Asthma

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Jan Hed, Clin Immunologist, MD, PhD
Karolinska Institutet, IMPI, Div of Clin Immunology
Huddinge University Hospital, Sweden
 
The statements below are based on conclusions from selected publications. Their intention is to highlight recent research and information that could be beneficial in allergy in vitro testing. They can include seemingly contradictory statements due to differences in selecting patient populations as well as in the study design.
  • Asthma is defined (1) according to the United States National Heart, Lung and Blood Institute as a chronic inflammatory disorder of the airways in which many cells play a role, in particular mast cells and eosinophils. In susceptible individuals, this inflammation causes symptoms that are usually associated with widespread but variable airflow obstruction that is often reversible, either spontaneously or with treatment, and that causes an associated increase in airway responsiveness to a variety of stimuli. 
     
  • With increasing age, particularly beyond 3 years, the diagnosis of asthma becomes progressively more definitive, and beyond 6 years of age, the NHLBI (1) definition can be accepted (2).
     
  • Childhood asthma begins in early childhood, with 80% of children experiencing their first episode of wheezing before the age of 3 years (3).
     
  • Lung function in early childhood appears to deteriorate from previously normal levels but does not deteriorate further from the age of 6 years (4) up to the age of 35 years, except in those with moderately severe childhood asthma (5).
     
  • Studies in twins have suggested that in more than half of the cases, susceptibility to childhood asthma is genetic (6).
     
  • There is now overwhelming evidence that allergy is a very important prerequisite for the development of asthma, and at least 75-90% of childhood asthmatics beyond 4-5 years of age have evidence of allergy (2).
     
  • Sensitization to both indoor and outdoor aeroallergens occurring early in life is strongly associated with the risk of developing asthma-like symptoms (7, 8), whereas sensitization to similar allergens later in life has less bearing on asthma (9).
     
  • Infants who subsequently develop asthma symptoms are more likely than other children to be sensitized to foods (10).
     
  • In patients with acute allergy to foods, associated asthma is an important risk factor for fatal or near-fatal anaphylaxis (11, 12).
     
  • Bronchial hyperreactivity was present in 29 of 40 children and young adults (mean age 12.3 years) with atopic dermatitis, whereas only 8 of them had a diagnosis of bronchial asthma (13).
     
  • Many asthmatic children have allergic rhinitis, and treatment of the rhinitis could have beneficial effects on the asthma (14).
     
  • In a 23-year follow-up study, patients who reported nasal symptoms were three times more likely to develop asthma than participants without rhinitis (15).
     
  • Between 11% and 32% of patients with allergic rhinitis had increased bronchial hyperreactivity in the range of responses observed in patients with asthma (16-19).
     
  • The prevalence of IgE sensitization to indoor allergens (house-dust mite and cat) (7,20) and Alternaria (21) is positively correlated with both the frequency of asthma and its severity.
     
  • Atopic patients without asthma present some degree of bronchial inflammation (22) and irregularly distributed subepithelial fibrosis of the bronchi (23).
     
  • Pollen has not been found to be associated with asthma in epidemiological studies (21, 24).
     
  • First-degree relatives of asthmatic subjects without asthma have a 75% prevalence of bronchial hyperreactivity, which may persist for several years without the development of symptoms (25).
     
  • An increased bronchial hyperreactivity was shown in 78% of children with atopic dermatitis and no history of asthma symptoms (26).
     
  • In population-based studies using multiple regression, sensitization to grass, ragweed, or tree pollens has not been shown to be an independent risk factor for asthma (20, 27-29).
     
  • Indoor allergens such as house dust mite, cat dander and cockroach allergens have been shown to be major independent risk factors for asthma (20, 27-38).

References:

    1. Global Strategy for Asthma Management and Prevention. NHLBI/WHO workshop report. Publication no. 95-3659. National Institutes of Health, Bethesda, MD, 1995.
    2. Warner JO, Naspitz CK, Cropp GJA. Third international pediatric consensus statement on the management of childhood asthma. Pediatr Pulmonol 1998;25:1-17.
    3. Wright AL, Taussig LM. Lessons from long-term cohort studies. Childhood asthma. Eur Respir J Suppl 1998;27:17s-22s.
    4. Martinez FD, Wright AL, Taussig LM, Holberg CJ, Halonen M, Morgan WJ et al. Asthma and wheezing in the first years of life. The Group Health Medical Associates. N Engl J Med 1995;332:133-8.
    5. Oswald H, Phelan P, Lanigan A, Hibbert M, Carlin JB, Bowes G et al. Childhood asthma and lung function in mid-adult life. Pediatr Pulmonol 1997;23:14-20.
    6. Duffy DL, Martin NG, Battistutta D, Hopper JL, Mathews JD. Genetics of asthma and hay fever in Australian twins. Am Rev Respir Dis 1990;142:1351-8.
    7. Sporik R, Holgate ST, Platts-Mills TA, Cogswell JJ. Exposure to house-dust mite allergen (Der p 1) and the development of asthma in childhood. A prospective study. N Engl J Med 1990;323:502-7.
    8. Henderson FW, Stewart PW, Burchinal MR, Voter KZ, Strope GL, Ivins SS et al. Respiratory allergy and the relationship between early childhood lower respiratory illness and subsequent lung function. Am Rev Respir Dis 1992;145:283-90.
    9. Peat JK, Salome CM, Woolcock AJ. Longitudinal changes in atopy during a 4-year period: relation to bronchial hyperresponsiveness and respiratory symptoms in a population sample of Australian schoolchildren. J Allergy Clin Immunol 1990;85:65-74.
    10. Sigurs N, Bjarnason R, Sigurbergsson F, Kjellman B, Björksten B. Asthma and immunoglobulin E antibodies after respiratory syncytial virus bronchiolitis: a prospective study with matched controls. Pediatrics 1995;95:500-5.
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    19. Braman SS, Barrows AA, DeCotiis BA, Settipane GA, Corrao WM. Airway hyperresponsiveness in allergic rhinitis. A risk factor for asthma. Chest 1987;91:671-4.
    20. Pet JK, Tovey E, Toelle BG, Haby MM, Gray EJ, Mahmic A et al. House dust mite allergens. A major risk factor for childhood asthma in Australia. Am J Respir Crit Care Med 1996;153:141-6.
    21. Gergen PJ, Turkeltaub PC. The association of individual allergen reactivity with respiratory disease in a national sample: data from the second National Health and Nutrition Examination Survey, 1976-80 (NHANES II). J Allergy Clin Immunol 1992;90:579-88.
    22. Djukanovic R, Lai CK, Wilson JW, Britten SJ, Roche WR, Howarth PH et al. Bronchial mucosal manifestation of atopy: a comparison of markers of inflammation between atopic asthmatics, atopic nonasthmatics and healthy controls. Eur Respir J 1992;5:538-44.
    23. Chakir J, Laviolette M, Boutet M, Laliberte R, Dube J, Boulet LP. Lower airways remodeling in nonasthmatic subjects with allergic rhinitis. Lab Invest 1996;75:735-44.
    24. Charpin D, Hughes B, Mallea M, Sutra JP, Balansard G, Vervloet D. Seasonal allergic symptoms and their relation to pollen exposure in south-east France. Clin Exp Allergy 1993;23:435-9.
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