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Medical Journal Review

October 2015

WAO Reviews - Editors' Choice

The Editors select articles for their importance to clinicians who care for patients with asthma and allergic/immunologic diseases, and whenever possible they seek articles that everyone can access freely. The Editors’ Choice comes to you each month from Juan Carlos Ivancevich, MD, WAO Web Editor-in-Chief, and summary author, John J. Oppenheimer, MD, FACAAI, FAAAAI, WAO Reviews Editor.

1. An Interleukin-33-Mast Cell-Interleukin-2 Axis Suppresses Papain-Induced Allergic Inflammation by Promoting Regulatory T Cell Numbers.

Morita H , Arae K, Unno H , Miyauchi K, Toyama S et al. An Interleukin-33-Mast Cell-Interleukin-2 Axis suppresses papain-induced allergic inflammation by promoting regulatory T Cell numbers. Immunity 2015; 42(3): 175 – 186. (doi:


This is an interesting study that via use of a mouse model brings into question some of our prior suppositions regarding the role of IL-33 in allergic inflammation.  It is known that the IL-33, which is produced by lung cells following their exposure to protease in allergens such as house dust mites, can induce an innate-type airway eosinophilia via the activation of natural helper cells (a member of the group 2 innate lymphoid cells) with resultant secretion of Th2 type-cytokines.  In light of the fact that IL-33 can also induce mast cells to secrete Th2 type-cytokines, it was believed that mast cells cooperate with natural helper cells in enhancing protease or IL-33 mediated innate-type airway eosinophilia.  Interestingly, however, the authors via use of a mast cell deficient KitW-sh/W-sh  mouse found that IL-33 and mast cells can actually play an anti-inflammatory role via IL-33 stimulated induction of mast cell derived IL-2 resulting in expansion of IL-10 producing CD4+CD25+Foxp3+ regulatory cells.  These Treg cells can then down-regulate tissue inflammation.  This certainly is an interesting finding that deserves further evaluation.

2. National and regional asthma programmes in Europe.

Selroos O, Kupczyk M, Kuna P, Lacwik P, Bousquet J et al. National and regional asthma programmes in Europe. European Respiratory Review 2015; 24(137). (doi:10.1183/160000617.00008114)

Full Text, Open Access

This is a very useful review of 7 national asthma programs associated with the European Asthma Research and Innovation Partnership which explores strategies to reduce asthma morbidity and mortality across Europe.  The author’s note that characteristics associated with a successful asthma program include: 1) improve early diagnosis and introduction of anti-inflammatory agents as first line therapy, 2) improve long-term asthma control, 3) implement simple self-management tool to proactively prevent asthma exacerbations and 4) develop effective education and networking with general practitioners, nurses and pharmacists.

3. Eustachian tube dysfunction: consensus statement on definition, types, clinical presentation and diagnosis.

Schilder AGM, Bhutta MF, Butler CC, Holy C, Levine LH et al. Eustachian tube dysfunction: consensus statement on definition, types, clinical presentation and diagnosis. Clinical Otolaryngology 2015; 40(5): 407-411. (doi:10.1111/coa.12475)

Full Text, Free

Following a recent systematic review which demonstrated a wide variation in diagnostic criteria for Eustachian Tube dysfunction (ETD) an expert panel was assembled with the goal of more clearly defining the entity and developing an evidence-based evaluation protocol.

The group consensus was that the ETD is a syndrome with a constellation of signs and symptoms suggestive of dysfunction of the Eustachian Tube (ET).  They further agreed that the diagnosis can be stratified into acute and chronic illness, with the latter lasting longer than 3 months.  They further stratified the illness into 3 subtypes: dilatory, baro-challenge induced and patulous.

With regard to evaluation of these subtypes, in dilatory dysfunction, there are signs on otoscopy and tympanometry of negative pressure in the middle ear.  In baro-challenge induced dysfunction, symptoms occur only on changes to ambient pressure.  In patulous dysfunction, presumed secondary to an abnormally patent ET, there is otoscopic or tympanometric evidence of excursion of the tympanic membrane with breathing.  It is hoped that this consensus paper can be used as a guide in future studies regarding ETD.

4. Medical Therapies for Adult Chronic Sinusitis. A Systematic Review

Rudmik L and Soler ZM. Medical therapies for adult chronic sinusitis. A systematic review. JAMA 2015;  314(9): 926-939. (doi:10.1001/jama.2015.7544)


It is well known that chronic rhinosinusitis (CRS) is a very prevalent illness, affecting 3-7% of the population, with resultant healthcare expenditures of over 9 billion dollars per year.  Although it was previously thought to be an entirely infectious illness, CRS is now recognized as an inflammatory disease of a multifactorial etiology.  In this systematic review Rudmik and Soler examine the efficacy of medical therapies in the treatment of adult CRS.  Through their systematic review they found that the evidence supports daily saline irrigation with topical corticosteroids as the first-line therapy in CRS.  They further demonstrate that a short course of systemic corticosteroids (1-3 weeks) or doxycycline (3 weeks) may be considered in patients with nasal polyps, while a prolonged course (3 months) of macrolide antibiotic may be considered in patients without nasal polyps.

5. Revisiting the Dutch hypothesis.

Postma DS, Weiss ST, van den Berge M, Kerstjens HAM, Koppelman GH. Revisiting the Dutch hypothesis. Journal of Allergy and Clinical Immunology 2015; 136(3): 521-519. (doi:

Full Text, Free

Postma and colleagues, in this review, provide us with a wonderful journey of our present understanding of asthma and COPD, by using the literature regarding the Dutch hypothesis as a framework. Unlike the British hypothesis, which stresses that there is no common origin or relationship between asthma and COPD, the Dutch hypothesis, derived from the work of Orie and Sluiter (which was the consequence of the Bronchitis Symposium of 1960), suggests that asthma and COPD have common origins and further that they are determined by endogenous (heredity, age and sex) as well as exogenous (environmental allergens, smoking, virus and air pollution) factors.  It is amazing how visionary Orie and Sluiter were when examining our present beliefs regarding risk factors (genetics, atopy, and bronchial hyperreactivity), clinical expression (lung function, reversibility of airway obstruction, eosinophilic inflammation or the airways, and role of bacterial inflammation) andimplications for clinical management in asthma and COPD.  In the end, the approach of Postma and colleagues  provides us a wonderful opportunity to review the literature regarding these illnesses, showing us how far we have come and how much further we still have to travel to truly unravel the mysteries of asthma and COPD.

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