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PubMed1996

Cost-effectiveness of adjuvant chemotherapy with cyclophosphamide+methotrexate+fluorouracil in patients with node-positive breast cancer.

BACKGROUND: The analysis of published survival curves can be used as the basis for incremental cost-effectiveness analyses in which two treatments are compared with each other in terms of cost per life year saved. In patients with node-positive breast cancer adjuvant chemotherapy with cyclophosphamide+ methotrexate+fluorouracil has been reported to improve survival in comparison with patients who are not given this treatment. METHODS: To assess the pharmacoeconomic profile of this adjuvant chemotherapeutic regimen in terms of cost per life-year gained, we conducted an incremental cost-effectiveness analysis in which the Gompertz model was used to calculate the lifetime estimate of the patient-years gained by treated subjects compared to controls. RESULTS: Using data from a published, controlled long-term trial involving 207 patients treated with cyclophosphamide+methotrexate+fluorouracil and 179 controls, we estimated that this adjuvant chemotherapy improved life expectancy by 357 patient-years per 100 subjects. Direct costs, which were almost exclusively related to the administration of chemotherapy, were estimated to be US $159,516 per 100 patients. On the basis of these data, adjuvant chemotherapy was found to imply an incremental cost of US $447 per life-year saved. CONCLUSIONS: The cost-effectiveness ratio of adjuvant chemotherapy with cyclophosphamide+methotrexate+fluorouracil in patients with node-positive breast cancer seems to be particularly favourable in comparison with estimates of cost per life-year saved previously calculated for other types of pharmacological intervention.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2006

Low-dose cyclophosphamide modulates galectin-1 expression and function in an experimental rat lymphoma model.

In recent years, one of the most important insights into tumor immunity was provided by the identification of negative regulatory pathways and immune escape strategies that greatly influence the magnitude of antitumor responses. Galectin-1 (Gal-1), a member of a family of highly conserved beta-galactoside-binding proteins, has been recently shown to contribute to tumor cell evasion of immune responses by modulating survival and differentiation of effector T cells. However, there is still scarce information about the regulation of Gal-1 expression and function in vivo. Here we show that administration of a single low-dose cyclophosphamide (Cy), which is capable of restraining metastasis in the rat lymphoma model L-TACB, can also influence Gal-1 expression in primary tumor, metastasis, and spleen cells and modulate the effects of this protein on T cell survival. A time-course study revealed a positive correlation between Gal-1 expression and tumor volume in primary tumor cells. Conversely, Gal-1 expression was significantly reduced in spleen cells and lymph node metastasis throughout the period studied. Interestingly, cyclophosphamide treatment was capable of restoring the basal levels of Gal-1 expression in primary tumors and spleens. In addition, this antimetastatic agent rendered spleen T cells from tumor-bearing animals resistant to Gal-1-induced cell death. Our results suggest that, in addition to other well-known functions of cyclophosphamide, this immunomodulatory agent may also modulate Gal-1 expression and function during tumor growth and metastasis with critical implications for tumor-immune escape and immunotherapy.

Animals↗
PubMed2004

Combined thalidomide and cyclophosphamide treatment for refractory or relapsed multiple myeloma patients: a prospective phase II study.

Thalidomide is an effective agent for patients with refractory multiple myeloma (MM) with a response rate of 30-40% at doses of 200-800 mg but with considerable side effects. We questioned whether lower doses of thalidomide in combination with a daily dose of cyclophosphamide might be an effective regimen with fewer side effects. We included 38 patients with relapsed or refractory MM. The median doses of thalidomide and cyclophosphamide were 100 and 95 mg/day, respectively. Side effects were observed in all patients, with neurotoxicity as the most troublesome. With a median follow-up of 14 months 84% of the patients responded, including 64% partial responses. The median time of progression-free survival was 30 months and the median overall survival time was 20 months. In conclusion, the results demonstrate that the combination of low-dose thalidomide with a daily dose of cyclophosphamide is an effective regimen with a high overall response rate and manageable side effects.

Aged↗
PubMed2003

Amifostine does not reduce the toxicity of the fludarabine and cyclophosphamide regimen in patients with chronic lymphocytic leukemia.

PURPOSE: Amifostine is an organic thiophosphate that may selectively protect normal tissues from the toxicities of chemotherapy. The combination of fludarabine and cyclophosphamide (FC) is highly active in patients with chronic lymphocytic leukemia (CLL). Infection is a serious toxicity of the FC regimen. METHODS: Amifostine was added to the FC regimen in a phase II study of 46 patients with CLL. Patients received FCA (fludarabine 30 mg/m(2) i.v. daily for 3 days, cyclophosphamide 300 mg/m(2) i.v. daily for 3 days, and amifostine 500 mg i.v. over 15 min daily for 3 days starting 30 min before cyclophosphamide) at intervals of 4-6 weeks for a maximum of six courses. RESULTS: Patients receiving FCA had equivalent rates of sepsis, early death, objective response and survival to those observed in a prior series of 78 patients treated with FC. Amifostine-associated toxicities included nausea, vomiting, and hypotension. CONCLUSION: The study amifostine regimen did not reduce the toxicity or activity of the FC regimen in patients with CLL.

Amifostine↗
PubMed2006

Population analysis of the pharmacokinetics and the haematological toxicity of the fluorouracil-epirubicin-cyclophosphamide regimen in breast cancer patients.

PURPOSE: The aims of the study were (a) to characterise the pharmacokinetics (PK), including inter-individual variability (IIV) and inter-occasion variability (IOV) as well as covariate relationships and (b) to characterise the relationship between the PK and the haematological toxicity of the component drugs of the fluorouracil (5-FU)-epirubicin (EPI)-cyclophosphamide (CP) regimen in breast cancer patients. PATIENTS AND METHODS: Data from 140 breast cancer patients, either within one of different studies or in routine clinical management, were included in the analyses. The patients were all treated with the fluorouracil-epirubicin-cyclophosphamide (FEC) regimen every third week for 3-12 courses, either in standard doses, i.e. 600/60/600 mg/m(2) of 5-FU, EPI and CP, respectively, or according to a dose escalation/reduction protocol (tailored dosing). PK data were available from 84 of the patients, whereas time-courses of haematological toxicity were available from 87 patients. The data analysis was carried out using mixed effects models within the NONMEM program. RESULTS: The PK of 5-FU, EPI and 4-hydroxy-cyclophosphamide (4-OHCP), the active metabolite of CP, were described with a one-compartment model with saturable elimination, a three-compartment linear model and a two-compartment linear model, respectively. No clinical significant correlation was found between PK across drugs. The unexplained variability in clearance was found to be less within patients, between courses (inter-occasion variability, IOV) than between patients (inter-individual variability, IIV) for EPI and 5-FU. For 4-OHCP, however, the IIV diminished by approximately 45% when significant covariates were included and the final population model predicts an IIV that is equal to IOV. Significant covariates for elimination capacity parameters were serum albumin (5-FU, EPI and 4-OHCP), creatinine clearance (5-FU), bilirubin (EPI) and body surface area (BSA) (4-OHCP). Elimination capacity of 5-FU and EPI was not related to BSA and for none of the studied drugs did body weight explain the PK variability. The time-course of haematological toxicity after treatment was well described by a semi-physiological model that assumes additive haematological toxicity between CP and EPI with negligible contribution from 5-FU. The influence of G-CSF could be incorporated into the model in a mechanistic manner as shortening the maturation time to 43% of the normal duration and increasing the mitotic activity to 269% of normal activity. CONCLUSIONS: The models presented describe the dose-concentration-toxicity relationships for the FEC therapy and may provide a basis for implementation and comparison of different individualisation strategies based on covariates, therapeutic drug monitoring and/or pharmacodynamic (PD) feedback. The PD model extends on previous semi-mechanistic models in that it also takes G-CSF administration into account.

Antineoplastic Combined Chemotherapy Protocols↗
PubMed2001

Primary breast tumor levels of suspected molecular determinants of cellular sensitivity to cyclophosphamide, ifosfamide, and certain other anticancer agents as predictors of paired metastatic tumor levels of these determinants. Rational individualization of cancer chemotherapeutic regimens.

PURPOSE: Cyclophosphamide is one of the most frequently used agents in the neoadjuvant, adjuvant, and high-dose chemotherapeutic treatment of breast cancers. Preclinical models indicate that cellular sensitivity to cyclophosphamide and other oxazaphosphorines, e.g., ifosfamide, is inversely related to the cellular content of two aldehyde dehydrogenases, viz ALDH1A1 and ALDH3A1, and glutathione. Breast tumor levels of these "determinants of cellular sensitivity to the oxazaphosphorines" are known to vary widely, and the decision as to whether or not to use an oxazaphosphorine as part of the therapeutic strategy to treat breast cancer in any given patient is likely to depend, in large part, on the levels of these determinants in that cancer. ALDH1A1, ALDH3A1, and glutathione levels can be easily quantified in primary breast tumors and in detectable metastatic breast tumors present in axillary lymph nodes because the amounts of tissue required for the desired analysis can be readily obtained, whereas these levels cannot be quantified in residual metastatic breast cancer cell populations, i.e., those that escape detection and/or that are inaccessible to surgical harvest. The inability to directly quantify residual metastatic breast cancer cell ALDH1A1, ALDH3A1, and glutathione levels would not preclude a rational decision with regard to the inclusion/exclusion of an oxazaphosphorine as part of the chemotherapeutic strategy intended to eradicate residual metastatic breast cancer cells if primary breast tumor levels of these determinants reliably predicted those in metastatic breast cancer cells. METHODS: ELISAs and spectrophotometric assays were used to quantify enzyme and glutathione levels in paired human primary and locally advanced metastatic breast tumor samples. RESULTS: Primary breast tumor ALDH1A1 and ALDH3A1 levels were highly predictive of their respective levels in paired metastatic breast tumors present in axillary lymph nodes (r2 = 0.80 and 0.85, respectively). On the other hand, those of glutathione were relatively poorly predictive of its levels in paired metastatic offshoots (r2 = 0.35). Primary breast tumor levels of some additional enzymes known to catalyze the detoxification/toxification of various anticancer agents, though not of cyclophosphamide, were poorly predictive (DT-diaphorase and glutathione S-transferases alpha, mu, and pi) or not predictive (cytochrome P450 1A1) of their respective levels in paired metastatic offshoots. CONCLUSION: Since ALDH1A1, ALDH3A1 and, to a lesser extent, glutathione levels in primary breast tumors reliably predicted those in detectable and easily accessible metastatic breast cancer cell populations, viz those in axillary lymph nodes, they are also likely to be predictive of these levels in undetectable and/or relatively inaccessible metastatic breast cancer cell populations. Thus, quantification of primary breast tumor ALDH1A1, ALDH3A1 and, to a lesser extent, glutathione levels prior to the initiation of not only neoadjuvant but also adjuvant and high-dose breast cancer chemotherapy is likely to be of value in the rational design of individualized chemotherapeutic regimens intended to eradicate breast cancer cells with a minimum of untoward effects.

Aldehyde Dehydrogenase↗
PubMed2001

Cyclophosphamide metabolism in children following a 1-h and a 24-h infusion.

PURPOSE: The pharmacokinetics and metabolism of cyclophosphamide (CPA) when given as a 1-h and a 24-h infusion to children were compared. METHODS: Thirteen children with a variety of different malignancies received an identical dose of cyclophosphamide as a 1- and 24-h infusion. In each case the concentration of CPA and its principal metabolites were measured by a thin-layer-chromatography-photographic-densitometry technique. RESULTS: Cyclophosphamide clearance was greater during the 24-h infusion, following time-dependent increases in the metabolism of the drug (autoinduction) (median 5.1 vs 3.1 l/h/m2: P = 0.037). Autoinduction was seen in five children (38%), producing a median end of infusion concentration of 49% (range 28-89%) of the maximum and was not accompanied by an increase in the production of the principal inactive metabolites carboxyphosphamide and dechloroethylcyclophosphamide. CONCLUSIONS: These results suggest potential benefits of prolonging the infusion of CPA in clinical practice.

Adolescent↗
PubMed1996

Phase II study of second-line treatment with high-dose cyclophosphamide in recurrent metastatic breast cancer.

A total of 78 patients with second recurrence or progression of histologically verified breast cancer were treated with single-agent cyclophosphamide given at 2.5 g/m2 by i.v. infusion every 3 weeks along with mesna support. All had previously been treated with epirubicin and cisplatin or epirubicin alone. Toxicity was predominantly hematologic: WHO grade III+IV toxicity was found in 95% of cases. The overall response rate was 26.7% (95% confidence limits, 15.8-41.4%), with 7% of patients achieving a complete response (CR) and 19.7%, a partial response (PR). The median duration of CRs and PRs was 11 and 5 moths, respectively. The response rate observed for patients previously treated with epirubicin alone was 30.5% in contrast to the 8.3% recorded for patients previously treated with cisplatin plus epirubicin. Thus, an indication of cross-resistance was absent between cyclophosphamide and epirubicin but possible between cyclophosphamide and cisplatin.

Adult↗
PubMed1999

Treatment of poor-prognosis extensive disease small-cell lung cancer with an all-oral regimen of etoposide and cyclophosphamide - a Southwest Oncology Group clinical and pharmacokinetic study.

PURPOSE: An all-oral regimen of etoposide and cyclophosphamide was developed for use in poor-prognosis extensive disease small-cell lung cancer. Limited pharmacokinetic sampling was used to derive a pharmacodynamic model predictive of myelosuppression early in the course of therapy. PATIENTS AND METHODS: Eligible patients were chemotherapy-naive and had extensive disease small-cell lung cancer with either SWOG performance status 2 or serum albumin <3.5 g/dl. The first cohort (n = 18) received etoposide orally at 50 mg daily and cyclophosphamide orally at 50 mg daily days 1-14 every 28 days. Due to good hematologic tolerance, the second cohort (n = 39) received both agents orally at 50 mg twice daily days 1-14 every 28 days. Plasma etoposide levels were determined in samples drawn at baseline, and at 1 h, 2 h, and 23.5 h (trough) after the first dose. Linear regression analysis was used to determine pharmacokinetic and demographic parameters predictive of myelosuppression. RESULTS: A total of 173 treatment cycles were delivered. Patients on the daily regimen had a 22% response rate (complete and partial), a 22% unconfirmed response rate, and a 5-month median survival, while patients on the twice-daily regimen had a 28% response rate (complete and partial), a 13% unconfirmed response rate, and a 7-month median survival. Granulocytopenia and alopecia were the most common toxicities seen. Significant granulocytopenia could be predicted for the twice-daily regimen according to the formula ln(AGC nadir)=7.80 - 1.88(trough), with an increased incidence of granulocytopenia if the etoposide trough value was >/=1.49 microg/ml. CONCLUSION: Oral etoposide and oral cyclophosphamide given days 1-14 every 28 days is well tolerated and results in an acceptable response rate and median survival in poor-prognosis (poor performance status or low serum albumin) extensive disease small-cell lung cancer. A trough etoposide level obtained within 24 h of starting therapy can predict severe granulocytopenia.

Administration, Oral↗
PubMed2006

Mitoxantrone versus cyclophosphamide in secondary-progressive multiple sclerosis: a comparative study.

Fifty secondary progressive multiple sclerosis (SPMS) patients who had lost one or more EDSS points in the prior two years were selected to receive either cyclophosphamide (25 patients, 13 females, 12 males, F/M = 1.08; mean age: 42.4 years; mean disease duration: 13.3 years; mean EDSS at study entry: 5.7) or mitoxantrone (25 patients, 14 females, 11 males, F/M = 1.27; mean age: 38.2 years; mean disease duration: 11.5 years; mean EDSS at study entry: 5.5). SPMS patients were treated for two years with clinical evaluation (relapse rate, disability progression) every three months and radiological imaging (conventional magnetic resonance imaging) before therapy initiation and at the end of the first and second years of therapy. Safety profile and costs of the two therapeutic protocols were also analysed. In terms of clinical and radiological measures the drugs exerted a quite identical effect on both, and produced a significant reduction in both relapse rate (mitoxantrone Mito): p = 0.001, cyclophosphamide (Cy): p = 0.003) and disability progression (Mito: p = 0.01; Cy: p = 0.01). Subgroups of mitoxantrone- and cyclophosphamide-responding patients were identified (14/25 and 17/25, respectively) and were characterized by a significantly shorter duration of the secondary progressive phase of the disease. In these subgroups, the improvement in the EDSS score at the end of therapy was highly significant (p<0.0001 for Mito, p = 0.0004 for Cy). The safety profiles of both drugs were acceptable; however, the Cy-based therapy protocol was significantly less expensive. We conclude that Cy should be considered as a therapeutic option in rapidly deteriorating SPMS patients.

Adult↗
PubMed2005

Bendamustine, vincristine and prednisone (BOP) versus cyclophosphamide, vincristine and prednisone (COP) in advanced indolent non-Hodgkin's lymphoma and mantle cell lymphoma: results of a randomised phase III trial (OSHO# 19).

PURPOSE: The purpose of this study was to compare the efficacy and toxicity of bendamustine, vincristine + prednisone (BOP) with a standard regimen of cyclophosphamide, vincristine + prednisone (COP) in patients with previously untreated advanced indolent non-Hodgkin's lymphoma (NHL) and mantle cell lymphoma. METHODS: A total of 164 patients with follicular lymphoma (grade 1/2), mantle cell lymphoma or lymphoplasmacytic lymphoma (immunocytoma) was randomised to treatment with vincristine 2 mg (day 1) and prednisone 100 mg/m2 (days 1-5) + bendamustine 60 mg/m2 (days 1-5) or + cyclophosphamide 400 mg/m2 (days 1-5) for a total of eight 21-day cycles. RESULTS: The rate of complete remission was 22% with BOP and 20% with COP. The projected 5-year survival rate was 61% with BOP and 46% with COP. The BOP-associated 5-year survival advantage almost reached significance in the subgroup of patients who responded to therapy (74% vs. 56%; P = 0.05), and did reach significance in responders who did not receive interferon maintenance therapy (70% vs. 47%; P = 0.03). Toxicity was acceptable in both treatment groups, although alopecia and leucopenia were more severe with COP. CONCLUSIONS: Bendamustine can efficaciously and safely replace cyclophosphamide, as used in standard COP therapy, for the treatment of patients with indolent NHL and mantle cell lymphoma. Long-term survival data suggest a clinically significant benefit for patients treated with BOP.

Adult↗
PubMed2006

Epirubicin, cyclophosphamide and weekly paclitaxel as neoadjuvant chemotherapy for stage II and III breast cancer.

PURPOSE: To assess the efficacy and the toxicity of a new combination of epirubicin, cyclophosphamide and paclitaxel as neoadjuvant chemotherapy for breast cancer. METHODS: Patients with stage II and III breast cancer received 3-4 cycles of epirubicin 75 mg/m(2) plus cyclophosphamide 600 mg/m(2) on day 1, and paclitaxel at a dose of 100 mg on days 1, 8, 15 and 22 on a 28-day cycle. RESULTS: Forty-nine patients were enrolled in the study. Stage II was present in 16 patients (32.7%) and stage III in 33 patients (67.3%). Relevant toxicities were nausea/vomiting grades III-IV in 6 patients (12.2%) and neutropenia grade III-IV in 33 patients (67.3%). The overall clinical response rate was 83.7%. Partial response was observed in 25 patients (51%), complete response in 16 patients (32.7%), stable disease in 7 patients (14.3%) and progression in 1 patient. Thirty-three non-inflammatory breast cancer patients underwent surgery, 29 with breast-conserving surgery (87.9%). Pathological complete response was found in 5 patients (15.1%). CONCLUSIONS: The combination of epirubicin, cyclophosphamide and weekly paclitaxel as given in this study is safe and shows good activity in the neoadjuvant setting of stage II and III breast cancer patients.

Adult↗
PubMed2001

Treatment of focal glomerulosclerosis with pulse steroids and oral cyclophosphamide.

Patients with steroid-resistant nephrotic syndrome often have an unsatisfactory long-term outcome and are at risk of developing chronic renal failure. We prospectively treated 65 children with idiopathic steroid-resistant nephrotic syndrome and focal segmental glomerulosclerosis (FSGS) with intravenous pulses of corticosteroids and oral cyclophosphamide. Dexamethasone (5 mg/kg) or methylprednisolone (30 mg/kg) was administered intravenously, initially 6 pulses on alternate days, followed by 4 fortnightly and 8 monthly pulses. Oral cyclophosphamide therapy was given for 12 weeks and tapering doses of prednisolone were administered for 52 weeks. The mean age at treatment was 85.7+/- 44.9 months. Five patients developed serious infections during administration of initial alternate-day pulses and were excluded. Of 59 patients who completed initial alternate-day therapy, 17 had complete and 8 partial remission; 34 (57.6%) patients did not respond to treatment. The median urine protein to creatinine ratio decreased from 10.0 to 0.75 (P<0.005) and serum albumin increased from 1.9 g/dl to 2.4 g/dl (P<0.01). The median duration of follow-up after stopping pulse therapy was 25.6 months. Thirty-four patients were followed for more than 3 years (median 4.5 years). Of these, 22 (64.7%) patients had a favorable outcome; persistent complete remission was seen in 15 patients and steroid-responsive relapses in 7. Seven patients had non- nephrotic-range proteinuria, 2 had nephrotic-range proteinuria, and 3 (8.8%) were in chronic renal failure. There was no significant difference in the short- and long-term outcome of patients with initial (n=28) and late resistance (n=31). The outcome in patients receiving intravenous dexamethasone (n=48) or methylprednisolone (n=11) was also similar. The chief side effects included worsening of height standard deviation score (47.4%), transient hypertension (42.5%), and serious infections (18.5%). We conclude that prolonged treatment with intravenous corticosteroids and oral cyclophosphamide is beneficial in patients with steroid-resistant FSGS. Expensive protocols can be successfully modified and used, depending upon the availability of health resources.

Administration, Oral↗
PubMed2005

Effect of cysteine protease inhibitor Ep-475 on TNF-alpha-independent cyclophosphamide-induced apoptosis in mouse lymphosarcoma LS cells.

Cyclophosphamide 1.5-2.0-fold increased activity of cathepsins B and L in tumor tissue of mouse lymphosarcoma LS and caused tumor regression. The effect was most pronounced on day 5 after treatment. Twofold treatment with a selective cathepsin inhibitor Ep-475 slightly stimulated tumor growth in control mice and significantly reduced the antitumor effect of cyclophosphamide. Lysosomal cysteine proteases cathepsins B and L are involved, but do not play a key role in TNF-alpha-independent apoptosis in LS cells induced by cyclophosphamide.

Animals↗
PubMed1978

Cyclophosphamide-induced remissions in advanced polyarteritis nodosa.

Two patients with far advanced polyarteritis nodosa involving multiple organ systems and with aneurysm formation demonstrable by celiac axis and renal arteriograms were treated with oral cyclophosphamide, 1 to 2 mg/kg/day, and alternate day prednisone therapy. Dramatic remissions of disease activity were achieved within weeks of initiation of therapy. Repeat angiograms obtained after one year revealed complete resolution of all aneurysms. Both patients are now receiving only cyclophosphamide and are maintained in complete remission 27 and 18 months after the start of therapy. Cyclophosphamide therapy can thus be highly effective even in far advanced polyarteritis nodosa.

Adult↗
PubMed1980

Recurrence of Wegener's granulomatosis after kidney transplantation. Successful re-induction of remission with cyclophosphamide.

A patient with Wegener's granulomatosis underwent successful kidney transplantation. After four years he had a recurrence of his disease while being maintained on azathiorpine. Substitution of cyclophosphamide for azathioprine resulted in a rapid remission of the Wegener's granulomatosis. Renal function has remained stable, and the patient has done well. As previous reports have suggested, it appears that cyclophosphamide is the immunosuppressive drug of choice in the treatment of Wegener's granulomatosis and that azathioprine is not as effective as cyclophosphamide in the treatment of this form of systemic vasculitis.

Adult↗
PubMed1984

Intravenous cyclophosphamide plus methylprednisolone in treatment of systemic rheumatoid vasculitis.

Systemic vasculitis in rheumatoid arthritis shows similarities to polyarteritis nodosa and may require equally aggressive therapy. Forty-five patients with systemic rheumatoid vasculitis were studied during treatment with either cyclophosphamide plus methylprednisolone given by intermittent bolus intravenous injection (21 patients) or a variety of other more conventional drug regimens (24 patients). In this open study, the intravenous treatment group had more severe initial disease, a higher incidence of neuropathy, and more frequent evidence of necrotizing arteritis on biopsy than the other treatment group. Despite this, intravenous cyclophosphamide plus methylprednisolone resulted in more frequent healing of vasculitic lesions including leg ulcers and neuropathy, a lower incidence of relapse, fewer serious complications, and a lower mortality than did other treatments. Toxic effects were similar in both study groups. Intravenous cyclophosphamide plus methylprednisolone is a useful early treatment for systemic rheumatoid vasculitis.

Adult↗
PubMed1986

Cyclophosphamide in the treatment of orbital vasculitis.

When vasculitis, an angiocentric and angiodestructive process, occurs in the orbit, the clinical presentation and radiographic findings resemble those of idiopathic inflammatory pseudotumor. Three patients, two men and a woman, 28 to 72 years old, initially thought to have "pseudotumor" failed to response to corticosteroid therapy. Orbital biopsy specimens in all patients disclosed vasculitis. There was no evidence of systemic vasculitis. High-dose prednisone effectively eliminated pain and reduced inflammation but did not adequately control fibrosis formation leading to ultimate loss of function. Each patient eventually lost an eye to this process. Therapy with cyclophosphamide, a B-cell cytotoxic drug, produced a prompt response in terms of eliminating pain, inflammation, and formation of fibrous tissue. Cyclophosphamide therapy has been instrumental in preserving sight in each patient's remaining eye. In such cases we believe the benefits of cyclophosphamide therapy outweight the known risks.

Adult↗