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I read a article related to asthma but I don't remember the link website. I'd like to share the information that I copied for person who has asthma.
Asthma is a clinical syndrome characterized by episodic reversible airway obstruction, increased bronchial reactivity, and airway inflammation. Asthma results from complex interactions among inflammatory cells, their mediators, airway epithelium and smooth muscle, and the nervous system. In genetically susceptible individuals, these interactions can lead the patient with asthma to symptoms of breathlessness, wheezing, cough, and chest tightness.

Causes or triggers of asthma can be divided into allergic and nonallergic etiologies. Aeroallergens can include seasonal pollen, mold spores, dust mites, animal allergens, and food (especially in children). Monosodium glutamate does not appear to be an allergen.

Nonallergic causes of asthma can include smoke, odors, cold air and weather, chemicals, medications (eg, aspirin and other nonsteroidal anti-inflammatory drugs [NSAIDs)], beta-blockers), exercise, hormonal changes (eg, pregnancy, menstrual cycle), and bisulfite food additives.

Genetic differences may alter susceptibility to asthma, as well as responsiveness to asthma medications. Significant genetic variation exists between and within racial and ethnic groups, but the issue is confounded by important coexisting economic, cultural, and environmental differences, including geography (place of birth)

Asthma-associated economic costs

In the United States, asthma is annually responsible for 1.5 million emergency department visits, 500,000 hospital admissions (third leading preventable cause), and 100 million days of restricted activity. Medical expenses, as well as lost work and productivity, cost an estimated $12.7 billion in 1998. In Western countries, the financial burden on patients ranges from $300 to $1,300 per patient year, increasing with more severe disease.

Worldwide, economic costs for asthma are more than those for tuberculosis and acquired immunodeficiency syndrome (AIDS) combined. Cost is associated with disease severity; more than half of all expenditures are attributed to the 10-20% of patients with the most severe disease.

Asthma risk factors

Risk factors for asthma include a family history of allergic disease, the presence of allergen-specific immunoglobulin E (IgE), viral respiratory illnesses, exposure to aeroallergens, cigarette smoke, obesity, and lower socioeconomic status.

A recent study by Zhang et al suggests that those children who are genetically predisposed to asthma may be at an even higher risk if they are overweight beyond infancy.

Data from the Prevention of Allergy: Risk Factors for Sensitization in Children Related to Farming and Anthroposophic Lifestyle (PARSIFAL) Study and the Multidisciplinary Study to Identify the Genetic and Environmental Causes of Asthma in the European Community Advanced (GABRIELA) Study reinforce the concept of the hygiene hypothesis. Using a cross-sectional design, the authors compared children living on farms to those in a reference group with respect to the prevalence of asthma and to the diversity of microbial exposure. The studies found that children who lived on farms had a lower prevalence of asthma and atopy and were exposed to a greater variety of environmental microorganisms than children in the reference group. The diversity of microbial exposure was inversely related to the risk of asthma (odds ratio for PARSIFAL, 0.62; 95% confidence interval [CI], 0.44-0.89; odds ratio for GABRIELA, 0.86; 95% CI, 0.75-0.99).

Allergy-associated asthma

Environmental exposure in sensitized individuals is a major inducer of airway inflammation, which is a hallmark finding in the asthmatic lung. Although triggers induce inflammation through different pathways, the resulting effects all lead to increased bronchial reactivity.

The importance of allergy in asthma has been well established. For example, exposure to dust mites in the first year of life is associated with later development of asthma and, possibly, atopy. Mite and cockroach antigens are common, and exposure and sensitization have been shown to increase asthma morbidity.

Allergies trigger asthma attacks in 60-90% of children and in 50% of adults. Approximately 75-85% of patients with asthma have positive (immediate) skin test results. In children, this sensitization is associated with disease activity.

Although most people with asthma have aeroallergen-induced symptoms, some individuals manifest symptoms with nonallergic triggers. About 3-10% of people with asthma are sensitive to NSAIDs. Approximately 5-10% of people with asthma have occupation- or industry-induced airway disease. Many individuals develop symptoms after viral respiratory tract infections.

Allergen avoidance and other environmental control efforts are feasible and effective. Symptoms, pulmonary function test findings, and airway hyperreactivity (AHR) improve with avoidance of environmental allergens. Removing even 1 of many allergens can result in clinical improvement. However, patients frequently are not compliant with such measures.

Etiology of Allergy-related Asthma

The etiology of asthma is likely multifactorial. Genetic factors may control individual predispositions to asthma. Genetics may also be associated with responses to medications. Variation in the beta-adrenergic receptor gene of the Arg-Arg type has been associated with adverse responses to inhaled, short-acting beta-agonist inhalers.

Genetics alone, however, cannot account for significant increases in asthma prevalence (see Epidemiology, below), as genetic factors take several generations to develop, and asthma and atopy are not always co-inherited.

One theory to explain the increased prevalence of allergic disease is that, with fewer infectious stimuli in the environment, the in utero TH 2 allergic cytokine state never switches to the TH 1 state.

Description of the allergic response

The allergic response in the airway is the result of a complex interaction of mast cells, eosinophils, T lymphocytes, macrophages, dendritic cells, and neutrophils. Inhalation-challenge studies with allergens reveal an early allergic response (EAR), which occurs within minutes and peaks at 20 minutes, following inhalation of the allergen.

Clinically, the manifestations of the EAR in the airway include bronchial constriction, airway edema, and mucus plugging. These effects are the result of mast cell–derived mediators. Four to 10 hours later, a late allergic response may occur, which is characterized by infiltration of inflammatory cells into the airway and is most likely caused by cytokine-mediated recruitment and activation of lymphocytes and eosinophils.

Antigen-presenting cells (ie, macrophages, dendritic cells) in the airway capture, process, and present antigen to helper T cells, which, in turn, become activated and secrete cytokines. Helper T cells can be induced by cytokines to develop into TH 1 (ie, by interferon-gamma, interleukin [IL]–2) or TH 2 (ie, by IL-4, IL-5, IL-9, IL-13) cells. Regulatory T cells (Treg) appear to play an important role in TH 2-cell response to allergens. Allergens drive the cytokine pattern toward TH 2, which promotes B-cell IgE production and eosinophil recruitment.

Subsequently, IgE binds to the high-affinity receptor for IgE, Fc-epsilon-RI, on the surface of mast cells and basophils; with subsequent exposure to the allergen, the IgE is cross-linked. This leads to degranulation of the mast cell and basophil. Preformed mast-cell mediators, such as histamine and proteases, are released, leading to the EAR.

Newly formed mediators, such as leukotriene C4 and prostaglandin D2, also contribute to the EAR.

Proinflammatory cytokines (IL-3, IL-4, IL-5, tumor necrosis factor-alpha [TNF-α]) are released from mast cells and are generated de novo after mast-cell activation. These cytokines contribute to the late allergic response by attracting neutrophils and eosinophils. The eosinophils release major basic protein, eosinophil cationic protein, eosinophil-derived neurotoxin, and eosinophil peroxidase into the airway, causing epithelial denudation and exposure of nerve endings.

The lymphocytes that are attracted to the airway continue to promote the inflammatory response by secreting cytokines and chemokines, which further potentiate the cellular infiltration into the airway.

The ongoing inflammatory process eventually results in hypertrophy of smooth muscles, hyperplasia of mucous glands, thickening of basement membranes, and continuing cellular infiltration. These long-term changes of the airway, referred to as airway remodeling, can ultimately lead to fibrosis and irreversible airway obstruction in some, but not most, patients.

Epidemiology of Asthma

Prevalence in the United States

The general prevalence of asthma is difficult to determine, because definitions and survey methods vary, but the incidence of the condition appears to be on the rise. The disease’s prevalence has been estimated as 10.9%, with asthma affecting more than 22 million people, including more than 6 million children.

International prevalence

Global Initiative for Asthma (GINA) researchers noted that, with regard to asthma in general, there have been increases in prevalence, morbidity, mortality, and economic burden over the past 40 years, especially in children. Asthma affects more than 300 million people worldwide, and some reports suggest that asthma prevalence is increasing by 50% every decade.

The highest recorded prevalences of asthma outside North America are in the United Kingdom (>15%), New Zealand (15.1%), and Australia (14.7%).

Asthma-associated morbidity and mortality

In the United States, mortality from asthma in general has increased, especially in children who live in inner-city areas, despite advances in disease understanding and therapy. The number of asthma-related deaths annually in the United States decreased from 5067 (1960-1962) to a low of 1870 (1975-1978), and then increased to 5429 (1993-1995).

Hospitalization and death rates are 50% higher for African American adults than white adults and 150% higher in children.

Worldwide, approximately 180,000 deaths annually are attributed to asthma; most deaths occur in persons older than age 45 years.

Increased morbidity is multifactorial; morbidity may be increased by increased exposure to indoor allergens, less exposure to viral infections early in life, more environmental pollution, overuse of short-acting beta-2 agonists, underuse of anti-inflammatory medications, and limited access to or education about health care.

Sex predilection

Boys have been shown to be at greater risk for asthma than girls. In children younger than 14 years, the prevalence of asthma is twice as high in boys as it is in girls.

This difference narrows with age, however; women aged 40 years have a greater prevalence of asthma than do men of the same age.

Age predilection

Disease onset can occur in people of any age, but children often present when younger than 6 years. Asthma is one of the most common chronic diseases of childhood.
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