Brittle asthma is a type of asthma distinguishable from other forms by recurrent, severe attacks. There are two subtypes divided by symptoms: Type 1 and Type 2,depending on the stability of the patient's maximum speed of expiration, or peak expiratory flow rate (PEFR). Type 1 is characterized by sustained, chronic variability of PEFR, while type 2 is distinguished by sudden unpredictable drops in PEFR where asthma symptoms are otherwise well controlled and the function of the lungs is not substantially impaired. Brittle asthma is one of the "unstable" subtypes of "difficult asthma", a term used to characterize the less than 5% of asthma cases that do not respond to maximal inhaled treatment, including high doses of corticosteroids combined with additional therapies such as long-acting beta-2 agonists. Acute severe asthma, also known as status asthmaticus, is an acute exacerbation of asthma that does not respond to standard treatments of bronchodilators (inhalers) and corticosteroids.  Asthma is caused by multiple genes, some having protective effect, with each gene having its own tendency to be influenced by the environment although a genetic link leading to acute severe asthma is still unknown.Symptoms include chest tightness, rapidly progressive dyspnea(shortness of breath), dry cough, use of accessory respiratory muscles, fast and/or labored breathing, and extreme wheezing. It is a life-threatening episode of airway obstruction and is considered a medical emergency. Complications include cardiac and/or respiratory arrest. The increasing prevalence of atopy and asthma remains unexplained but may be due to infection with respiratory viruses.

Inflammation in asthma is characterized by an influx of eosinophils during the early-phase reaction and a mixed cellular infiltrate composed of eosinophils, mast cells, lymphocytes, and neutrophils during the late-phase (or chronic) reaction. The simple explanation for allergic inflammation in asthma begins with the development of a predominantly helper T2 lymphocyte–driven, as opposed to helper T1 lymphocyte–driven, immune milieu, perhaps caused by certain types of immune stimulation early in life. This is followed by allergen exposure in a genetically susceptible individual. Specific allergen exposure (e.g., dust mites) under the influence of helper Th2 helper T cells leads to B-lymphocyteelaboration of immunoglobulin E (IgE) antibodies specific to that allergen. The IgE antibody attaches to surface receptors on airway mucosal mast cells. One important question is whether atopic individuals with asthma, in contrast to atopic persons without asthma, have a defect in mucosal integrity that makes them susceptible to penetration of allergens into the mucosa.

Manuscripts with relevance to the scope can be submitted to our Email: hematology@scitecjournals.com or bloodres@peerjournal.org Online Submission Hematology