The role of allergy in otitis media with effusion

The role of allergy in chronic otitis media with effusion (OME) is controversial. New evidence from cellular biology and immunology explain the basics of allergic reactions and allow more accurate diagnosis of allergies and inflammatory disease throughout the unified airway. This article examines the epidemiologic, methodological, and immunologic studies of allergic causes of OME, including (1) evidence for and against OME as an allergic disease, (2) allergy as a cause for eustachian tube obstruction, (3) examination of the most sensitive diagnostic tests for allergy, and (4) the effect of treatment of underlying allergies in improving and resolving middle ear disease.     

Tobacco intervention teachable moments for pediatric otolaryngologists: Atopy and second hand smoke exposure among children

Objectives

Pediatric otolaryngology clinics have tremendous access to children with allergic conditions, yet no research has evaluated in this setting environmental tobacco smoke and the occurrence of atopic diseases.

Methods

Caregivers or parents of 201 consecutive patients in a Hungarian pediatric otolaryngology clinic were queried on otolaryngologic conditions; self-reported diagnoses of atopic diseases; and tobacco smoke exposure.

Results

A history of asthma was reported in 10.3% of children; 38.7% had at least one parent who smoked. Fifteen out of the 20 children with asthma (75.0%) had at least one parent who smoked. Having a diagnosis of hay fever and having a parent who smoked greatly increased the odds of having a diagnosis of asthma.

Conclusions

Second hand smoke exposure among children in an otolaryngology clinic was common, and was associated with co-existing atopic conditions. Pediatric otolaryngologists have an important opportunity to address parental smoking as part their care of children.     

The number and function of T regulatory cells in obese atopic female asthmatics

Background: Mechanisms underlying the association between asthma and obesity remain poorly understood. Obesity appears to be a risk factor for asthma, and obese asthmatics fare poorly compared to lean asthmatics. Objectives: To explore the possibility that reduced regulatory T cell (Treg) number and function contribute to the obesity-asthma association. We concentrated on obese females with childhood-onset asthma, since Treg may be involved in this phenotype. Methods: We recruited 64 women (ages 18–50) into four groups: lean (BMI 18–25 kg/m²) controls (n = 17) and asthmatics (n = 13), and obese (BMI ≥ 35 kg/m²) controls (n = 17) and asthmatics (n = 17). Asthmatics had atopy and childhood-diagnosed asthma. We assessed lung function, asthma control and quality of life. Peripheral blood CD4+/CD25+/FoxP3+ Treg cells were identified and counted by flow cytometry and expressed as % total CD4+ T cells. We assessed Treg cell function by the ability of CD4+/CD25+ Treg cells to suppress autologous CD4+/CD25- responder T cell (Tresp) proliferation and measured as % suppression of Tresp cell proliferation. Results: Obese asthmatics had worse lung function, asthma control, and quality of life compared to lean asthmatics. Compared to lean or obese control groups, the number of Treg cells in the obese asthmatics was approximately 1.58- or 1.73-fold higher. The ability of Treg cells from obese-asthmatics to suppress Tresp cell proliferation was reduced. Conclusions: Obese, atopic women with childhood diagnosed asthma demonstrate increased Treg cell number and mildly decreased Treg cell function. Our data do not support the view that reduced Treg cell number contributes to this obese-asthma phenotype.     

Increasing risk of asthma without other atopic diseases in school children: A repeated cross-sectional study after 13 years

Some children develop asthma and other atopic diseases, others asthma without atopic diseases. To better understand secular trends, we estimated the relative increase in asthma in children with (atopy related asthma) and without (non-atopy related asthma) other atopic diseases (eczema or hay fever) in two samples of school children born, 1965–1975 (n = 1674) and 1978–1988 (n = 2188). By analysing the samples as historical cohorts, age-specific prevalence rates were estimated and incidence rates were calculated (number of new cases by 1000 personyears under risk). Cox regression was used to estimate the relative risk (RR) of asthma by year of birth. The point prevalence of asthma was 1.9% (95% CI: 1.4–2.4) in the 1965–1975 cohort and 4.6% (95% CI: 3.8–5.4) in the 1978–1988 cohort for three-year old children, and remained fairly constant throughout childhood. The age-specific prevalence of non-atopy related asthma increased relatively more from 1965–1975 to 1978–1988 compared to atopy related asthma. The age-specific incidence rates of asthma showed that the RRs comparing the two cohorts tended at all ages to be highest for non-atopy related asthma. The relative risks of non-atopy related asthma by gender and birth cohort, showed that the effect of cohort was higher for non-atopy related asthma, aRR: 4.0 (95% CI: 2.5–6.5), than for atopy-related asthma aRR: 2.0 (95% CI: 1.3–3.2). Children without other atopic diseases have a higher relative risk of being diagnosed with asthma than children with other atopic diseases across all ages comparing two samples of school children born 1965–1975 and 1978–1988.