Asthma - Update on New Therapies - Twitter summary from #CSACI15 meeting

Twitter summary made possible by:

Dr. Paul O'Bryne from @McMasterU: "Asthma - Update on New Therapies". Paul O'Byrne to kick off the morning symposium with a talk on new and emerging asthma therapies. From @lee_jasonk: An honour & pleasure to introduce my personal hero Dr. Paul O'Byrne, Chair of Medicine @McMasterU & Director of the Firestone.

GINA 2015 update - stepwise approach to therapy - before any 'step up' confirm diagnosis, adherence and inhaler technique (DAT).

5-8% with severe or refractory asthma despite "maximal" guideline therapy, responsible for large fraction of costs. Dr O'Byrne: severe refractory asthma: 5 to 8% of asthmatics in Canada. 5-8% of severe asthmatics will not respond to standard asthma therapy.


Potential biologics for asthma treatment - anti-IL5 (meoplizumab and resulizumb), IL5R, IL4R, IL13, anti-TSLP. Several current/potential biological targets for asthma tx, IL-4, 5, 13, IgE, TSLP, receptors.

Reduction in severe asthma exacerbations has to be the most important outcome measure. Asthma exacerbations and reduced oral steroid use are probably the most important outcomes for biological agents. Biologics, though expensive, might be very useful in severe asthma, reducing oral corticosteroid use and asthma exacerbation.

Use the lowest effective dose given least frequently - this is important for biologics given the high costs.


Mepolizumab substantially improves exacerbation a in steroid dependent asthma, according to NEJM. Nair paper - pivotal trial showing benefit of mepolizumab for prednisone dependent eosinophilic asthma. Mepolizumab (anti-IL5) has been shown to significantly decrease exacerbations in well-selected asthma pts.

DREAM study of mepolizumab showed reduction in severe exacerbations for eosinophilic asthma - Lancet 2012.

Use the lowest effective dose given least frequently - this is important for biologics given the high costs. Example: 75mg of mepolizumab IV shown to be equivalent to 100mg subcutaneously by Ortega et al in 2014.

Current FDA-approved dose of mepo (100mg) may not fully control airway eosinophilia, may be insufficient for some patients.

Benralizumab (IL5-receptor alpha mAb)

Benralizumab (IL5-receptor alpha mAb) effective in preventing relapse after acute severe asthma. Benralizumab is an anti-IL5 receptor antibody - shown to reduce exacerbations/admissions to hospital in the 0.3mg/kg dose.


Reslizumab (different anti-IL5 drug) also shown to reduce severe exacerbations, especially in those older than 40 yo. Reslizumab given to patients with late-onset asthma with elevated blood eosinophils reduced exacerbations and improved FEV1.


IL4R alpha subunit is the common receptor for both IL4 and IL13. Lebrikizumab is an anti-IL13 mab - benefit is seen entirely in patients with elevated periostin. Lebrikizumab (anti-IL13) effective for improved lung function, but only in those with high periostin (marker of IL13 activity).

De Boever study of an anti-IL13 Mab showed an increase in blood eosinophil counts - unexplained. Surprising, using anti-IL13 increases eosinophils, an unexplained finding. No improvement in ACQ-7 or FEV1 in another study of anti-IL13.


Tralokinuab (anti-IL13) for moderate to severe asthma - those with high periostin sputum levels were the only ones to benefit .

Dr. O'Bryne points out that neither of the previous two studies looked at rates of severe exacerbations. Hanania et al Thorax 2015 - able to show significant reductions in severe exacerbations with anti-IL13 in the periostin-high group. Striking reduction in exacerbations with lower doses of lebrikizumab (not with higher dose) in those with high periostin.


Dupilumab is an anti-IL4R alpha Mab - showed reductions in exacerbations in asthmatics with elevated eosinophils. Dupilumab (anti-IL4Ra) prevented loss of control/exacerbations as meds decreased in asthma with elevated eosinophils.

Dupilumab given q2 wks improved FEV1 and reduced exacerbations, irrespective of eosinophil counts - Wenzel study.

Dupilumab significantly decreased severe exacerbations in a recent trial in a dose-dependant fashion.


QGE031 - new anti-IgE MAb that has much higher affinity binding to IgE than omalizumab. High affinity anti IgE may be better than omalizumab in asthma.

New trial is studying a new high affinity anti-IgE monoclonal antibody, reportedly better than Omalizumab.

AMG 157

AMG 157 is a MAb against TSLP - marked reduction in FENO levels, sputum eosinophils and blocked responses to allergen challenge. AMG157 (anti-TSLP) recently shown to have beneficial effects as well, but very preliminary data.

Inflammatory phenotyping most useful way to identify asthma pts who may benefit from novel therapeutics (ie Anti-IL-5).

Bronchial thermoplasty

Bronchial thermoplasty - Dr Nair/Cox think it is best for persistent non-inflammatory asthma with high degree of variable hyperresponsiveness.

ACAAI Tweetup! Meet allergists who will update Twitter with the latest allergy news from #ACAAI meeting

Here is the list of the allergists who are planning to use Twitter to post updates from the #ACAAI meeting. The list is open for edit, please feel free to add your own info.

The list shows the availability of the allergists by date and if they are planning to attend the Tweetup (a meeting of people who use Twitter or are following the tweets). If interested in a real life meeting Tweetup during the #ACAAI, sign up in the spreadsheet above. This will be the First Annual Tweetup during ACAAI!

Here is the Tweetup info - come meet us for a chat at:

Convention Center, Room 101B (PDF map)
Saturday, November 7th, 1:00 – 2:00 pm

The room is at street level, left of Ballroom A, in front of Exhibit Hall A (see the map above).

This is a free, informal event, no ticket required. Suggested topics: how to tweet? why to tweet? who to follow? research projects using social media, Twitter for patient education, etc.

The Tweetup will be hosted by Ves Dimov @Allergy and Daniel Ramirez Jr @AllergySA

The hashtag for the meeting is #ACAAI

The hashtag for the 2015 annual meeting of the American College of Allergy, Asthma and Immunology (ACAAI) is #ACAAI

Type #ACAAI in Twitter Search box to find all recent updates from  #ACAAI

You can also find info about the #ACAAI15 hashtag on the website of Symplur:

How to use Twitter to post updates from #ACAAI meeting

See examples of best practice by  @MatthewBowdish and @DrAnneEllis posted here: (tweets were summarized in a series of blog posts by me). For example, the tweets from 2012 AAAAI meeting reached more than 250,000 people.

I would strongly encourage you to post updates on Twitter from the CME conferences that you are planning to attend in the future. Here is how to do it: Twitter for Physicians: How to use Twitter to keep track of the latest news and scientific meetings, and share information with colleagues and patients.

WAO TV Social Media Guide for Allergists

Here is WAO TV Social Media Guide for Allergists:

Dr Stukus: How to use Twitter to engage patients

Dr Bowdish: Best practices for Twitter use by allergists

Dr Bowdish: How to use Twitter during a scientific conference: AAAAI, ACAAI, etc.

Dr Ramirez: How allergists can use Facebook for patient education


The impact of social media on a major international emergency medicine conference -- Neill et al. -- Emergency Medicine Journal

PLOS ONE: Tweeting the Meeting: An In-Depth Analysis of Twitter Activity at Kidney Week 2011

Tweeting the Meeting: Investigating Twitter Activity At the 2012 AAAAI Conference - Disclaimer: I am one of the authors.

How to share up to 4 photos in a single Tweet - Great for conference posters - see example

How to Make the Most of A National Scientific Conference

Air pollution and childhood asthma and allergy - Twitter summary from #CSACI15 meeting

Twitter summary made possible by:

Michael Brauer from UBC on air pollution and childhood asthma and allergy. Michael Bauer speaking on air pollution & asthma.

During wild fires we see increased use of ventolin and asthma exacerbations.

Correlation between PM2.5 levels (wildfire smoke) and salbutamol dispensations.

However, meta analysis shows no correlation of prevalence of asthma and pollution. Recent meta analysis shows no correlation between air pollution levels and asthma rates. The trend over time is decreased air pollution in wealthier countries while asthma rates have climbed.

Dr Brauer: Air pollution clearly exacerbates pre-existing asthma but there previously didn't appear to be links to asthma development.

Truck traffic

More truck traffic near home correlates with increased risk of asthma in 2009 study. Dr Brauer related an article that showed that reported increased truck traffic was linked to increased risk of asthma.

Small but significant association in Dutch PIAMI cohort between PM2.5 levels (traffic pollution) and asthma prevalence. More recent meta analysis looking at PM2.5 (traffic-related air pollution) specifically suggested an association with asthma.

If you look specifically at traffic pollution only, it may interact with genetic profile to predispose to asthma. Dr Brauer's group found link in BC between traffic pollution exposure and increased risk of asthma. No word on how many VW's were involved.

Now looking at traffic pollution and asthma genetics (TAG) to see if there might be a gene x environment effect. Confirmed that certain alleles coupled with pollution exposure associated with asthma, not with AR though.

In the @CHILDSTUDY, air pollution does seem to have a link towards increased risk of atopy/asthma. Air pollution does not affect development of asthma if child is greater than 6 years old.

Air pollution is fairly low in Canada but traffic related pollution is present. Mitigation strategies may be helpful. 32% of the population lives in areas influenced by traffic and 36% of primary schools in large Canadian cities.

Traffic-related air pollution in Canada, defined as fewer than 500m from highway or fewer than 100m from major road, could affect 1/3 population.

This is the definition of a 'Traffic Influence Zone:

Residential 'Greenness' appears to reduce the incidence of childhood asthma. Likely to be multi-factorial though.

13% of incident childhood asthma attributable to traffic related air pollution. Estimated 13% of incident childhood asthma in Vancouver attributable to traffic pollution.

Does traffic-related air pollution contribute to development of asthma? Growing evidence suggests consistent association.

Dr. Brauer showed very interesting data on traffic-related air pollution and asthma, hot spots near roads in Canadian cities.

Ali Hosseini from @PollutionLab is discussing how combined exposure to diesel exhaust and allergen enhances allergic inflammation.

Coal burning

Pollution such as from coal burning are not linked to asthma development but there is new concern re: ultra-fine particles. Pollutions caused by coal burning such as what used to be noted in East Germany is not a risk factor for asthma development.

Gut microbiota and development of allergic disease - Twitter summary from #CSACI15 meeting

Twitter summary made possible by:

Stuart Turvey from UBC on gut microbiota and the development of allergic disease. Microbiome influences on allergy /asthma. Human body has 10x as many bacteria as human cells. The body has 10X the number of bacterial cells than human cells. Stuart Turvey says it is time to rethink our relationship with bacteria and its importance to health.

The Microflora hypothesis

The microflora hypothesis - early life exposures affect composition of intestinal microbiota. Early life factors influence intestinal microbiota.

The Microflora hypothesis: early life exposures affect the composition of intestinal microbiota. That influences immunity.

From CHILD study: looked at bacterial 16S rRNA in stool samples at 2 times points in infancy, V3 region specifically. The gut microbiota at 3 months and 1 year were analyzed to determine which bacteria are present via RNA analysis. The gut microbiota at 3 months and 1 yr were analyzed to determine which bacteria are present via 16S RNA analysis. Microbiota results then compared to patient phenotype (wheezing or not, atopic/sensitized or not). They compared 319 children in the @CHILDSTUDY with 74 controls, 87 atopic only, 136 wheeze only and 22 subjects with both.

FLVR bacteria

No major differences in 1-year stool samples, but intriguing differences in 3-month samples: followed up with quantitative PCR. Several species "FLVR" shown to be significantly lower in 3-month stool of future atopic wheezers. FLVR bacteria were different in 3 months but not so much in year 1. Faecalibacterium, Lachnospira, Veillonella, and Rothia are the gut microbes labelled FLVR. At 1 year of age the microbiota were identical but there were differences at age 3 months between atopic and non-atopic.

FLVR supplementation in sterile OVA asthma mouse model showed protection against airway inflammation. These FLVR microbes appear protective against the development of atopy/asthma as shown by putting them in mouse models. FLVR - Faecalibacterium, Lachnospira, Veillonella & Rothia.

Short chain fatty acid: end-product of bacterial fermentation of carbohydrates. Acetate was lower in atopic wheezers.

Early life microbial dysbiosis is associated with enhanced risk of asthma and allergic disease. Early life microbial "dysbiosis" (lack of gut diversity) associated with enhanced risk asthma and allergic disease.

Dr. Turvey (UBC): Atopy PLUS Wheeze = significantly increases asthma by 3-years of age

Asthma is the most common chronic disease in childhood in Canada. 1 in 3 Canadians will be diagnosed with asthma at some point, and 30% of health care billings for children due to asthma.

Here are links to Dr Turvey's microbiome/asthma research (along with @MeghanAzad):

Atopic march and asthma - Twitter summary from #CSACI15 meeting

Twitter summary made possible by:

Dr Becker from Manitoba speaking on development of atopic conditions & life trajectories. Dr Allan Becker from U of Manitoba on the CHILD study and the determinants of allergic disease.

Hygiene hypothesis and allergy epidemic

.@allanbecker2 points out that the Hygiene Hypothesis was actually first stated by a Canadian Dr John Gerrard in 1976. A reminder that Canadian allergist John Gerrard postulated the hygiene hypothesis in 1976. John Gerrard 1976 postulated this inverse relationship. Give us this day our daily germs (Immunology Today 1998).

UN general assembly described slow motion epidemic in 2011. UN called non-communicable diseases, including allergy, an epidemic unfolding in slow motion.

Almost half of all children wheeze in the pre-school years. About 1/2 of preschool children will have at least one episode of wheezing. The question: which become asthmatic?

Early changes in lung function by age 3

Things get set off in early life. Pulmonary function while in normal range is in the low range and follows this trend. Structural modification is set by age 10. But kids are not born this way, it occurs around 2-3 years of life. Evidence of airway remodeling in recurrent/frequent wheezers already identified by age 3. Airway remodelling in asthmatic children can already be present at the age of 29 months. The more severe and frequent the airway inflammation, the greater the likelihood of structural changes/remodeling. The Dunedin study showed that asthma was present at childhood. Irreversible structural changes might start early. We need to focus on young kids with window of opportunity to prevent the development of allergies & asthma. Airway remodeling can occur in toddler years, adding more evidence to treat persistent asthma/wheezing.

Canadian Asthma Primary Prevention Study (CAPPS)

CAPPS stands for Canadian Asthma Primary Prevention Study headed by Dr Becker - multidimensional interventional study. Small but significant changes in lung function in young children with asthma dx (age 7) compared to controls in CAPPS study.

Skin test positive status highly associated with asthma: Atopy at 1 yr is the most significant risk factor asthma at age 7 yr

Marked increase in risk for persistent wheeze in teens if positive SPT by age 2. Skin test positive much more likely to develop persistent wheezing. Early life atopy a strong predictor of asthma. Skin test positive status highly associated with asthma at 7 yo in @allanbecker2's study.

Dr. Becker: If you are allergic (skin test positive) in first 2y of life, there is an increased risk for persistent asthma by teen yrs.

Risk factors for asthma at 7 years: Male child, Mother with asthma, Father/sibling with asthma, Atopy at 1 year RSV. Atopy (positive SPT) at age is a bigger risk for persistent asthma than maternal history, RSV, other risk factors, in CAPPS study. Atopy at 1 yr is the most significant risk factor asthma at age 7 yr. Atopy the age of 1 seems to be a huge determinant of likelihood of asthma at age 7. Timing of atopy, even if it disappears, is a risk for developing asthma.

Factors critical to development of asthma: genes, environment AND atopy in early life (in particular food allergy). Factors critical to development of asthma: genes, environment AND atopy in early life (in particular). Genetics play a big role in allergy and asthma, “choose your parents wisely.”

PFT changes worse at 15 years with all wheezy phenotypes: transient wheeze less than late onset less than persistent wheeze.

Canadian healthy infant longitudinal development study @CHILDSTUDY

Child study looked at enviro factors. @CHILDSTUDY came about to fully study the determinants of asthma/atopy in Canadian children.

The @CHILDSTUDY, perhaps luckily, studied the role of gut microbiota. A lot of the articles on this from @MeghanAzad.

It's cool that scientific studies have Twitter handles now, example @CHILDSTUDY - investigators worldwide take note, find a good Twitter handle.

Reminder about CTS/CPS position paper: Diagnosis and management of asthma in preschoolers:
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