Inhaled steroids as prophylaxis for delayed pulmonary toxicity syndrome inbreast cancer patients undergoing high-dose chemotherapy and autologous stem cell transplantation
Ds. Mcgaughey et al., Inhaled steroids as prophylaxis for delayed pulmonary toxicity syndrome inbreast cancer patients undergoing high-dose chemotherapy and autologous stem cell transplantation, BIOL BLOOD, 7(5), 2001, pp. 274-278
Purpose. To evaluate the efficacy of inhaled fluticasone propionate (Floven
t) as prophylaxis against delayed pulmonary toxicity syndrome (DPTS) and de
cline in pulmonary function in breast cancer patients undergoing high-dose
chemotherapy with the conditioning regimen of cyclophosphamide, cisplatin,
and carmustine (CPB) followed by autologous stem cell transplantation (ASCT
).
Patients and Methods. Sixty-three consecutive patients with multinode-posit
ive or metastatic breast cancer undergoing high-dose chemotherapy with CPB
and ASCT who were treated at the Duke University Adult Bone Marrow Transpla
nt Program. Ad patients were started on inhaled fluticasone propionate, 880
mug every 12 hours, for 12 weeks from the start date of their CPB conditio
ning regimen. Pulmonary function tests (PFTs) with. a single-breath diffusi
ng capacity of carbon monoxide (DLCO) were performed pre-ASCT as well as ap
proximately 6 and 12 weeks post-ASCT. DPTS was defined as follows: (1) deve
lopment of a nonproductive cough and dyspnea with or without fever, plus a
fall in DLCO to less than 60% predicted; or (2) decline in DLCO to less tha
n 50% predicted with or without symptoms.
Results: Pulmonary function tests were done on all patients pre-ASCT, on 56
of tile 63 patients at a median of 44 days (range, 25 to 73 days) post-ASC
T, and on 51 of the 63 patients at a median of 96 days (range, 50 to 190 da
ys) post-ASCT. The PFTs showed an average of an 8% (+/- 26%) and 21% (+/- 2
2%) decline in DLCO. These declines compare favorably with our historical c
ontrol group of 45 consecutive breast cancer patients undergoing ASCT with
CPB as a conditioning regimen, who experienced average declines in DLCO of
29% (+/- 18%) (P < .001) and 33% (+/- 18%) (P < .001) at comparable time pe
riods post-ASCT. Delayed pulmonary toxicity syndrome occurred in 35% of tre
ated patients compared to 73% of the historical controls (P = .0003). No pa
tients died of DPTS or pulmonary problems, and there were no fungal pneumon
ias.
Conclusion: Inhaled fluticasone propionate may decrease the incidence of DP
TS in patients treated with CPB as a conditioning regimen for ASCT, as well
as help to preserve pulmonary function as measured by DLCO. These results
are worthy of further study in a randomized clinical trial.