PMID- 28044257
OWN - NLM
STAT- MEDLINE
DCOM- 20180220
LR  - 20181113
IS  - 1179-2000 (Electronic)
IS  - 1177-1062 (Linking)
VI  - 21
IP  - 3
DP  - 2017 Jun
TI  - Targeted Therapy for Severe Asthma: Identifying the Right Patients.
PG  - 235-247
LID - 10.1007/s40291-016-0252-x [doi]
AB  - Asthma affects over 300 million people worldwide. Most asthmatics are well 
      controlled with inhaled corticosteroids and long-acting beta-agonists; however, a 
      proportion of patients are unresponsive and attain limited disease control. This 
      group represents a considerable healthcare and financial burden, particularly 
      patients who experience frequent exacerbations and require hospital admission. 
      Development of new biological agents and disease biomarkers has provided novel 
      avenues for treatment. These treatments have been highly successful, reducing 
      exacerbations and yielding modest improvements in quality of life and lung 
      function. However, only a proportion of severe asthmatics respond to this 
      targeted treatment, highlighting the heterogeneity of severe asthma. One of the 
      first biological therapies targeted immunoglobulin E (IgE) and demonstrated 
      modest benefit but could only be used in a subgroup of patients. Recent research 
      has shown that treatment aimed at the T helper-2-(Th(2))-high pathways and 
      cytokines such as interleukin (IL)-5, IL-4, and IL-13 may also be effective in 
      another partially overlapping subgroup. A blood eosinophil count over a defined 
      threshold (generally >/=300 cells/mul) was a reliable biomarker and identified the 
      majority of responders in this group. Further discovery and validation of 
      biological markers to define asthmatic phenotypes that may benefit from 
      biological treatments remain an area of intense interest and research. We review 
      the latest information pertaining to biological agents and demonstrate how 
      patient responders may potentially be identified for treatment.
FAU - Low, Kathy
AU  - Low K
AD  - Lung and Sleep Medicine, Monash University and Medical Centre, 246 Clayton Road, 
      Clayton, Melbourne, VIC, 3168, Australia.
FAU - Bardin, Philip G
AU  - Bardin PG
AD  - Lung and Sleep Medicine, Monash University and Medical Centre, 246 Clayton Road, 
      Clayton, Melbourne, VIC, 3168, Australia. philip.bardin@monash.edu.
AD  - Hudson Institute, Melbourne, VIC, Australia. philip.bardin@monash.edu.
LA  - eng
PT  - Journal Article
PT  - Review
PL  - New Zealand
TA  - Mol Diagn Ther
JT  - Molecular diagnosis & therapy
JID - 101264260
RN  - 0 (Anti-Asthmatic Agents)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (Antibodies, Monoclonal, Humanized)
RN  - 0 (Biomarkers)
RN  - 0 (Cytokines)
RN  - 35A26E427H (reslizumab)
RN  - 37341-29-0 (Immunoglobulin E)
RN  - 71492GE1FX (benralizumab)
RN  - 90Z2UF0E52 (mepolizumab)
SB  - IM
MH  - Anti-Asthmatic Agents/pharmacology/*therapeutic use
MH  - Antibodies, Monoclonal/pharmacology/therapeutic use
MH  - Antibodies, Monoclonal, Humanized/therapeutic use
MH  - Asthma/*drug therapy/*etiology
MH  - Biomarkers/blood
MH  - Cytokines/antagonists & inhibitors/metabolism
MH  - Humans
MH  - Immunoglobulin E/metabolism
MH  - Molecular Targeted Therapy/methods
MH  - Th2 Cells/metabolism/pathology
MH  - Treatment Failure
EDAT- 2017/01/04 06:00
MHDA- 2018/02/21 06:00
CRDT- 2017/01/04 06:00
PHST- 2017/01/04 06:00 [pubmed]
PHST- 2018/02/21 06:00 [medline]
PHST- 2017/01/04 06:00 [entrez]
AID - 10.1007/s40291-016-0252-x [pii]
AID - 10.1007/s40291-016-0252-x [doi]
PST - ppublish
SO  - Mol Diagn Ther. 2017 Jun;21(3):235-247. doi: 10.1007/s40291-016-0252-x.