000			03688nam a2200325 4500
001			ESSALUD
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040			_aBMG
041			_aeng
100			_aNathan, Steven D. _eAutor _953690
245			_aPhase 3 trials of inhaled treprostinil for idiopathic pulmonary fibrosis
300			_apáginas: 115-126
520			_aBackground: Two phase 3, randomized trials of inhaled treprostinil for idiopathic pulmonary fibrosis (IPF) were conducted on the basis of preclinical and clinical evidence of an antifibrotic mechanism. TETON-2 was completed first, and results were published; the results of TETON-1 and of both trials combined are reported here. Methods: In the double-blind TETON-1 trial, we randomly assigned patients with IPF to receive inhaled treprostinil or placebo (12 breaths four times daily). The primary end point was the change in forced vital capacity (FVC) at week 52. Secondary end points, which were analyzed in a prespecified order to control for multiplicity, were clinical worsening (the first occurrence of death from any cause, hospitalization for a respiratory cause, or a relative decline of ≥10% in the percentage of predicted FVC) and acute exacerbation of IPF (each assessed in a time-to-event analysis), survival, change in percentage of predicted FVC, quality of life, and change in diffusion capacity of the lungs for carbon monoxide at week 52. Results: A total of 598 patients underwent randomization and received at least one dose of treprostinil (299 patients) or placebo (299 patients). Of these, 434 completed the assessments through week 52 (218 in the treprostinil group and 216 in the placebo group). The mean age of the patients was 73.0 years, 77.3% were men, and 77.6% were receiving background antifibrotic therapy; the percentage of predicted FVC at baseline was 74.6%. The median change in FVC at week 52 was −43.3 ml (95% confidence interval [CI], −92.1 to −9.1) with treprostinil and −196.2 ml (95% CI, −227.1 to −155.6) with placebo (difference, 130.1 ml; 95% CI, 82.2 to 178.1; P<0.001). Clinical worsening occurred in 95 patients (31.8%) with treprostinil and in 133 patients (44.5%) with placebo (hazard ratio, 0.67; 95% CI, 0.52 to 0.88; P=0.003). No significant difference was observed in the time to an IPF exacerbation, and no further inferences regarding secondary end points were made. The most frequent adverse event was cough (reported in 54.8% of the patients in the treprostinil group and 33.1% patients in the placebo group). Discontinuation of treprostinil or placebo occurred in 40.5% and 32.8% of the patients, respectively, with adverse event being the primary reason (20.7% and 14.7%). Efficacy and safety outcomes were similar in analyses of the combined trial data. Conclusions: In patients with IPF, treatment with inhaled treprostinil led to a smaller decline in FVC and fewer clinical-worsening events than placebo over the course of 52 weeks.
650			_aMEDICINA CLÍNICA _933681
650			_aENFERMEDAD PULMONAR INTERSTICIAL _953691
650			_aMEDICINA CLINICA AMBULATORIO _953692
650			_aFIBROSIS PULMONAR _953693
650			_aNEUMOLOGÍA _925628
650			_aCUIDADOS INTENSIVOS _95208
700			_aSmith, Peter _953694
700			_aDeng, Chunqin _953695
700			_aKing, Christopher S. _953696
700			_aDe Salvo, Maria _953697
700			_aWeigt, S. Samuel _953698
700			_aPandya, Sahil _953699
773	0		_022717 _922635 _dMassachusetts NEJM Group _oNEJM002 _tThe New England Journal of Medicine _wESSALUD _x0028-4793
942			_cARTICULOS _e2026-07-30 _zsqb
999			_c22729 _d22729