Asthma and COPD - Twitter summary from 2014 #ACAAI meeting



From @DrAnneEllis: What a great looking panel! #ACAAI - Busse, Lieberman and Panettieri http://t.co/LWtq1XwHSZ

Dr Panettieri presented on COPD:

As an allergist, what do I need to know about COPD? Is the USA - COPD is entirely smoking related, according to Dr Panettieri. COPD is unlikely to occur in anyone under the age of 40, except if there is alpha 1 antitrypsin deficiency. COPD is characterized by persistent airflow limitation that is progressive and an enhanced chronic inflammatory response in airways.

Fun Fact: The lung has the surface area of a tennis court.

70% of COPD have bronchial hyperresponsiveness - methacholine challenge and pre-post SABA PFTs can't reliably distinguish from asthma. True emphysema that we remembered from our Netter diagrams in medical school only occurs in 20% of COPD patients.

IL-6, CRP gene SNPs associated with COPD.

Phenotypes in COPD: asymptomatic, ventilatory limited, muscle limited, gas exchange limited.

Lung inflammation drives systemic inflammation, leading to blood vessel activation and endothelial dysfunction, it enhances CAD/CVD. Systemic manifestation of COPD: Cardiovascular Disease, Osteoporosis, Respiratory Infections, Anxiety/Depression, Diabetes, Lung CA, Bronchietasis. COPD amplifies heart disease, manifested by arrhythmias, angina, acute MI, CHF, CVA, etc.

Osteoporosis/osteopenia is more frequent with greater spirometric severity in COPD.

There is a skeletal muscle dysfunction in COPD - these patients’ anaerobic threshold occurs much earlier leading to lactic acidosis. Lower BMI predicts increased mortality in COPD.

COPD patients have a high rate of depression and depression leads to non-adherence (important idea for other diseases too!!). Prevalence of depression in COPD patients is between 20 to 60%. Co-morbid Depression increases the rate of acute exacerbations of COPD.

There are a variety of COPD biomarkers in sputum, BAL and blood, some more fruitful than others, to help identify at-risk patients.

It patients with COPD have secondary pulmonary hypertension, prognosis is dramatically worse.

Dr Panettieri pointed out the health problems associated with e-cigarettes including inhalation of formaldehydes. “COPD will develop if you smoke tobacco, marijuana, or cabbage". Dr Panettieri's point being, it's the smoking of any vegetable matter and incomplete combustion that leads to lung damage and COPD.

Dr Phil Lieberman presented on "Asthma as COPD: Pulmonary remodeling". Fun fact, only about 15% of Phillips are spelled with 2 L's. (according to Phillip Lieberman :).

Lung remodeling is simple - Injury causes scarring that leads to aberrant healing that results in remodeling. “Easy peasy.”

Asthmatics as a group demonstrate an accelerated decline in FEV1 as they age compared with normal population.
Normal peak of FEV1 occurs by age 18 to 25, there is a decline of about 10 to 30 ml thereafter. Adults asthmatics decline more rapidly. Childhood asthmatics - their peak FEV1 by age 18 to 25 is lower than healthy controls. A cohort of 228 asthmatics was followed up to 31 yrs: 16% developed irreversible obstruction; correlated with low initial FEV1 and less ICS.

Patients with asthma and irreversible airflow obstruction decline in FEV1 at similar rate to COPD patients. Children with baseline abnormalities in high resolution CT chest at baseline were less likely to improve FEV1 with ICS/LABA therapy.

Lung remodeling can begin very early in life, as early as 3 months of age. Dr Lieberman believes that irreversible damage to asthmatic lungs can be prevented, but notes that view is controversial. PFTs are not only way to see remodeling in severe asthmatics. CT scans can be used to follow airway wall thickness.

Duration, severity, bronchial reactivity, gender, eosinophil levels and IgE level all affect progression of remodeling. Patients with highly variable presence of eosinophils in sputum decline FEV1 faster that those with low eosinophils or high constant eosinophils.

IgE and FEV1 in Tenor Study: FEV1 was lower in patients with high IgE across all age levels (IgE higher than 100 IU). In Tenor Study: FEV1 was lower in asthmatics with high IgE levels (greater than 100) across all age groups. "Asthmatic lungs are stiff".

According to NHANES, allergic skin test reactivity correlated with a more rapid decline in FEV1 and FEV1/FVC.

Dr Bill Busse presented on Severe Asthma vs COPD - Therapeutic Dilemmas.

Asthma commonly begins before age 40, COPD rarely does so. Nighttime awakenings is not common in COPD.

25% of patients with asthma smoke. 90% of COPD patients (in US) are smokers or ex-smokers.

Five clusters of obstructive lung diseases have been identified via genetic analysis - AJRCCM 2010;181:315.

"COPD-Asthma Overlap Syndrome" is a persistent airflow limitation with several features of both asthma and COPD. Treatment of Asthma-COPD Overlap Syndrome depends on features of the individual patient, Asthma more than COPD or COPD more than Asthma.

Asthma/COPD overlap syndrome: persistent airflow limitations, several features usually associated with both asthma and COPD. Males seem to be a greater risk of overlap syndrome, likely due to higher rates of smoking, this may change as more women smoke now.

Overlap syndrome is not well studied - patients get excluded from asthma studies because they smoke; they are also excluded COPD studies because of reversibility.

CRP is elevated in COPD but not asthma. Unknown status of this biomarker in the Overlap syndrome. If asthma symptoms are predominant: Anti-inflammatory treatment, if COPD is predominant (and mild), primary therapy is long acting bronchodilators. Asthma patients rarely have a decrease in the DLCO - we need to get complete PFT's in overlap patients.

As many of 50% of older adults w/obstructive airways disease have overlapping diagnoses of asthma and COPD. HRCT, FENO and blood eosinophils can help distinguish asthma from COPD. COPD and asthma may be distinct entities in younger patients but as people age overlaps are more common and it associated with other comorbidities.

There is some debate now whether using ICS in treatment of mild COPD patients could put them at greater risk for respiratory infections.

Steroid non-responders is where we will see the best role for the new biological therapies.

Dr Panettieri: Most US pulmonologists don't look at percent predicted FEV1 now but rather compare absolute FEV1 to the lower limit of normal. A resting Sa02 of 91% is profoundly abnormal, it should trigger a 6 min walk test and consider home 02. Allergists should do more 6-minute walk tests in our COPD/asthma patients.

This is a Twitter summary from 2014 #ACAAI meeting. The post is a part of series. See the rest here: http://allergynotes.blogspot.com/search/label/ACAAI

The Twitter summary was made possible by @MatthewBowdish and @DrAnneEllis

Several allergists did a great job posting updates from the 2014 meeting of the #ACAAI. I used the website “All My Tweets” to review the tweets. For comparison, here are the tweets from previous #ACAAI meetings (scroll down the page for the past years): http://allergynotes.blogspot.com/search/label/ACAAI

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