Small airway involvement is present in all stages of asthmatic disease despite been referred to as 'silent zone'

This review provides an update on the importance of the peripheral, small airways in asthma. As the small airways account for less than 10% of total airway resistance, thus having little impact on standard lung function measures such as forced expiratory volume and peak flow, they have been referred to as the 'silent zone'.

Small airway involvement is present in all stages of asthmatic disease, and is related to important clinical phenotypes such:

- nocturnal asthma
- exercise-induced asthma
- difficult-to-control asthma
- patients with the risk of repeated asthma exacerbations

Uncontrolled small airway inflammation is related to airway remodeling and progression of the disease, with a more rapid decline in the lung function.

In order to control the disease, we need to target small airway inflammation, which is difficult to reach by standard inhaled medications. A better understanding of the role small airways are playing in asthma shows that the 'silent zone' is not silent at all.


The role of small airway disease in asthma. Bjermer L. Curr Opin Pulm Med. 2014 Jan;20(1):23-30. doi: 10.1097/MCP.0000000000000018.

Image source: Spirometry, from Wikipedia, the free encyclopedia, GNU Free Documentation License.

Uvular Angioedema Due to ACE Inhibitor - NEJM

Angioedema is a swelling that is similar to hives, but the swelling is under the skin instead of on the surface.

In this NEJM case report, treatment with 6.25 mg of captopril was started 6 hours after cardiac stent placement, and 30 minutes after administration the patient reported difficulty swallowing and throat pain. The uvula was markedly edematous and erythematous:

Uvular angioedema, or Quincke's disease, was diagnosed, and treatment with antihistamines and glucocorticoids was started. Improvement was rapid, and the edema completely resolved within 24 hours.

Isolated uvular angioedema is usually caused by an immediate (type I) hypersensitivity reaction. Mast-cell degranulation can occur after exposure to an immunologic or nonimmunologic stimulant, such as a drug, as was the case in this patient.

Angiotensin-converting–enzyme (ACE) inhibitors can cause isolated uvular angioedema, and although this response to ACE inhibitors is uncommon, it is important to be aware of it, since it can lead to obstructive respiratory distress.

Angioedema (AE) Classification (click to enlarge the image)


Isolated Uvular Angioedema — NEJM, 2014

2014 #WorldAllergyWeek : Anaphylaxis is the most severe allergic reaction - see how you can prevent and treat it

#WorldAllergyWeek is an annual campaign by the World Allergy Organization (WAO) to feature a specific allergic condition. This year the topic is anaphylaxis.

Join us during World Allergy Week 2014 and increase awareness of Anaphylaxis - When Allergies Can Be Severe and Fatal. There are many ways you can participate, see how:

A tweet a day, make #allergy go away! Here is my suggestion: post the following tweets to your Twitter account (you can change the URL if you want to):

Anaphylaxis is a severe, whole-body allergic reaction to an allergen #WorldAllergyWeek

Anaphylaxis happens quickly after allergen exposure, is severe, and involves the whole body #WorldAllergyWeek

Anaphylaxis affects between 1.5% and 5% of people #WorldAllergyWeek

To participate in #WorldAllergyWeek this year, I recorded 2 videos interviews for WAO TV with world experts during 2014 AAAAI. Feel free to link, post on Twitter, and embed the interviews in your own website:

Dr Lieberman: Anaphylaxis in America - YouTube

Dr Lockey: World Allergy Organization Anaphylaxis Guidelines 2013 update - YouTube

Disclaimer: I'm a Member of the World Allergy Organization (WAO) Web Editorial Board, Editor of the World Allergy Organization (WAO) Small Airways Working Group site, and Editor of WAO TV. I also co-authored the WAO Anaphylaxis Guidelines for 2012 and 2013.

Image source: Insect stings are among the causes of anaphylaxis; Bee, Wikipedia, GNU Free Documentation License.

Top Asthma Articles for April 2014

Here are my suggestions for some of the top articles about asthma for April:

23 million Americans have asthma, of whom 12 million experience an asthma exacerbation every year

Obesity was associated with significant lung restriction in children with and without asthma. Obesity was not associated with significantly altered airway or systemic inflammation in asthmatic children.

Use of Written Asthma Action Plans: 27% of parents had them - 80% felt they were useful, but only 55% looked at them -- Wallet Written Asthma Action Plan (WAAP) Compared to a Full-Page Plan: 90% of parents felt they were useful

Framing Asthma: Content Analysis in US Newspapers - Fear cues present in 43% of articles, 28% contained a stigma cue

Exposures to molds in school classrooms of children with asthma: Mold was present in 100% of classrooms

NYTimes on the hight cost of allergy and asthma medications: "The Soaring Cost of a Simple Breath"

Should All Patients with Asthma Receive Statins? - No, 1 in 50 patients on statins develops diabetes

Regional and near-roadway pollutants decrease children's lung function

Here is Advair's replacement by GSK: Once-daily fluticasone/vilanterol reduces risk of asthma exacerbations

Regional and near-roadway pollutants decrease children's lung function

In the UK, FeNO is used in primary practice to guide ICS initiation, dosing and identify poor ICS adherence

Bed covers reduce exposure to dust mite and improve adult atopic asthma

The term “asthma” should be avoided in describing the chronic pulmonary disease of prematurity

RCT of azithromycin in smokers with asthma: clear evidence demonstrating lack of efficacy

Inhaled corticosteroids may increase risk of tuberculosis in an intermediate-TB-burden country (South Korea)

FDA Approves New, Once-daily COPD Combination Therapy: Anoro Ellipta is umeclidinium (LAMA) and vilanterol (LABA)

Single inhaler "as needed" SMART therapy (ICS/LABA) may work better than standard b.i.d. ICS/LABA combo (Cochrane)

The articles were selected from Twitter @Allergy and RSS subscriptions. Some of the top allergy accounts on Twitter contributed links. I appreciate the curation provided by @Aller_MD @AllergyNet @IgECPD @DrAnneEllis @AACMaven @AllergieVoeding @allergistmommy @mrathkopf @wheezemd.

Please feel free to send suggestions for articles to allergycases AT gmail DOT com and you will receive an acknowledgement in the next edition of this publication.

Food protein-induced enterocolitis syndrome (FPIES) 2014 review

This summary is based on 3 review articles about FPIES published in March 2014 in the journal Current Opinion Allergy Clinical Immunology.

What is FPIES?

Food protein-induced enterocolitis syndrome (FPIES) is a poorly understood non-IgE-mediated food hypersensitivity, primarily affecting infants and toddlers. FPIES is one of the Adverse Food Reactions (see the classification below):

Adverse Food Reactions (click to enlarge the image).

What causes FPIES?

Foods and local intestinal imbalance between TNF-α and TGF-β play a role in the FPIES etiology.

There is regional variation in common triggering foods, rates of combined cow milk and soy FPIES and multiple food group FPIES.

WAO TV: Dr Greenhawt dfiscussed Food Protein Induced Enterocolitis Syndrome (FPIES) In a National Cohort - YouTube

How common is FPIES?

PIES is regarded as a rare non-IgE-mediated gastrointestinal allergic disorder. Older nonpopulation-based studies reported an average of 1-15 cases presenting to allergy clinics a year, but recent studies have reported figures as high as 90 cases a year. The yearly incidence of FPIES in one Australian study was one in 10,000 infants less than 2 years of age. FPIES is not as rare as once thought.

What are the symptoms of FPIES?

Patients frequently present with multiple reactions, which are characterized by projectile, repetitive vomiting (emesis), dehydration, lethargy, and failure to thrive.

Chronic FPIES typically presents in neonates, whereas acute FPIES is primarily a disorder of young infants. FPIES has a slight male predominance; eczema and a family history of atopy are commonly present at diagnosis; almost one in 10 infants have coexistent IgE food allergies and siblings are rarely affected.

How to diagnose FPIES?

Despite the severity of presentation, the diagnosis is frequently delayed, and patients often undergo extensive and invasive evaluation prior to reaching the diagnosis.

How to manage FPIES?

After FPIES has been diagnosed and avoidance of the culprit food prescribed, the most important management needs are as follows:

1. Avoid recurrence of acute FPIES episodes due to accidental ingestion of culprit food. It may be useful to give patients' families an action plan.

2. The principal suggested treatments of acute FPIES episode are intravenous fluids and steroids, whereas the use of epinephrine and ondansetron requires further study. In mild-to-moderate cases, oral rehydration should be sufficient.

3. Dietary introduction of at-risk foods is a difficult area. In children with FPIES, in addition to the identified culprits, some foods may not be tolerated (typically cow's milk, legumes, cereals, poultry). It has been suggested to avoid introducing these foods during the baby's first year. Otherwise, they may be given for the first time in hospital, performing an oral food challenge.

4. Acquisition of tolerance. Children affected by cow's milk-FPIES have a good chance of acquiring tolerance by the time they reach age 18-24 months. For other culprit foods, insufficient data are available to indicate the appropriate time, so that it is suggested that an oral food challenge be performed about 1  year after the last acute episode.

Where is future FPIES research headed?

Multicenter studies are necessary to reevaluate and modify the oral food challenge criteria. Research on the pathophysiology of FPIES reactions is necessary to provide insight into the evidence-based approach to diagnosis and management of FPIES. Registries are needed to understand the phenotype, triggers, and prevalence of FPIES.


Definition, etiology, and diagnosis of food protein-induced enterocolitis syndrome. Feuille E1, Nowak-Węgrzyn A. Curr Opin Allergy Clin Immunol. 2014 Mar 31. [Epub ahead of print]

Epidemiology of food protein-induced enterocolitis syndrome. Mehr S1, Frith K, Campbell DE. Curr Opin Allergy Clin Immunol. 2014 Mar 31. [Epub ahead of print]

Clinical management of food protein-induced enterocolitis syndrome. Sopo SM1, Iacono ID, Greco M, Monti G. Curr Opin Allergy Clin Immunol. 2014 Mar 31. [Epub ahead of print]
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