Login to your account

Username *
Password *
Remember Me

Blog With Right Sidebar

Immunotherapy in allergies: an update.

The allergen specific immunotherapy is the administration, in IgE-mediated allergic patients, of a specific allergen in a gradually increased number to provide protection against allergic symptoms and inflammatory reaction. The current immunotherapeutic approaches occur by modulating the release of inflammatory mediators involved in allergic reaction and consequently the inhibition of allergic inflammatory process.

Since 1997 several World Associations of Allergy, Asthma and Immunology, have reviewed this issue, seeking to establish standards for its use. Also many publications about the immunotherapy's efficacy, as well as, several guidelines on the use of immunotherapy in the treatment of allergic are available.

This article will focus on the most current evidence about the immunotherapy in allergies regarding its mechanism of action, effectiveness and practical considerations.

A Systematic Review of Long-Acting β2-Agonists Versus Higher Doses of Inhaled Corticosteroids in Asthma.

To compare the efficacy of inhaled corticosteroids (ICS) plus long-acting β2 agonist (LABA) versus higher doses of ICS in children/adolescents with uncontrolled persistent asthma.

METHODS:Randomized, prospective, controlled trials published January 1996 to January 2012 with a minimum of 4 weeks of LABA+ICS versus higher doses of ICS were retrieved through Medline, Embase, Central, and manufacturer's databases. The primary outcome was asthma exacerbations requiring systemic corticosteroids; secondary outcomes were the pulmonary function test (PEF), withdrawals during the treatment period, days without symptoms, use of rescue medication, and adverse events.

RESULTS:Nine studies (n = 1641 patients) met criteria for inclusion (7 compared LABA+ICS versus double ICS doses and 2 LABA+ICS versus higher than double ICS doses). There was no statistically significant difference in the number of patients with asthma exacerbations requiring systemic corticosteroids between children receiving LABA+ICS and those receiving higher doses of ICS (odds ratio = 0.76; 95% confidence interval: 0.48-1.22, P = .25, I(2) = 16%). In the subgroup analysis, patients receiving LABA+ICS showed a decreased risk of asthma exacerbations compared with higher than twice ICS doses (odds ratio = 0.48; 95% confidence interval: 0.28-0.82, P = .007, I(2)= 0). Children treated with LABA+ICS had significantly higher PEF, less use of rescue medication, and higher short-term growth than those on higher ICS doses. There were no other significant differences in adverse events.

CONCLUSIONS:There were no statistically significant group differences between ICS+LABA and double doses of ICS in reducing the incidence of asthma exacerbations but it did decrease the risk comparing to higher than double doses of ICS.

Inflammatory Mediators in Induced Sputum and Airway Hyperresponsiveness in Cough Variant Asthma during Long-Term Inhaled Corticosteroid Treatment.

Objective. This study aimed to investigate improvements in inflammatory mediator levels in induced sputum and airway hyperresponsiveness (AHR) in cough variant asthma (CVA) during long-term inhaled corticosteroid (ICS) treatment.

Patients and Methods. Patients with CVA (N = 35) and classic asthma (N = 26) and healthy subjects (N = 24) were recruited into this study. All patients were treated with budesonide (400 μg/day). Measurement of inflammatory mediators in induced sputum and PD20-FEV(1) (the accumulated provocative dose resulting in a 20% decrease in FEV(1)) in histamine-challenged subjects was performed every three months after the start of medication. Interleukin- (IL-) 5 and IL-10 were assayed by ELISA, and the percentage of eosinophils was detected with Giemsa stain. Trends during the follow-up period were analyzed using a general linear model.

Results. Inflammatory mediator levels in induced sputum and PD20-FEV(1) in patients with CVA and classic asthma differed from those in the control group, although no differences were found in the two asthmatic groups. PD20-FEV(1) significantly increased in CVA patients after ICS treatment for 3 months, while classic asthma patients exhibited a delayed change in AHR. After ICS treatment, levels of IL-5 and IL-10 as well as the percentage of eosinophils in the CVA group were altered at 3 months and 6 months, respectively. Accordingly, the level of inflammatory mediators in classic asthma changed more slowly.

Conclusion. CVA has a greater improvement in airway inflammation and airway hyperresponsiveness (AHR) than classic asthma with respect to inhaled corticosteroid (ICS). Short-term ICS considerably reduces AHR although longer treatment is required for complete control of airway inflammation.

Foetal exposure to maternal passive smoking is associated with childhood asthma, allergic rhinitis, and eczema.

We examined the hypothesis that foetal exposure to maternal passive smoking is associated with childhood asthma, allergic rhinitis, and eczema.

Methods. The study was a population-based cross-sectional survey of Hong Kong Chinese children aged ≤14 years carried out in 2005 to 2006.

Results. Foetal exposure to maternal passive smoking was significantly associated with wheeze ever (OR 2.05; 95% CI 1.58-2.67), current wheeze (OR 2.06; 95% CI 1.48-2.86), allergic rhinitis ever (OR 1.22; 95% CI 1.09-1.37), and eczema ever (OR 1.61; 95% CI 1.38-1.87). Foetal exposure to maternal active smoking was significantly associated with asthma ever (OR 2.10; 95% CI 1.14-3.84), wheeze ever (OR 2.46; 95% CI 1.27-4.78), and current wheeze (OR 2.74; 95% CI 1.24-6.01) but not with allergic rhinitis ever (OR 1.01; 95% CI 0.70-1.46) or eczema ever (OR 1.38; 95% CI 0.87-2.18). The dose response relationship between wheeze ever and current wheeze with increasing exposure, from no exposure to maternal passive smoking and then to maternal active smoking, further supports causality.

Conclusion. There is significant association between foetal exposure to maternal passive smoking and maternal active smoking with childhood asthma and related atopic illnesses. Further studies are warranted to explore the potential causal relationship.

Aspirin Sensitivity and Chronic Rhinosinusitis with Polyps: A Fatal Combination.

Aspirin-exacerbated respiratory disease (AERD) refers to aspirin sensitivity, chronic rhinosinusitis (CRS), nasal polyposis, asthma, eosinophil inflammation in the upper and lower airways, urticaria, angioedema, and anaphylaxis following the ingestion of NSAIDs. Epidemiologic and pathophysiological links between these diseases are established.

The precise pathogenesis remains less defined, even though there is some progress in the understanding of several molecular mechanisms. Nevertheless, these combinations of diseases in patients classified by AERD constitute a fatal combination and may be difficult to treat with standard medical and surgical interventions.

This paper reviews in brief the epidemiology, clinical features, diagnosis, molecular pathogenesis, and specific therapies of patients classified by AERD and postulates future attempts to gain new insights into this disease.

Search