Asthma Bronchial Asthma

More complex causes of the disease, the most that is a multi-gene genetic diseases, genetic factors and environmental factors affected by the double effect.

(A) of the genetic factors of asthma and genetic relationship has been the growing attention.According to information on the family, think early studies that asthma is a single-gene genetic diseases, believe some scientists, is that autosomal dominant (autosomal dominant) of the disease, there are considered, an autosomal recessive (autosomal recessive be inherited) of the disease. At present the view that asthma is a multi-gene genetic diseases, the heritability of 70% to 80%. Multi-gene genetic diseases are caused situated in different pairs of disease genes on chromosomes by the interaction of these genes have no obvious difference was recessive, their effect on the phenotype is weak, but cumulative effects of disease or by environmental factors larger. Therefore form the Role of bronchial asthma through a series of small but cumulative effects of disease genes, the genetic factors that determine the genetic basis of disease risk, such as an individual sensitivity. By genetic factors and environmental factors and decide whether an individual is, the possibility that susceptibility to asthma susceptibility. said inheritance of genetic factors in the size of measurable role in the pathogenesis of size, the higher the heritability of genetic factors, role in the pathogenesis of size, the higher the heritability of genetic factors in the pathogenesis said the greater role. Many survey data show that more members of patients with a high prevalence of asthma prevalence in the population, and the closer genetic relationship, the higher prevalence rate, in a pedigree, the more the number of patients, their relatives, the prevalence higher; patients serious the disease, the higher prevalence of their relatives. Wang Mingang children with asthma and other investigations, and Ⅱ Ⅰ level of asthma prevalence, and compared with the control group, asthma group Ⅰ level of asthma prevalence at 8.2%, Ⅱ grade relative prevalence was 2.9%, theformer prevalence of asthma was significantly higher than the latter. The control group Ⅰ, Ⅱ were degree of asthma prevalence of 0.9% and 0.4%, lower than the prevalence of the asthma group Ⅰ, Ⅱ degree of asthma prevalence.

An important feature of asthma is the existence of the airway hyperresponsiveness, have on human and animal studies have shown that some genetic factor controlling the airway response to stimuli from the environment. Xiaodong, Zhang, etc. inhalation method with tissue in 40 asthmatic children and 34 healthy children, parents, the responsiveness of the airways, asthma, increased most kids with parents in varying degrees of airway responsiveness measured PC20 11.6mg/ml average, and normal children PC20 parents were more than 32mg/ml, shows the existing family members of patients with asthma, bronchial hyperresponsiveness of the airways basis, hyperresponsiveness of the airways in asthma genetic inheritance plays an important role.

Currently, asthma genes have not yet entirely clear, but studies have shown that certain genes may have asthma, and IgE specific genes regulate the immune response genes. 11q12q13 autosomal genes with asthma, IgE reactivity control; abroad in recent years closed serum total IgE genetic research, that the total IgE genes located on chromosome 5, the regulation, control of specific immune response is not IgE-regulating genes, and controlled by immune response genes, immune response genes with high discrimination power of the antigenic molecules in the immune response in mice confirmed the chromosome 17 gene in the MHC region is located.Research has shown, is that human chromosome 6 loci HLA DR region immune response genes control the occurrence of a specific antigen immune response. Therefore regulate the pathogenesis of asthma by the IgE immune response genes and the interaction between genes.In addition, the nervous system and may be sensitive airways in various cell receptors to the state, be some enzymes such as the congenital absence or genetic factors. In short, should the relationship between asthma and genetic, further study to early diagnosis, to facilitate early prevention and treatment.

(B) the formation of stimulating factors of asthma and recurrent disease, which often lead many complex factors together.

1, sucks sucks in two types of specificity and nonspecific. The former, such as dust mites, pollen, fungi, animal hair, etc., non-specific inhaled materials such as sulfuric acid, sulfur dioxide, chlorine, ammonia. Occupational asthma specific inhalation, such as toluene diisocyanate, phthalic anhydride, ethylenediamine, penicillin, protease, amylase, silk, animal hair or excreta, etc. In addition, there are nonspecific formaldehyde, formic acid and so on.

2, infection of the formation and attack of asthma and recurrent respiratory infections. In asthma patients, the existence of bacteria, viruses, mycoplasmas and specific IgE, when the corresponding antigen inhalation may stimulate asthma. Virus infection can directly damage airway epithelium, resulting in increased responsiveness of the airways. Some scientists believe the virus infection by interferon, IL-1 produced to increase the release of histamine basophil. In the suckling period, respiratory viruses (particularly respiratory syncytial virus) infection shows a wide variety of symptoms of asthma. Since the parasites such as roundworms, hookworms cause of asthma, seen in the rural areas still.

3, causes relationship of food are often seen in asthma, particularly in infants and young children due to poor nutrition of the phenomenon of an asthma attack susceptible to food allergies, but gradually decreased with age. The most common cause of food allergy is fish, shrimp, crab, eggs, milk and so on.

4, climate change, though, the air temperature, air temperature, pressure and (or) changes in the air ions trigger asthma, so that during the cold season or in winter when the climate changed more disease.

5, the mentally ill nervous, emotional factors, Yuannu will be to promote an asthma attack, the general view that it is through the cerebral cortex and vagal reflex or induced hyperventilation.

6, sports some 70% to 80% of asthma patients after an exhausting exercise-induced asthma, exercise-induced asthma, or known as exercise-induced asthma. A typical case is in motion 6 to 10 minutes after the end of Exercise 1 to 10 minutes bronchospasm obvious, many patients from 30 to 60 minutes in their own recovery. About 1 hour after training refractory period, while the 40% pass to 50% of patients not re-exercise bronchospasm. Clinical features include cough, chest tightness, shortness of breath, wheezing, and auscultation to listen to wheeze.While lacking some of the typical patient with asthma after exercise performance, but the lung function before and after exercise can be found in bronchospasm. The disease more often in young people. If the given cromolyn sodium, ketotifen or aminophylline may reduce or prevent seizures. This study suggests that physical exertion by hyperventilation, which is in the respiratory mucosa of moisture and heat loss, respiratory epithelium temporary molar concentration is too high, leading to bronchial smooth muscle contraction.

7 may, asthma and Drug Some medications cause an asthma attack, such as propranolol of β2-adrenergic receptor blocking and asthma. About 2.3% to 20% of asthma patients, the aspirin-induced asthma medication and called the aspirin asthma. Patients with nasal polyps and aspirin because of poor tolerance, which in turn associated to aspirin triad disease. The clinical symptoms are: Aspirin may cause severe asthma symptoms more than 2 hours after administration there, even as late as 2 to 4 hours. Patients with other anti-inflammatory drugs and non-steroidal anti-inflammatory drugs may cross-react; children with asthma onset before the age of more thanł, but are mainly middle-aged patients, from 30 to 40 years welcome; women than men, the ratio of men to women of approximately 2:3; attack no significant seasonal, serious condition, they stubbornly, mostly dependent on hormones, more than half have nasal polyps, often with perennial allergic rhinitis and (or), sinusitis, nasal Sometimes after polypectomy increased asthma symptoms or trigger, common inhalant allergen skin test negative often isolated, serum total IgE were normal; family have less allergic disease. At its pathogenesis is not yet fully understood, it was considered possible in patients with bronchial COX medium for an infectious (possibly viral) effects of aspirin sensitive cyclooxygenase inhibitory drugs, namely, a division of ASA intolerance. So, when patients with aspirin-containing drugs, the effects of arachidonic acid metabolism, inhibition of prostaglandin synthesis, so PGE2/PGF2α disorders, so that to increase leukotriene formation, leading to strong and persistent contraction of bronchial smooth muscle.

8th Menstruation, pregnancy and asthma, many women with asthma during the menstrual period 3 to 4 days prior to the increase of the phenomenon of asthma, which can be a sudden drop after the first progesterone. If the patient will be issued monthly, but injected by the amount of not more than those with progesterone can prevent in a timely manner, sometimes to severe premenstrual asthma. The influence of pregnancy on asthma is not regular, asthma symptoms were worsening, but most do not change much of their condition. The role of pregnancy on asthma, especially in the mechanical effects and asthma-hormonal changes in the third trimester of pregnancy, such as the uterus grows, increases the diaphragm position so that residual volume, expiratory reserve volume and functional residual capacity with different degrees of decay and ventilation and oxygen consumption have increased. When asthma is treated properly, will not have a negative impact on pregnancy and birth.

(A) the frequency of allergic asthma and allergy related, has been recognized as an important type Ⅰ allergy. Were mostly atopic constitution, often accompanied by other allergic diseases, as allergens enter the body, stimulate the body may, after synthesis of IgE titers high, and the binding to mast cells and basophils high Fcε surface receptor (FcεR1), also some B-cells, macrophages, monocytes, eosinophils, NK cells and a low affinity Fcε platelet surface receptors (FcεR2) combined. However FcεR2 affinity IgE below FcεR1 about 10 to 100 times. If the allergen in the body back into FcεR can be combined, the IgE cross-linking, a variety of active synthesis and release medium, which bronchial smooth muscle contraction, mucus secretion, vascular permeability and inflammatory cell infiltration. And the role of inflammatory cells in the media can release under a variety of media, so that the inflammation of the airways.can be divided by asthma after allergen inhalation in the period of rapid reaction Asthma (IAR), delayed-type asthmatic reaction (LAR) asthmatic reaction and biphasic type (DAR). IAR almost immediately, while inhaled allergens can interact with 15 to 30 minutes, 2 hours after return to normal in the record. LAR is late onset, occurred about 6 hours, lasted longer, up to several days. Some of the severe asthmatic patients with delayed-reaction is closely related to clinical symptoms and lung function and permanent impairment of the hand, and often the drugs have crime, inhaled corticosteroid therapy was initiated. In recent years, LAR clinical significance has attracted the attention of people. LAR complex mechanism, not only with IgE degranulation mediated the mast cells and were mainly caused by inflammation of the respiratory tract, may cause mast cell degranulation and leukotriene-Re-(LT be involved), prostaglandin (PG), thromboxane (TX) and thus the release Medium delay. Some studies show that mast cell degranulation response is not clear, the immune system, non-immune stimuli such as exercise, cold air, inhaled sulfur dioxide activate mast cells and release particles. If the asthma is a large number of inflammatory cells into the interplay of many participating mediators and cytokines involved are a chronic inflammatory disease that was LAR by the result of inflammation of the airways, mast cells compared with primary effector cells and eosinophils, neutrophils, monocytes , lymphocytes and platelets for the secondary effects of the system, these cells large amounts of inflammatory mediators, activation and share the airways target organs, which bronchial smooth muscle spasm, microvascular leakage, mucosal edema, neuronal responses in mucus hypersecretion excitement, patients significantly increased airway responsiveness.Clinically, the general bronchodilators alone is not easy to damage limitation, and use of inhaled corticosteroids and cromolyn sodium treatment may prevent the occurrence of LAR.

In bronchial asthma and allergic Ⅲ the relationship between the dispute has continued.Traditional view of exogenous type Ⅰ allergy asthma are expressed as the IAR, and endogenous allergic asthma is a type Ⅲ (Arthus phenomenon), showed LAR. But results show that most secondary LAR to IAR, LAR significantly dependent on the IAR. Therefore, not all types Ⅲ LAR are allergic.

(B) of the airway inflammation in asthmatic airway inflammation in the pathogenesis of research in recent years, important progress in this area. Bronchial asthma and participate airway inflammation in patients with a variety of cells, particularly mast cells, eosinophils and T lymphocytes in, and there are more than 50 types of inflammatory mediators and cytokines more than 25 types of interaction between chronic respiratory Livet inflammation of the opposite sex. Airway inflammation in asthma patients with reversible airway obstruction and nonspecific bronchial hyperreactivity important factor. Asthma airway inflammation process has three steps, namely activation and IgE-FcεR start to promote the release of inflammatory mediators and cytokines and adhesion molecules on leukocyte transmembrane movement. If the allergen in the body to recognize B-cell antigens and activation, the activation means: T, B cells recognize antigen expression of different epitopes were activated; B endocytosis, processing and integration of major histocompatibility antigen complex (MHC â…¡) was the complex after the release of Th IL-4, IL-5 identified for further promotion of B-cell activation. Activated B cells produce specific IgE antibodies in accordance with, the latter again with the mast cells, eosinophils, and other cross-linking, then the effect of the allergens produced, the release of inflammatory mediators. Known mast cells, eosinophils, neutrophils, epithelial cells, macrophages and endothelial cells have the ability to produce inflammatory mediators, has written to the media reports, may, in the rapid release media (such as histamine are shared), secondary production of medium (PG, LT PAF , etc.) and particles derived medium (such as heparin) categories. Airway inflammation in mast cells is the largest primary effector cells, mast cells, may release histamine, eosinophil chemotactic factor (ECF-A), neutrophil chemotactic factor (NCF-A), LT and other media. Alveolar macrophages in the initiation of inflammation in asthma may also play an important role, may release its activation TX, PG, and platelet-activating factor (PAF) and other media. ECF-A on eosinophil chemotaxis, and induce the release of major basic protein (MBP), eosinophilic cationic protein (ECP), eosinophil peroxidase (EPO), eosinophil neurotoxin (EDN), PAF can LTʢ, etc., MBP, EPO fall epithelial cells of the airway sensory nerve endings exposed, in the hyperreactivity of the airways. MBP can activate mast cells release EPO medium. NCF-A can increase the neutrophil chemotaxis, and release of LT, PAF, PGS, free oxygen radicals and lysosomal enzymes, the inflammatory reaction.LTC4 and LTD4 are potent agents bronchoconstriction and increased mucus secretion and vascular permeability increase induced promotion. LTB4 may neutrophils, eosinophils, monocytes, chemotaxis, aggregation and secretion media and so on. PGD2, PGF2, PGF2α, PGI2, and TX are powerful agents of respiratory contraction. PAF, the bronchial and chemokines, activation of eosinophils and other inflammatory cells induce contraction increased microvascular leakage, it is important to inflammation of asthma. In recent years, found that epithelial cells of the airways and endothelial cells produce endothelin (ET5) is airway contraction and the reconstruction of the main media, induced ET1 by far the strongest known bronchial smooth muscle contraction is agent is its strength of contraction and nerve LTD4Bradykinin 100 times, 1000 times acetylcholine, ET submucosal gland secretions also encourage and promote smooth muscle cells and fibroblast proliferation effect. can pro-inflammatory cytokines TNF may airways stimulates smooth muscle cells ET1, which aggravated not only the contraction of smooth muscles, increases the smooth muscles of the airway contractile response itself to abnormal proliferation of cells from the respiratory tract causing conversion result of the respiratory tract, can become chronic important reason for persistent asthma. Adhesion molecules (adhesion molecules, AMS) are a class can cell adhesion glycoprotein to mediate, was a large number of research data confirms that adhesion molecules play an important role in the pathogenesis of asthma, the inflammation of the airways, sticky Adhesion Molecule-mediated leukocyte adhesion to endothelial cells and endothelial cross-transfer to sites of inflammation.

Standard desensitization therapy: A therapy for patients with allergies in determining the source, the preparation of the allergen in different concentrations of vaccine formulations, administration of small to large, because of the low dose of the vaccine clinical effects of treatment are often not increased and the high dose of vaccine treatment, there may be excessive side effects. It is therefore necessary to increase for patients with the long-term, repeated vaccinations on tolerance to these allergens, so as to achieve the purpose of controlling or relieving symptoms. This process requires parents and keep their children with patience and active support to a satisfactory effect.