Relationship Found Between Mild Asthma and Poor Clinical Outcome

Addressing Asthma

by David A. Stempel, MD
October 29, 2003

 

Introduction
The topic of mild asthma was addressed at the 60th Annual Meeting of the American College of Allergy, Asthma and Immunology in San Antonio, Texas. Asthma is a disease characterized by significant variability. Exposure to allergen or common viral respiratory tract infections may trigger an exacerbation. These flares of symptoms will respond to therapy or reverse spontaneously. Furthermore, there is a diurnal variation in the intensity of asthma reflecting time of day differences in mediator release and endogenous glucocorticoid and catecholamine levels. The 1997 National Heart, Lung, and Blood Institute (NHLBI) Guidelines for the Diagnosis and Management of Asthma[1] established criteria for disease severity classification. Daytime symptoms for patients with mild persistent asthma occur more than twice a week but less than daily and for nighttime symptoms occur between 2 and 4 times a month. Does disease variability limit the applicability of this classification scheme?
 
The Agency for Healthcare Research and Quality (AHRQ) was contracted to perform the evidence-based review for the 2002 NHLBI guideline update. In their discussion of disease classification, the AHRQ stated that "asthma is a chronic disease characterized by differing frequencies of daily symptoms, exacerbations, and remissions, (and) characterizing disease severity is problematic."[2] AHRQ noted that disease severity was confounded by the lack of inclusion of use of inhaled corticosteroids or other controller medications, the duration of asthma, or the presence of atopy. In their review, the AHRQ suggested the use of 3 classifications of persistent asthma: mild-moderate, moderate, and severe.

Mild Asthma

Inflammatory Pathology In the first presentation of this symposia, James Donahue, MD,[3] Chief of Pulmonary Division and Critical Care Medicine, University of North Carolina School of Medicine, Chapel Hill, North Carolina, presented some of the background for this discussion. From a clinical perspective, the difficulty with asthma is that disease severity is frequently underestimated by both patients and healthcare workers. Patients underreport symptoms and physicians underdiagnose disease severity. Patients may be diagnosed as being intermittent asthmatics if symptoms alone are assessed. When patients' medications are factored into the disease classification, then 40% of intermittent asthmatics now appear to have persistent disease.
 
Inflammation noted on biopsy is recognized in the guidelines as a common feature of all levels of persistent asthma. Disease severity is based on clinical assessment rather than biopsy data. Donahue next presented a paper by Van den Toorn and colleagues[4] that demonstrated that young adults with asthma in remission, no symptoms for greater than 1 year, still had evidence of active airway inflammation. Biopsies of their airways looked more like patients with active asthma than individuals who never had asthma. The asthmatics in remission had evidence of increased major basic protein, elevated levels of exhaled nitrous oxide, and increased collagen deposition in their subbasement membrane, all indicating evidence of ongoing inflammation in their airway biopsies. This study raises some very critical issues. Clinically, these patients do not have evidence of persistent asthma, but pathologically, their asthma is still active. How should they be classified? Should they be treated? Even patients with milder disease can be at risk for serious exacerbations. The question was raised as to whether this ongoing inflammation places these patients at greater risk for relapse. This study also suggests that children with asthma may not outgrow their asthma.
 
Donahue then reviewed the study by Moore and colleagues,[5] who performed allergen challenge in patients with both mild and moderate persistent asthma. Patients were grouped by the impairment in lung function and degree of airway hyperreactivity. After allergen challenge, the authors quantitated the changes in cellular response and cytokine and protein concentrations. These responses were the same for both mild and moderate persistent asthmatics. Post-challenge, there were similar increases in total cells, eosinophils, and macrophages. Cytokine and protein concentrations increased with the same intensity in both groups of patients and were not distinguished by disease severity. This study confirms the difficulty in disease severity classification and illustrates how the inflammatory process and risk of exacerbation is similar across severity stratifications.
 
In a study by Louis and colleagues,[6] 3 groups of patients with asthma were investigated. They were classified as intermittent, mild to moderate, and severe persistent asthmatics. In this study, the authors were able to differentiate by disease severity with greater evidence of eosinophils and macrophages in the sputum as disease severity increased. Tryptase levels and increased albumin in the sputum, though, did not correlate as strongly with disease severity. What was important in this paper is the finding of significant inflammation even in the patients with intermittent disease. Inflammation is a potential risk factor for severe consequences of asthma and warrants appropriate therapy. How we classify disease severity has a direct bearing on how we treat patients with asthma.

When Do You Treat Mild Asthma and With How Much?

Harold S. Nelson, MD,[7] addressed the question of therapy of mild asthma. The National Asthma Education and Prevention Program (NAEPP) presents as goals of therapy the treatment and prevention of symptoms and exacerbations. Potential complications of mild asthma include decreased quality of life, exacerbations, airway remodeling, and even death. Approximately 40% of patients have mild intermittent or persistent asthma, according to the Asthma in America study. However, in a recent publication by Fuhlbrigge and colleagues,[8] they explored disease classification. When patients were assessed based on short- and long-term symptoms, researchers found that up to 60% of patients had mild intermittent to mild persistent disease. When the functional impact of the disease was included in the assessment of disease severity, this number fell to 22%, reflecting the large majority of patients now diagnosed with moderate to severe persistent asthma.
 
Dr. Nelson noted that patients with asthma and normal daytime spirometry may still have significant impact on their quality of life. In the OPTIMA trial,[9] 33% of patients with mild asthma with normal lung functions and mild symptoms treated with placebo had a severe asthma exacerbation over the subsequent year. These events were severe enough to cause a hospitalization, emergency department visit, require prednisone, or a 25% variability in their peak flow rate on 2 consecutive days. Treatment of these patients with inhaled corticosteroids reduced the rate of exacerbations by more than 50%. In this trial, there was a second group of patients who were being treated with inhaled corticosteroids at the time of enrollment. These patients were "mildly symptomatic." When these patients were treated with the combination of inhaled corticosteroids and a long-acting inhaled bronchodilator, there was a further reduction in the rates of serious exacerbations. This study describes the importance of recognizing the patients at risk for an exacerbation and the need to use appropriate preventive medications to reduce the risk of these flares of disease.
 
Several studies have demonstrated that patients with more mild asthma are at risk for sudden death from asthma. Dr. Nelson discussed the paper by Robertson and associates[10] that studied 51 children who had died of asthma. This study retrospectively investigated whether children were correctly assessed for disease severity based on medical records and interviews. One third of the fatalities were in children with perceived mild asthma. Whether their disease was truly mild or the perception of their disease as mild is not as important as the fact that these children were undertreated. Most were not on controller therapy with inhaled corticosteroids.
 
Dr. Nelson next reviewed the evidence for the 2002 Update of the NAEPP Guidelines. The Childhood Asthma Management Program[11] demonstrated the value of using inhaled corticosteroids in the treatment of children with a baseline forced expiratory volume in 1 second (FEV1) of 94% who were considered mild to moderate persistent asthmatics. Children treated with inhaled corticosteroids had a 40% to 45% reduction in hospitalizations, emergency department visits, and prednisone use -- all significant reductions in severe exacerbations. No significant adverse effects were noted with this treatment.
 
The guideline review demonstrated that use of other controller medications as primary therapy, including theophylline, salmeterol, or leukotriene modifiers, did not appear to be as effective as inhaled corticosteroids. To illustrate this point, he reviewed a study by Busse and colleagues[12] that demonstrated greater improvement in lung function, symptom-free days, albuterol use, and nighttime awakenings. This is one of the articles that was used in the AHRQ evidence-based review.
 
Dr. Nelson concluded his presentation with 2 important questions. First is the question of when to treat. Patients should be treated if they do not meet the goals of the asthma guidelines, including symptoms, pulmonary function, and prevention of exacerbations. Second is the question of how much to treat. One may start with monotherapy with low-dose inhaled corticosteroids but increase to add a long-acting inhaled bronchodilator if the goals of therapy are not achieved. Mild asthmatics are at risk for serious exacerbations and should receive appropriate controller therapy.
The Role of Immunotherapy in Mild Asthma The third presentation at the symposium was by Peter S. Creticos, MD,[13] of Johns Hopkins Asthma and Allergy Center, Baltimore, Maryland. This was a discussion on the role of immunotherapy in the treatment of mild asthma. The success of immunotherapy in asthma is based on the proper selection of patients. Patients with mild disease appear to be good candidates, with some evidence demonstrating that this therapy may modify disease progression. Caution needs to be exercised in the treatment of patients with more severe disease because of the greater risk of side effects from the treatment. Dr. Creticos then reviewed the literature comparing the value of immunotherapy for various allergens. This is an area of intense research and potential for significant change in disease pathology.
 
This symposium demonstrated the need for appropriate assessment of disease severity and implementation of therapy to prevent the consequences of untreated or under-treated asthma. The NAEPP has developed evidence-based guidelines to address the therapy of asthma. Disease classification is dependent on appropriate clinical assessment. Inflammation is an important component of all persistent asthma and potentially even intermittent asthma. The intrinsic variability of asthma must be reflected in disease classification.
References

  1. National Heart, Lung, and Blood Institute. Expert Panel Report 2: Guidelines for the Diagnosis and Management of Asthma. July 1997, NIH Publication No. 97-4051.
  2. Agency for Healthcare Research and Quality Publication No. 01-E044.
  3. Donahue J. Symposium. Mild asthma: is "mild" asthma the wrong word? Inflammatory pathology of mild asthma. Program and abstracts of the 60th Annual Meeting of the American College of Allergy, Asthma and Immunology; November 15-20, 2002; San Antonio, Texas.
  4. van den Toorn LM, Overbeek SE, De Jongste JC, Leman K, Hoogsteden HC, Prins J-B. Airway inflammation is present during clinical remission of atopic asthma. Am J Respir Crit Care Med. 2001;164:2107-2113.
  5. Moore WC, Hasday JD, Meltzer SS, Wisnewski PL, White B, Bleecker ER. Subjects with mild and moderate asthma respond to segmental allergen challenge with similar, reproducible, allergen-specific inflammation. J Allergy Clin Immunol. 2001;108:908-914.
  6. Louis R, Lau LCK, Bron AO, Roldaan AC, Radermecker M, Djukanovi_ R. The relationship between airways inflammation and asthma severity. Am J Respir Crit Care Med. 2000;161:9-15.
  7. Nelson HS. Symposium. Mild asthma: is "mild" asthma the wrong word? Mild asthma: when to treat and how much. Program and abstracts of the 60th Annual Meeting of the American College of Allergy, Asthma and Immunology; November 15-20, 2002; San Antonio, Texas.
  8. Fuhlbrigge AL, Adams RJ, Guilbert TW, et al. The burden of asthma in the United States: level and distribution are dependent on interpretation of the National Asthma Education and Prevention Program Guidelines. Am J Respir Crit Care Med. 2002:166:1044-1049.
  9. O'Byrne PM, Barnes PJ, Rodriguez-Roisin R, et al. Low-dose inhaled budesonide and formoterol in mild persistent asthma. The OPTIMA Randomized Trial. Am J Respir Crit Care Med. 2001;164:1392-1397.
  10. Robertson CF, Rubinfeld AR, Bowes G. Pediatric asthma deaths in Victoria: the mild are at risk. Pediatr Pulmonol. 1992;13:95-100.
  11. The Childhood Asthma Management Program Research Group. Long-term effects of budesonide or nedocromil in children with asthma. N Engl J Med. 2000;343:1054-1063.
  12. Busse W, Raphael GD, Galant S, et al. Low-dose fluticasone propionate compared with montelukast for first-line treatment of persistent asthma: a randomized clinical trial. J Allergy Clin Immunol. 2001;107:461-468.
  13. Creticos PS. Symposium. Mild asthma: is "mild" asthma the wrong word? Immunotherapy for mild asthma. Program and abstracts of the 60th Annual Meeting of the American College of Allergy, Asthma and Immunology; November 15-20, 2002; San Antonio, Texas.

 

For more information contact:
Alan L. Wozniak, CIAQP
(800) 422-7873 ext. 802
info@pureaircontrols.com