This Twitter summary from the 2013 meeting of the American College of Allergy, Asthma & Immunology (#ACAAI) was based on tweets by the following allergists/immunologists:
Robert Silge, MD @DrSilge
Andrew Nickels @AndrewNickelsMD
Dr. Dave Stukus @AllergyKidsDoc
Yesim Demirdag @DrYesimDem
Jason K Lee @lee_jasonk
Severe asthma was discussed Dr. Szefler: Severe asthma is found in the schools, not medical centers - care is too sporadic.
Severe asthma as defined by ATS: 1 of the following:
- PO steroids for more than 50% of past year
- continuous high dose ICS
- 2 of 7 minor criteria.
The WHO definition of severe asthma includes frequent severe exacerbations and/or adverse reactions to medications and/or chronic morbidity. The WHO definition is more holistic perhaps.
The WHO defines 3 severe asthma groups:
- untreated severe asthma
- difficult to treat asthma
- treatment resistant asthma
Very poorly controlled asthmatics have roughly double the indirect costs of other groups. Half that cost is due to missed school.
Severe asthma is difficult to treat due to long term irreversible effects of inflammation. Perhaps we are not using Xolair (anti-IgE) early enough for asthma - we may need to change guidelines to allow this.
Robert Rogers @choirdoc: Hardly surprising: If ICS/LABA is needed to achieve asthma control, stopping LABA leads to loss of control.
Severe asthma - differential diagnosis and management (click to enlarge the image):
Mechanisms of severe asthma are multiple and complex. There is a new approach to severe asthma - immunomodulators are here, but we don't know how and when to use them most effectively. Dr. Szefler sees future as large patient databases help refine phenotypes and appropriate treatment for severe asthma.
New immunomodulators are coming: anti IL5, IL13, and IL4/13. All focus on Th2 pathway. We need medications that target dendritic cells in asthma inflammation, not just focus on eosinophilic inflammation.
How to prevent fall exacerbations?
Summer vacation from asthma controllers may be wrong approach. Patients may need to step up then to prevent autumn flares.
Inner city asthma consortium is working on a study to increase ICS and/or start anti-IgE in summer to try and prevent fall flares.
Similarities and differences of asthma and COPD
Dr. Kraft discussed similarities and differences of asthma and COPD. The "Dutch hypothesis": asthma and COPD are similar disease vs the "English hypothesis" - they are very different diseases.
As patients age the overlap of COPD and asthma increases. Among age 70 and above patients, over half of patients have features of both. Both asthma and COPD are progressive diseases that are affected by age.
There is also an overlap in risk factors for asthma & COPD. Smoking exposure, maternal smoking, respiratory infections, air pollution, and occupational exposures are common risk factors.
Lung function declines more rapidly in asthmatic patients who also smoke. COPD progresses even after the patient quits smoking.
Greater bronchial hyper responsiveness in COPD correlates with increased mortality rate.
Take home message on overlap and treatment of COPD and asthma: treat the clinical features, same medications may be of benefit despite what name disease has (for example, tiotropium may benefit asthma patients). Examples: anti-inflammatory medications can help COPD, tiotropium may help asthma.
Tiotropium addition may improve lung function in severe asthma.
Would biologics such as omalizumab help in COPD, in those with high eosinophil levels & features of atopy? Studies are ongoing.
Immunology of COPD
Dr. James Li from Mayo Clinic presented the McGovern Lecture on Immunology of COPD
The basement membrane (BM) changes in asthma include compact, homogenous, thickened BM. In COPD: non-homogenous, variably thick, fragmented BM.
Both innate and adaptive immune system have a role in COPD. Oxidative stress, increased infection, hypoxia, autophagy are all caused by cigarette smoke and trigger innate immune response in COPD.
Inflammatory markers linked to COPD exacerbations
Inflammatory markers are linked to COPD exacerbations. We can perhaps check CRP, fibrinogen, and leukocyte count to gauge risk.
Markers of systemic inflammation (WBC, CRP, fibrinogen) can be useful to predict morbidity/mortality in COPD.
Eosinophils as a biomarker in COPD
One study looked at serum eosinophils in flares. Blood eosinophil count greater than 2% may be a biomarker for ICS therapy.