Asthma: Difference between revisions
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==Etiology== | ==Etiology== | ||
According to the USA's [[National Heart, Lung, and Blood Institute]] of the [[National Institutes of Health]], "atopy, the genetic predisposition for the development of an immunoglobulin E (IgE)-mediated response to common aeroallergens, is the strongest identifiable predisposing factor for developing asthma". <ref>National Heart, Lung, and Blood Institute, [http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=asthma3.TOC&depth=2 Guidelines for the Diagnosis and Management of Asthma], National Institutes of Health, 2002.</ref> | According to the USA's [[National Heart, Lung, and Blood Institute]] of the [[National Institutes of Health]], "atopy, the genetic predisposition for the development of an immunoglobulin E (IgE)-mediated response to common aeroallergens, is the strongest identifiable predisposing factor for developing asthma". <ref>National Heart, Lung, and Blood Institute, [http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=asthma3.TOC&depth=2 Guidelines for the Diagnosis and Management of Asthma], National Institutes of Health, 2002.</ref> | ||
[[Atopy]], although genetically predetermined, is exacerbated by environmental factors. [[Diesel]] gas emissions were shown to increase atopy in asthma in the same way as allergen exposure itself. As was emphasised by the researchers who isolated this effect, the demonstration of such a modification in the expression of genetic predispositions, which was achieved through epigenetic mechanisms, urges researchers to adopt a "new paradigm" in asthma and atopy management.<ref name="pmid18042818">{{cite journal |author=Liu J, Ballaney M, Al-alem U, ''et al'' |title=Combined inhaled diesel exhaust particles and allergen exposure alter methylation of T helper genes and IgE production in vivo |journal=Toxicol. Sci. |volume=102 |issue=1 |pages=76-81 |year=2008 |month=March |pmid=18042818 |doi=10.1093/toxsci/kfm290 |url=}}</ref> | [[Atopy]], although genetically predetermined, is exacerbated by environmental factors. [[Diesel]] gas emissions were shown to increase atopy in asthma in the same way as allergen exposure itself. As was emphasised by the researchers who isolated this effect, the demonstration of such a modification in the expression of genetic predispositions, which was achieved through epigenetic mechanisms, urges researchers to adopt a "new paradigm" in asthma and atopy management.<ref name="pmid18042818">{{cite journal |author=Liu J, Ballaney M, Al-alem U, ''et al'' |title=Combined inhaled diesel exhaust particles and allergen exposure alter methylation of T helper genes and IgE production in vivo |journal=Toxicol. Sci. |volume=102 |issue=1 |pages=76-81 |year=2008 |month=March |pmid=18042818 |doi=10.1093/toxsci/kfm290 |url=http://www.pubmedcentral.nih.gov/articlerender.fcgi?tool=pubmed&pubmedid=18042818}}</ref> | ||
==Pathophysiology== | ==Pathophysiology== | ||
Revision as of 00:49, 4 May 2008
Definition
Epidemiology
Etiology
According to the USA's National Heart, Lung, and Blood Institute of the National Institutes of Health, "atopy, the genetic predisposition for the development of an immunoglobulin E (IgE)-mediated response to common aeroallergens, is the strongest identifiable predisposing factor for developing asthma". [1] Atopy, although genetically predetermined, is exacerbated by environmental factors. Diesel gas emissions were shown to increase atopy in asthma in the same way as allergen exposure itself. As was emphasised by the researchers who isolated this effect, the demonstration of such a modification in the expression of genetic predispositions, which was achieved through epigenetic mechanisms, urges researchers to adopt a "new paradigm" in asthma and atopy management.[2]
Pathophysiology
Diagnosis
Prognosis
Treatment
Treatment of acute exacerbations
The U.S. National Asthma Education and Prevention Program defines exacerbations as:[3]
- Mild. "Dyspnea only with activity (assess tachypnea in young children)"; peak expiratory flow rate ≥70 percent predicted or personal best
- Moderate. "Dyspnea interferes with or limits usual activity"; peak expiratory flow rate 40−69 percent predicted or personal best
- Severe. "Dyspnea at rest; interferes with conversation"; peak expiratory flow rate <40 percent predicted or personal best
- Life threatening. "Too dyspneic to speak; perspiring"; peak expiratory flow rate <25 percent predicted or personal best
Chronic treatment
Drug therapy
Long-acting beta-agonists may help[4]; however, they should not be used without corticosteroids and maybe should not be used in African American patients.[5] They might be safe as long as corticosteroids are used. According to a meta-analysis by the Cochrane Collaboration, when used with corticosteroids the relative risk for asthma-related death is increased at 1.34 although this increase was not statistically significant with a confidence interval of 0.30 to 5.97.[4]
Monitoring
A systematic review by the Cochrane Collaboration found that monitoring sputum eosinophils can guide treatment[6] The review identified three randomized controlled trials that found that benefit from adjusting anti-inflammatory medications to maintain less than 2 to 8% eosinophils in sputum.
Regarding peak expiratory flow rate monitoring, according to a meta-analysis of randomized controlled trials by the Cochrane Collaboration, peak flow monitoring is equivalent to symptom monitoring.[7] The U.S. National Asthma Education and Prevention Program recommends peak expiratory flow rate monitoring for selected patients.[3]
References
- ↑ National Heart, Lung, and Blood Institute, Guidelines for the Diagnosis and Management of Asthma, National Institutes of Health, 2002.
- ↑ Liu J, Ballaney M, Al-alem U, et al (March 2008). "Combined inhaled diesel exhaust particles and allergen exposure alter methylation of T helper genes and IgE production in vivo". Toxicol. Sci. 102 (1): 76-81. DOI:10.1093/toxsci/kfm290. PMID 18042818. Research Blogging.
- ↑ 3.0 3.1 National Asthma Education and Prevention Program: Expert Panel Report III: Guidelines for the diagnosis and management of asthma. Bethesda, MD. National Heart, Lung, and Blood Institute, 2007. (NIH publication no. 08-4051). Available from www.nhlbi.nih.gov/guidelines/asthma/asthgdln.htm. (Accessed September 1, 2008).
- ↑ 4.0 4.1 Walters EH, Gibson PG, Lasserson TJ, Walters JA (2007). "Long-acting beta2-agonists for chronic asthma in adults and children where background therapy contains varied or no inhaled corticosteroid". Cochrane Database Syst Rev (1): CD001385. DOI:10.1002/14651858.CD001385.pub2. PMID 17253458. Research Blogging.
- ↑ Salpeter SR, Buckley NS, Ormiston TM, Salpeter EE (2006). "Meta-analysis: effect of long-acting beta-agonists on severe asthma exacerbations and asthma-related deaths". Ann. Intern. Med. 144 (12): 904-12. PMID 16754916. [e]
- ↑ Petsky H, Kynaston J, Turner C, et al (2007). "Tailored interventions based on sputum eosinophils versus clinical symptoms for asthma in children and adults". Cochrane database of systematic reviews (Online) (2): CD005603. DOI:10.1002/14651858.CD005603.pub2. PMID 17443604. PMID 17443604. Research Blogging.
- ↑ Powell H, Gibson PG (2003). "Options for self-management education for adults with asthma". Cochrane Database Syst Rev (1): CD004107. PMID 12535511. [e]