamide administration, compared with the respective control groups. The increase in the number of type II cells was accompanied by the intensification of fibroplasia processes within the interstitium of the interalveolar septa of the lungs. Ultrastructural exponents of active participation of type II cells in fibroplasia processes were found.

Animals↗
PubMed1975

Kinetics of the reactive cell clones after immunosuppression and induction of tolerance: (1) inhibition of 19 S and 7 S plaque-forming cells in the primary and secondary immune response to sheep red blood cells by cyclophosphamide and 036.5122 (Asta).

The kinetics of the reactive cell clones after primary and secondary immunization with SRBC1) modified by cyclophosphamide and a newly synthesized cyclophosphamide analogue 036.5122 (Asta), have been studied. After primary immunization, both substances caused a severe and dose dependent depletion of 19 S PFC2). The 7 S PFC in the late primary response were only slightly inhibited by cyclophosphamide in low dose ranges, indicating, that sensitization could not be prevented by this substance. In contrast, 0.36.5122 was fully able to suppress 7 S PFC. Thus, treatment with 0.36.5122 after primary immunization can fully prevent the expression of the specific response. Experiments dealing with inhibition of a secondary immune response revealed that both test substances were able to strongly suppress the 19 S as well as the 7 S PFC. In general, 036.5122 demonstrates a higher suppressive potency, and the timing of its application for optimal suppression is less delicate than that of cyclophosphamide. 036.5122 was equally well inhibitory, whether given directly before or after antigenic challenge. The hypothesis is discussed, whether the immunosuppressive effect of 036.5122 given before antigenic challenge in the secondary immune response is due to cytotoxic damage of antigen reactive clones stimulated by persisting antigen.

Animals↗
PubMed1999

Cyclophosphamide-induced bladder cancer.

Cyclophosphamide is a known risk factor for the development of bladder cancer. We report 3 cases of cyclophosphamide-induced bladder carcinoma in 2 individuals treated for Wegener's granulomatosis and in 1 patient with neuroblastoma. Included is a review of the literature on the relative risk of cyclophosphamide therapy, the mechanisms by which the drug induces bladder cancer, and suggestions on how to minimize the deleterious effects of the drug. We conclude that cyclophosphamide should be used in the lowest possible dose and that patients receiving more than 20 g of the drug should undergo routine urinalysis for microscopic hematuria every 3-6 months for up to 11 years after the treatment has been discontinued. Dosages as small as 600 mg in the pediatric population may warrant lifelong monitoring.

Journal Article↗
PubMed1979

Aspirin, cyclophosphamide, and dexamethasone effects on experimental secondary herpes simplex uveitis.

The effects of aspirin, cyclophosphamide, and dexamethasone on secondary herpes simplex uveitis were studied in rabbits. Neither daily treatment with aspirin (rectal suppositories, 650 mg begun 24 hours before challenge) nor cyclophosphamide injections every two days (80 mg begun eight days before challenge) had any effect on the severity of the uveitis, on the rise in intraocular pressure (IOP), or on the host's immune responses. As in the control animals, infectious herpes simplex virus (HSV) could not be isolated from iris tissues of either aspirin- or cyclophosphamide-treated rabbits. On the other hand, twice-daily treatment with topical dexamethasone (0.1% drops begun 24 hours before challenge) lessened the severity of the uveitis appreciably and suppressed the rise in IOP, but iris tissues yielded infectious HSV in two of ten eyes. Although the dexamethasone had no effect on the neutralizing-antibody or macrophage migration inhibition factor, it markedly suppressed the chemotactic activity of the aqueous humor for both polymorphonuclear leukocytes and macrophages.

Animals↗
PubMed1992

Immunotherapy with a tumor-infiltrating lymphocyte clone, soluble antigen, and cyclophosphamide.

A tumor-specific cytotoxic T-lymphocyte clone derived from bulk cultures of tumor-infiltrating lymphocytes attenuated the outgrowth of methylcholanthrene (MCA)-induced fibrosarcomas in C3H/HeJ mice. In 4-hour chromium 51-release assays, bulk cultures of tumor-infiltrating lymphocytes showed nonspecificity for MCA-induced tumors (MCA-F, MCA-D, MCA-SP), YAC-1, and EL-4. In contrast, a cytotoxic T-lymphocyte-cloned line specifically killed MCA-F, but not MCA-D or MCA-SP. Cytotoxic T-lymphocyte line 8 protected syngeneic hosts in local and systemic adoptive transfer assays. Hosts bearing 4-day-established MCA-F tumor cells received single agents or combinations of isoelectrophoretically purified butyl alcohol-extracted tumor-specific transplantation antigen (1 microgram/wk), cyclophosphamide (20 mg/kg on days 4 and 11), and/or cytotoxic T-lymphocytes (1 x 10(7) cells on days 7 and 14). While the mean tumor diameter was 11.6 +/- 1.3 mm in untreated hosts or after single treatments, the combination of tumor-specific transplantation antigen and cyclophosphamide along with the cytotoxic T-lymphocyte clone resulted in tumor diameters of 1.8 +/- 0.5 mm. The triple combination prolonged host survival from 39.6 +/- 1.6 to 57.2 +/- 4.7 days compared with antigen and cyclophosphamide treatment.

Animals↗
PubMed1999

Determination of cyclophosphamide and ifosphamide in urine at trace levels by gas chromatography/tandem mass spectrometry.

A specific and sensitive method based on gas chromatography/tandem mass spectrometry with on-column injection was developed to quantify simultaneously cyclophosphamide and ifosphamide in urine by using trophosphamide as an internal standard. The urine samples were extracted with diethyl ether and derivatization was performed with heptafluorobutyric anhydride. The detection limits of cyclophosphamide and ifosphamide in urine samples were 0.1 and 0.5 ng ml(-1), respectively, with a signal-to-noise ratio of 3 : 1. The sensitivity, the specificity and the low cost of the instrumentation involved make this method suitable for economical analysis on a large scale, such as for the biological monitoring of occupational exposure to cyclophosphamide and ifosphamide in production plants and in hospitals during their pharmacological use.

Cyclophosphamide↗
PubMed1996

Evaluation of adjuvant estramustine phosphate, cyclophosphamide, and observation only for node-positive patients following radical prostatectomy and definitive irradiation. Investigators of the National Prostate Cancer Project.

In 1978 the National Prostate Cancer Project launched two protocols evaluating adjuvant therapy following surgery (Protocol 900) or irradiation (Protocol 1,000) for clinically localized prostate cancer. All patients underwent staging pelvic lymphadenectomy. Following definitive treatment, patients were randomized to either cyclophosphamide 1 gram/m2-IV every 3 weeks for 2 years, estramustine phosphate 600 mg/m2-po daily for up to 2 years, or to observation only. Patient accession closed in 1985 and includes 184 to Protocol 900 (170 evaluable) and 253 to Protocol 1,000 (233 evaluable). Lymph node involvement was identified in 198 patients (49% of total), 29% in Protocol 900, 63% in Protocol 1,000. Median progression-free survival (PFS) for patients with nodal involvement in Protocol 1,000 receiving estramustine phosphate adjuvant was longer (37.3 mo) compared to cyclophosphamide (30.9 mo) and to no treatment (20.9 mo). Median PFS for patients with limited nodal disease in Protocol 1,000 was longer (39.9 mo), regardless of adjuvant, compared to extensive nodal disease (20.7 mo). However for patients with extensive nodal involvement, those receiving adjuvant estramustine phosphate experienced a significantly longer median PFS (32.8 mo) compared to adjuvant cyclophosphamide (22.7 mo) and no adjuvant (12.9 mo). We conclude that adjuvant estramustine phosphate is of benefit in prostate cancer patients with extensive pelvic node involvement receiving irradiation as definitive treatment.

Antineoplastic Agents, Alkylating↗
PubMed1997

A dose-intensive, cyclophosphamide-based regimen for the treatment of recurrent/progressive or advanced solid tumors of childhood: a report from the Australia and New Zealand Children's Cancer Study Group.

BACKGROUND: Children with solid tumors that progress or recur after conventional multimodality therapies have a very poor prognosis. In a pilot study, vincristine, etoposide, and dose-escalated cyclophosphamide (VETOPEC) was shown to be a promising salvage regimen. Continued accrual of patients and increased duration of follow-up has resulted in substantial experience with VETOPEC. METHODS: Between May 1991 and March 1994, 56 pediatric patients from 6 centers were enrolled in this study; 44 had recurrent or progressive tumors (Group A) and 12 had newly diagnosed, advanced tumors with a very poor prognosis (Group B). The VETOPEC regimen was comprised of vincristine, 0.05 mg/kg, on Days 1 and 14; etoposide, 2.5 mg/kg, on Days 1, 2, and 3; and fractionated, dose-escalated cyclophosphamide on Days 1, 2, and 3. The initial cyclophosphamide dose was 90 mg/kg (2.7 g/m2)/cycle with an escalation of 15 mg/kg/cycle in each subsequent cycle, to a maximum (over 6 cycles) of 165 mg/kg (5.0 g/m2)/cycle. Tumor response was evaluated every two to three cycles and included central review of imaging. RESULTS: The combined and partial response rates for Groups A and B were 66% (25 of 38 patients) and 91% (10 of 11 patients), respectively. In Group A, best evaluable responses and event free (EF) survivors were observed with: brain tumors (7 of 9 patients; 2 EF at 39 and 45 months [mos], respectively), Wilms' tumor (6 of 7 patients; 3 EF at 37-49 mos), and lymphoma (4 of 4 patients; 2 EF at 52 and 59 mos, respectively); in Group B best evaluable responses and EF were observed with: neuroblastoma (5 of 6 patients; 1 disease free at 57 mos) and rhabdomyosarcoma (4 of 4 patients; no survivors). Hematologic toxicity was limiting despite support with myeloid growth factors in 33 patients. Four deaths in Group A and one in Group B were directly associated with this toxicity. Specifically, no cases of drug-related myocardial toxicity or pneumonitis were observed. CONCLUSIONS: This chemotherapy regimen with its intense scheduling produced a high response rate and appreciable survival in patients with a variety of recurrent, progressive, or advanced solid tumors of childhood.

Adolescent↗