Bronchoalveolar Lavage Aggravating Acute Exacerbations Of Idiopathic Pulmonary Fibrosis: When Is It Contraindicated In The Diagnostic Workup?

Author(s):  
Edwin L. Annan ◽  
Jaspreet S. Ahuja ◽  
Alan Legasto ◽  
Ravindra Rajmane
2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Ryo Yamazaki ◽  
Osamu Nishiyama ◽  
Sho Saeki ◽  
Hiroyuki Sano ◽  
Takashi Iwanaga ◽  
...  

AbstractSome patients with idiopathic pulmonary fibrosis (IPF) undergo recurrent acute exacerbations (AEs). This study aimed to elucidate the risk factors for recurrent AEs of IPF (AE-IPF). Consecutive patients with IPF admitted for their first AE-IPF between January 2008 and December 2018 were retrospectively recruited. Of 63 patients admitted for an AE-IPF and discharged alive, 9 (14.3%) developed a recurrence of AE within 1 year. The mean time to recurrence was 233 ± 103 days. Total doses (mg/month and mg/kg/month) of corticosteroids administered over day 1 to 30 after the AE were significantly higher in patients without recurrences of AE-IPF (5185 ± 2414 mg/month, 93.5 ± 44.0 mg/kg/month) than the doses in patients with recurrences (3133 ± 1990 mg/month, 57.2 ± 37.7 mg/kg/month) (p = 0.02 and p = 0.03, respectively). However, no differences were observed between the total doses of corticosteroids administered over days 31 to 60, 61 to 90, 91 to 120, and 151 to 180 after the AE. Furthermore, differences between the administration rates of immunosuppressive and antifibrotic treatments administered to the 2 patient groups were not significant. An increased total dose of corticosteroid administered over day 1 to 30 after an AE-IPF was associated with a decreased risk of subsequent recurrence of AE-IPF within 1 year after the first AE.


2013 ◽  
Vol 61 ◽  
pp. 160-163 ◽  
Author(s):  
Foteini Malli ◽  
Fotini Bardaka ◽  
Irene Tsilioni ◽  
Eleni Karetsi ◽  
Konstantinos I. Gourgoulianis ◽  
...  

2017 ◽  
Vol 83 (5) ◽  
Author(s):  
Gaetano Rea ◽  
Giuseppe Fiorentino ◽  
Antonio Corcione ◽  
Maurizia Lanza ◽  
Francesco Perna ◽  
...  

1991 ◽  
Vol 71 (5) ◽  
pp. 1688-1693 ◽  
Author(s):  
D. A. Schwartz ◽  
R. A. Helmers ◽  
C. S. Dayton ◽  
R. K. Merchant ◽  
G. W. Hunninghake

To investigate factors that determine bronchoalveolar lavage (BAL) cellularity in patients with idiopathic pulmonary fibrosis (IPF), we compared BAL cells in patients with IPF (n = 83) to both nonsmoking (n = 111) and smoking (n = 19) normal volunteers. Patients with IPF had higher concentrations of BAL total cells and alveolar macrophages than nonsmoking volunteers and more BAL neutrophils and eosinophils than normal volunteers regardless of smoking status. Among patients with IPF, the numbers of alveolar macrophages, neutrophils, or eosinophils were strongly associated with either smoking status or pack-years of cigarette smoking. In fact, after accounting for cigarette smoking, using multivariate analysis, the only additional factors that were found to be associated with BAL cellularity were age (macrophages and eosinophils) and the percent predicted forced expired volume in 1 s (neutrophils). Additional multivariate models failed to identify a significant relationship between BAL cellularity and either the type of immunosuppressive therapy or other physiological measures of lung function. We conclude that cigarette smoking strongly influences BAL cellularity in patients with IPF. These findings suggest that cigarette smoking may have a role in the pathogenesis of IPF or may adversely affect the prognosis in patients with IPF.


2020 ◽  
Vol 273 ◽  
pp. 103323 ◽  
Author(s):  
David Bennett ◽  
Elena Bargagli ◽  
Nicola Bianchi ◽  
Claudia Landi ◽  
Antonella Fossi ◽  
...  

Breathe ◽  
2020 ◽  
Vol 16 (3) ◽  
pp. 200086
Author(s):  
Christopher J. Brereton ◽  
Helen E. Jo

An acute exacerbation of idiopathic pulmonary fibrosis (AEIPF) is a potentially fatal complication of an already debilitating disease. Management is currently centred on delivering excellent supportive care and identifying reversible triggers. Despite growing international awareness and collaboration, no effective therapies have been identified. Corticosteroids are often the mainstay of treatment; however, the evidence base for their use is poor. Here, we review our current understanding of the disease process and how to manage it, with a focus on the role of corticosteroid therapy.


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