Childhood asthma

Smoking is, by far, the most important etiological risk factor for COPD occupational exposures also eontribute. Genetic deficiency of the arprotease inhibitor enzyme is another proved, but rare, cause. Other postulated risk factors include increased airways responsiveness to nonspecific stimuli, asthma, childhood respiratory infections, and air pollution (24). The potential role of particulate air pollution in the causation of COPD or other respiratory diseases remains imclear. 

Asthma affects 3—5% of the population and is one of the most common chronic illnesses (7—9). Both the frequency and severity of asthma appear to be increasing (10—13). Acute, severe asthma has the potential to be fatal. The disease may first appear ia childhood and iadividuals so affected can suffer recurrent episodes throughout their Hves or they may "outgrow" the condition at puberty. On the other hand, there is also adult-onset asthma. These people show no symptoms as children or as young adults, but suddenly develop symptoms later ia life. There have been many reports of bronchial infections preceding the appearance of asthma. However it is not known whether these infections contributed to the development of the disease or whether iadividuals who are already predisposed to asthma ate more likely to experience bronchospasms as a result of a bronchial infection (14). 

An economic externality exists whenever the wellbeing of some individual is affected by the economic activities of others without particular attention to the welfare of that individual. For example, smog-related illnesses such as bronchitis and exacerbated cases of childhood asthma have been blamed, to some extent, on the emissions of nitrogen oxides from automobiles and large fossil-fuel-burning power plants. These illnesses have high treatment costs that are not... 

There are few definitive data to substantiate the efficacy of LTRA therapy in refractory asthma, except for patients with aspirin-sensitive asthma. This is a fairly uncommon form of asthma that occurs generally in adults who often have no prior (i.e., childhood) history of asthma or atopy, may have nasal polyposis, and who often are dependent upon oral corticosteroids for control of their asthma. This syndrome is not specific to aspirin but is provoked by any inhibitors of the cycloxygenase-1 (COX-1) pathway. These patients have been shown to have a genetic defect that causes... 

Schmidt JR, Vignati AJ, Pagash RM, Simmons VA, Evans RL. Web-based distributed data management in the Childhood Asthma Research (CARE) network. 

Pogash RM, Haak T, Grella V, Zimmerman R, Doty L. Using the web for secnrely managing the asthma Clinical Research Network (ACRN) and the Childhood Asthma Research And Education (CARE) network. Controlled Clin Trials 2004 1.1.4 387-98(12). 

Novak, Z., Nemeth, L, Gyurkovits, K., Varga, S.I. and Mat-kovics, B. (1991). Examination of the role of free radicals in bronchial asthma in childhood. Clin. Chim. Acta 201, 247-251. 

Asthma results from a complex interaction of genetic and environmental factors however, the underlying cause is not well understood. There appears to be an inheritable component, as the presence of asthma in a parent is a strong risk factor for the development of asthma in a child. This risk increases when a family history of atopy is also present.13 Approximately 50% of asthma can be attributed to atopy, and atopic asthma is more common in children than adults.3 Furthermore, atopy in childhood asthma is the strongest prognostic factor for continued asthma as an adult.1,3... 

Genetic factors cannot explain the recent rapid rise in asthma prevalence. Asthma appears to require both genetic predisposition and environmental exposure. Many patients with occupational asthma develop the disease late in life upon exposure to specific allergens in the workplace. Environmental influences in utero or in infancy may contribute to the development of asthma. Maternal smoking during pregnancy or exposure to secondhand smoke after birth increases the risk of childhood asthma.3 Adult-onset asthma is not uncommon and may be related to atopy, nasal polyps, aspirin sensitivity, occupational exposure, or a recurrence of childhood asthma. 

D. Hariparsad, N. Wilson, and C. Dixon, Oral tar-trazine challenge in childhood asthma Effect on bronchial reactivity, Clin. Allergy, 14, 81 (1984). 

Asthma is the most serious of the atopic diseases and has become epidemic, affecting more than 155 million individuals in the developed world. It is the most common chronic childhood disease in developed nations [1], and carries a very substantial direct and indirect economic cost worldwide [2]. A number of pharmacological treatments have been developed for asthma. These treatments have a modest efficacy overall, due in part to widely variable individual responses to asthma drugs. Because of such variability, it is clear that some of the substantial resources expended on asthma medication, estimated to exceed U.S. 3 billion per annum in the U.S. alone [3], would be better spent targeting those patients who... 

Asher MI, Keil U, Anderson HR et al. International Study of asthma and allergies in childhood (ISAAC) rationale and methods. Eur Respir J 1995 8 483-491. 

The International Study of Asthma and Allergies in Childhood (ISAAC) Steering Committee. Worldwide variation in prevalence of symptoms of asthma, allergic rhinoconjunctivitis, and atopic eczema ISAAC. Lancet 1998 351 1225-1232. 

Holt, P.G., A potential vaccine strategy for asthma and allied atopic diseases during early childhood, Lancet, 344, 456, 1994. 

The onset of asthma might depend on both genetic and environmental components. In childhood the expression of IFN-7 is fundamental in determining the future T-cell development. In fact, defective IFN-7 early in life favors a Th2 cell development probably as a result of increased IL-6 production by DCs or mast cells and/or IL-4 production by natural killer or other cells. The increased GATA-3 expression in the lung of asthmatics points in this direction. The defect in T-bet or its genetic modification in asthmatics underlines the... 

Palmer LJ, Celedon JC, Weiss ST, Wang B, Fang Z, Xu X Ascaris lumbricoides infection is associated with increased risk of childhood asthma and atopy in rural China. Am J Respir Crit Care Med 2002 165 1489-1493. 

Melen, E., Bruce, S., Doekes, G., et al. (2005) Haplotypes of G protein-coupled receptor 154 are associated with childhood allergy and asthma. Am. J. Respir. Crit. Care. Med. 171, 1089-1095. 

Srivastava, P., Helms, P. J., Stewart, D., Main, M., and Russell, G. (2003) Association of CCR5 Delta 32 with reduced risk of childhood but not adult asthma. Thorax. 58, 222-226. 

Kemp, T., Pearce, N., Fitzharris, P., et al. (1997) Is infant immunization a risk factor for childhood asthma or allergy Epidemiology. 8, 678-680. 

Several studies have attempted to correlate increased numbers of hospital admissions with variations in photochemical-oxidant pollution. The California Department of Public Health study of excess mortalhy also investigated hospital admissions as a possible health indicator of oxidant pollution. Admissions to Los Angeles County General Hospital in September through December 1954 for childhood asthma, tuberculosis, other respiratory diseases, and all other causes were examined. No significant association with oxidant concentrations was found. 

For example, childhood exposure to lead can result in reduced IQ, which can affect an individual throughout their lifetime. Similarly, childhood asthma can have a severe impact on an individual s ability to play and socialize. 

The causes may include household dust, droppings from dust mites, and mold. Asthma-related illness resulted in over 100,000 children visiting a hospital and losing over 10 million school days. A very different kind of long-term disability results from childhood lead exposure. The US Centers of Disease Control estimated that over one million US children have elevated blood lead levels due to household exposures. 

Site has information on childhood asthma and the Master Home Environmentalist Program. 

Late onset wheezing asthma, symptoms often persist throughout childhood and into adult life. An allergic/atopic background including eczema, upper airway inflammation in patients and/or family histories may be observed. 

L C. Inflammation of the airway is a hallmark of asthma. The use of antiinflammatory drugs, such as inhaled corticosteroids, is critical to the long-term control of asthma. No credible data indicate either that asthma is psychosomatic or that it develops in response to vaccinations against childhood diseases. Asthma is a disease limited to the airways. It does not involve the lung parenchyma. Although upper respiratory tract infections can exacerbate asthma symptoms, asthma is not caused by infection, nor is it communicable. 

A special problem caused by inhaled corticosteroids is the occurrence of oropharyngeal candidiasis. The risk of this complication can be reduced by having patients gargle water and spit after each inhaled treatment. Hoarseness can also result from a direct local effect of inhaled corticosteroids on the vocal cords. These agents are remarkably free of other short-term complications in adults but may increase the risks of osteoporosis and cataracts over the long term. In children, inhaled corticosteroid therapy has been shown to slow the rate of growth, but this effect appears to be transient Asthma itself delays puberty, and there is no evidence that inhaled corticosteroid therapy in childhood influences adult height. 

Yoshihara S et al Effects of early intervention with inhaled sodium cromoglycate in childhood asthma. Lung 2006 184 63. [PMID 16622775]... 

Kozyrskyj AL, Ernst P, Becker AB. 2007. Increased risk of childhood asthma from antibiotic use in early life. Chest. 131 1753-1759. 

A two-part review was published in 2002, addressing the difficulties of assessing the effects of asthma therapy on childhood growth and reviewing the published literature based on the authors recommendations (136,137). In the first part (136), a simple classification system for growth studies was developed ... 

Gregson RK, Rao R, Murrills AJ, Taylor PA, Warner JO. Effect of inhaled corticosteroids on bone mineral density in childhood asthma comparison of fluticasone propionate with beclomethasone dipropionate. Osteoporos Int 1998 8(5) 418-22. 

Price J, Hindmarsh P, Hughes S, Effthimiou J. Evaluating the effects of asthma therapy on childhood growth principles of study design. Eur Respir J 2002 19(6) 1167-78. 

The Childhood Asthma Management Program Research Group. Long-term effects of budesonide or nedocromil in children with asthma. N Engl J Med 2000 343(15) 1054-63. 

Balfour-Lynn L. Growth and childhood asthma. Arch Dis Child 1986 61(ll) 1049-55. 

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