Severe asthma and death in a worker using methylene diphenyl diisocyanate MDI asthma death

Author(s):  
Adam V. Wisnewski ◽  
Ryan Cooney ◽  
Michael Hodgson ◽  
Kristinza Giese ◽  
Jian Liu ◽  
...  
2010 ◽  
Vol 44 (4) ◽  
pp. 2
Author(s):  
HEIDI SPLETE
Keyword(s):  

2007 ◽  
Vol 37 (5) ◽  
pp. 36
Author(s):  
MICHELE G. SULLIVAN

Pneumologie ◽  
2017 ◽  
Vol 71 (S 01) ◽  
pp. S1-S125
Author(s):  
I Pouliquen ◽  
D Austin ◽  
N Gunsoy ◽  
SW Yancey

2020 ◽  
Author(s):  
K Jamal Jameel ◽  
S Yanik ◽  
E Bülthoff ◽  
F Yusuf ◽  
B Struck ◽  
...  

2020 ◽  
Author(s):  
M Castro ◽  
J Corren ◽  
TB Casale ◽  
S Quirce ◽  
MS Rice ◽  
...  
Keyword(s):  

2021 ◽  
Vol 42 (1) ◽  
pp. e8-e16 ◽  
Author(s):  
Angelica Tiotiu

Background: Severe asthma is a heterogeneous disease that consists of various phenotypes driven by different pathways. Associated with significant morbidity, an important negative impact on the quality of life of patients, and increased health care costs, severe asthma represents a challenge for the clinician. With the introduction of various antibodies that target type 2 inflammation (T2) pathways, severe asthma therapy is gradually moving to a personalized medicine approach. Objective: The purpose of this review was to emphasize the important role of personalized medicine in adult severe asthma management. Methods: An extensive research was conducted in medical literature data bases by applying terms such as “severe asthma” associated with “structured approach,” “comorbidities,” “biomarkers,” “phenotypes/endotypes,” and “biologic therapies.” Results: The management of severe asthma starts with a structured approach to confirm the diagnosis, assess the adherence to medications and identify confounding factors and comorbidities. The definition of phenotypes or endotypes (phenotypes defined by mechanisms and identified through biomarkers) is an important step toward the use of personalized medicine in asthma. Severe allergic and nonallergic eosinophilic asthma are two defined T2 phenotypes for which there are efficacious targeted biologic therapies currently available. Non-T2 phenotype remains to be characterized, and less efficient target therapy exists. Conclusion: Despite important progress in applying personalized medicine to severe asthma, especially in T2 inflammatory phenotypes, future research is needed to find valid biomarkers predictive for the response to available biologic therapies to develop more effective therapies in non-T2 phenotype.


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