Current internationally recognized guidelines indicate that symptomatic asthmatics using a low to medium inhaled corticosteroid dose (400–800 µg/day of beclomethasone or equivalent) alone should preferentially be commenced on a long-acting agonist ß2 prior to an leukotriene receptor antagonists LTRA (British guideline on the management of asthma 2003; GINA Workshop Report 2004). However, two recent large trials have performed head to-head comparisons of add-on long-acting ß2 agonist versus LTRA as therapeutic adjuncts to inhaled corticosteroids, using exacerbation frequency (rather than lung function and symptoms) as the primary end point. (more…)

The genetic basis of asthma heritability has been extensively studied and the studies are yielding some understanding. There is, as yet, no set genetic pattern that predicts presence of asthma or defines it severity. There are usually reasons or risk of asthma factors that makes someone susceptible to asthma and respiratory allergy problems. Asthma doesn’t just happen randomly to anyone without asthma gene factors risk factors.

Let’s consider some asthma risk factors and see how they increase the chance that a individual will have the asthma signs or symptoms of cough, wheezing, as well as shortness of breathing associated with the disease. After determining your personal risk factors for asthma, decide on the ones you can control as well as try to make some lifestyle changes. Avoidance of the risk factors you can control is important in preventing asthma symptoms. While you cannot change your own gender to family history, you can avoid smoking with asthma, breathing polluted air, and obesity. Take control of your asthma by controlling the asthma risk factors. By understanding all of the risk factors, you are able to prevent to control your asthma.

Genetic factors cannot explain the rise in asthma prevalence, morbidity, or mortality. However, a small change in the prevalence of relevant environmental exposures could explain a significant rise in disease prevalence among genetically susceptible individuals. Gene-environment interaction, defined as the co-participation of genetic and environmental factors, is particularly relevant to the etiology of asthma morbidity, especially in individuals who experience a disproportionate burden of environmental exposures. Relevant exposures include smoking, stress, nutritional factors, infections, allergens, and occupational asthma exposures. In addition, racial/ethnic variability in the distribution of genetic polymorphisms can potentially modify the response to pharmacotherapeutic agents, such as the ß 2 -adrenergic receptor. A genetic polymorphism in the ß 2 -adrenergic receptor gene has been associated with asthma severity, as well as with the susceptibility to develop asthma among individuals who smoked.

Childhood asthma happens more frequently in boys than in girls. It is still not known precisely why this occurs even though some experts find a young male’s airway size is small compared to the female’s airway, that may contribute to increased risk of wheezing after a cold or perhaps other viral infection. Around age 20, the ratio of asthma between people is the same. At age 40, more females than men have adult asthma.

The inherited genetic makeup predisposes you to having asthma. In fact, it’s thought that three-fifths of all asthma cases are hereditary. Based on CDC report, if a person has a parent with asthma, there is 3 to 6 times more probably to develop asthma than someone who does definitely not have a parent with asthma.

Allergen-specific immunotherapy is highly effective in the treatment of IgE-mediated allergy diseases such as rhinitis, conjunctivitis, asthma, and venom allergy hypersensitivity. It is the only treatment that leads to lifelong tolerance against previously disease-causing allergens due to restoration of the normal immunity. (more…)

The intracellular forkhead winged transcription factor Foxp3 (forkhead box P3) appears to be specifically expressed by naturally occurring Treg cells, particularly in mice, although in humans there is evidence of upregulation of Foxp3 in all T cells on activation. Foxp3 is required for the development and function of naturally occurring regulatory t cells (treg) and expression is sufficient to convert non-regulatory CD4+CD25T cells into cells with regulatory activity. Conversion of peripheral CD4+CD25 naive T cells to Foxp3+CD4+CD25 foxp3+ Treg cells can be induced by TGF-ß. In a murine asthma model, these TGF-ß-induced Treg prevented house-dust mite-induced allergic pathogenesis or infection pathogenesis in lungs. A single independent report has suggested that IL-4 and IL-13 also induce Foxp3+CD25+ Treg from CD4+CD25precursors. (more…)

A variety of proinflammatory cells, mediators, and cytokines orchestrate the development of airway hyperresponsiveness, which results in the episodic airflow obstruction characteristic of asthma. As a consequence, modulation of the underlying disease process with antii-nflammatory agents is firmly established as being the cornerstone of successful management. Inhaled corticosteroids are the most potent antiinflammatory agents available and satisfactorily suppress underlying airway inflammation in most individuals. (more…)

Normally present at very low levels in plasma, antibodies of the immunoglobulin E (IgE) isotype were first discovered in 1967, decades after the description of IgA, IgG, and IM. IgE antibodies are produced primarily by plasma cells in mucosal-associated lymphoid tissue and their levels are uniformly elevated in patients suffering from atopic conditions like allergic rhinitis, asthma and atopic dermatitis. Production of allergen-specific IgE in atopic individuals is driven both by a genetic predisposition to the synthesis of this isotype as well as by environmental factors, including chronic allergen exposure. (more…)

This study was similar to the study of Harrison and colleagues, which looked at doubling the dose of inhaled corticosteroid during an asthma exacerbation. This study investigated whether doubling the dose of budesonide inhalation in patients on regular inhaled budesonide would be beneficial during an asthma exacerbation. (more…)

Allergic rhinitis and asthma are common comorbidities. Like asthma, the presence of a genetic component in allergic rhinitis has been well established. To identify genetic linkage regions unique to allergic rhinitis, as well as those shared by allergic rhinitis and asthma, a genome screen study was conducted. A total of 295 families in the French Epidemiological Study on the Genetics and Environment of Asthma (EGEA) containing 1317 subjects were genotyped for 396 microsatellite markers. The families included had two siblings with DNA available and at least one asthmatic subject. Three definitions of allergic rhinitis were used, two binary and one categorical. To investigate linkages specific to allergic rhinitis (without asthma), linkage analyses were also conducted in 185 families with at most one asthmatic sib. (more…)

This study examined the genetic basis of sensitization to house dust mite allergy allergens. A genome scan was conducted using 603 microsatellite markers in 82 nuclear families (366 individuals) of German, British and Portuguese origin with at least two affected siblings. Sensitization to Dermatophagoides pteronyssinus was assessed by determining specific IgE antibody levels detected by immunochemiluminometric assay and immunosorbent assay and categorized as positive or negative relative to a predetermined cut-off point. (more…)

Anti-IgE therapy could be particularly beneficial for patients with concomitant asthma and rhinitis as it targets a common factor in the two diseases. Omalizumab is significantly more efficacious than placebo in preventing asthma exacerbations and in improving disease-related quality of life scores when added to standard asthma and rhinitis therapies. (more…)