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Asthma — diagnosis and over-diagnosis

This was first pointed out in the area of asthma in sports in 1999 by a National Olympic Committee Medical Officer. Over-diagnosis gave rise to a false epidemic of asthma in sport. The main reason for this was that athletes wished to use beta-2 sympathomimetics (a World Anti-Doping Agency (WADA)-banned substance until 2008) for their perceived improvement in endurance performance or, in high doses, their anabolic effects.

This was followed by a concerted effort to have the European criteria for diagnosis of asthma accepted by the sports community. This was done first by the European Respiratory Society3 and then by WADA11,14 and finally in the consensus statement of the International Olympic Committee Medical Council in 2008.5 The over-diagnosis of asthma in the general community was highlighted in 200612 and subsequently got widespread coverage in the public press13.

There is no doubt that asthma is more common in athletes, with swimmers leading the prevalence.7,8,9 There are many explanations for this and ongoing research is being done to try to explain this phenomenon.

There is even an argument that asthma improves performance, resulting in more Olympic medals for asthmatic swimmers than for swimmers without asthma.10

As there is no difference between clinical asthma and sports asthma, there is a need for objective tests in the diagnosis of all forms of asthma. A history and physical examination at rest are rarely able to confirm a diagnosis of asthma in an athlete. They certainly cannot diagnose several of the mimics stated in the differential diagnosis (Table 1), nor assess the severity of airflow obstruction. We have learned a lot about asthma by observing the probable false epidemic of asthma that occurred in athletes in the 1990s and 2000s.

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Table 1: Differential diagnosis for asthma

Description of asthma

Asthma is a syndrome of the respiratory airways typified by recurrent, episodic symptoms associated with variable airway obstruction that is reversible, either spontaneously or with treatment; the presence of airway hyper-responsiveness; and chronic airway inflammation.

There is a high prevalence of these features in active, competitive athletes, often in the form of exercise-induced asthma (EIA) or exercise-induced bronchoconstriction (EIB).

EIA may be defined as a transient airway-narrowing induced by exercise in an individual with asthma, while EIB represents reduction in lung function only after exercise, even in the absence of a previous asthma diagnosis.1,2,4

This has lead to two main phenotypes of asthma:

  • The first is the classification of asthma as a disease, manifested as atopy, thereby including eczema, allergic rhinitis, conjunctivitis and raised levels of IgE and eosinophils in the description.
  • The second category describes asthma as a physiological variable on exercise in the form of induced bronchial hyper-reactivity, without reference to atopy or chronic disease.

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Table 2: What is not asthma

Discussion

The first case illustrates a definite diagnosis of asthma1,2 with low-normal spirometry at rest before and after exercise. A methacholine test was positive at 1mg and an excellent response to therapy at rest and after a pharmacological challenge, was demonstrated over months. This is our classical asthmatic patient, with a minimally-elevated IgE. Her treatment was in a stepwise fashion.1

Case report 1

This first case provides detail, while the other two cases will not mention negatives of history, tests and physical examination.

MH is a 56-year-old teacher with a persistent dry cough. She also complained of sputum but no haemoptysis. Dyspnoea was present to a mild degree intermittently and she had chest pain under her left scapula. She has a history of asthma for 20 years and attended her physician regularly for it. She has not been to an emergency department, nor has she been hospitalised for it. She has had one course of systemic steroids, one use of home nebuliser and many bronchodilators and steroids by inhalation over the years.

Family history is negative for asthma. Allergy tests were normal; she is a non-smoker and has no symptoms suggestive of sinusitis or reflux oesophagus. She never had a diagnosis of eczema nor of allergic conjunctivitis.

She has been on a Xanthine (phyllocontin) for 20 years. She has also been on Premarin and Coversyl (an ACE inhibitor) for two years for hypertension. This latter drug was stopped, as it can be a cause of chronic cough. She had Symbicort (a beta-2 agonist and a corticosteroid by inhalation) added to her therapy, to be used intermittently, in the past months.

Physical examination was unremarkable, with no evidence of rhonchi or crackles.

Chest and sinus x-rays were normal. Serum IgE was minimally elevated at 103 (-100) and total eosinophil count was normal in the peripheral blood.

Resting spirometry was normal, with an FEV-1 of 2.0 L (83 per cent predicted) and no bronchodilator effect. An exercise challenge test was negative. A methacholine challenge test was abnormal, with a drop in FEV-1 of 29 per cent at 1mg. With an increase and regular use of Symbicort, there was still a 25 per cent drop in FEV-1 at 1mg (still positive for bronchoconstriction after challenge).

She was given a home nebuliser with a steroid (Flixotide 2mg) and an anticholinergic, plus a beta-2 agonist (Combivent), one nebule twice a day. Her methacholine test was negative for bronchoconstriction at 16mg three months later. Her baseline FEV-1 improved to 2.16 L (91 per cent predicted after 18 months, with a negative test for bronchoconstriction. Treatment was continued and she was told to follow-up six-monthly or sooner if any deterioration occurred in her condition.

The second case illustrates the over-diagnosis of asthma made clinically. When objective criteria were applied, the athlete was found to have supernormal lung function at rest and no signs of a physiologically- or pharmacologically-induced airflow obstruction.

Why did the athlete persist with inhaled bronchodilators and steroids? An explanation may be that inhaled beta-2 agonists act as a placebo.

A teleological explanation is that he had fully developed his lung volume (lung cellular growth stops at age seven years; volumes increase for a variable number of years after that). His chest cage may have been still developing and would do so to the age of 28, +/– three years. This larger lung volume and smaller lung cage may have given him a perception of restriction. A new functional test of lung performance is badly needed in respiratory medicine to see whether there are unidentified changes in lung function in certain patients.

There was a 50 per cent drop in the incidence of asthma with the introduction of testing for anti-asthma drugs in sport.5,11 It has been claimed since the mid-2000s that asthma is over-diagnosed in other conditions such as obesity and diabetes.11

Case report 2

PH is a 17-year-old youth international rugby player. He complains of night cough, increased mucous and tiredness. On exercise, he gets a feeling of restriction of his lungs. He gets two significant pulmonary episodes per year but never goes six weeks without pulmonary symptoms, especially when training. Each significant episode lasts about two weeks.

He uses an antihistamine (Neoclarityn) in the morning. He favours a once-a-day steroid by inhalation, Asmanex and Symbicort before matches and as rescue medicine.

He has a history of reflux oesophagitis and mild nasal symptoms. He is 6ft 2 inches tall and weighs 93kg. His lungs were clear to auscultation and heart was normal.

FEV-1 was 130 per cent predicted at 6.05 L, with a 3 per cent bronchodilator response. Volumes and diffusion were at 110 per cent predicted. An exercise challenge test was done for 18 minutes, with a 2 per cent bronchoconstriction (negative for exercise-induced asthma). A methacholine test was negative at 16mg.

He was advised to stop Asmanex and Neoclarityn two weeks later and Symbicort after four weeks. A trial of therapy for his UGIT and nose were recommended. It was recommended that repeat tests be done in six-to-12 weeks off all anti-asthma drugs.

The third case is only seen in sport and possibly occupational asthma. It is better referred to as EIB to avoid the athlete carrying an insurance-adverse diagnosis of asthma for life.

This form of EIB/asthma is usually associated with a lymphocyte infiltration of the airways. It is more related to an environmental stimulus than a significant, intrinsic disease pathophysiology (normal IgE and eosinophils in blood and airways).

Sequential bronchial biopsies and functional assessment have shown changes in histology that correlates with functional changes in swimmers.6,8

There is a school of thought that says it may be just a physiological response to exercise. This would be the shift of perfusion and ventilation from the dependant part of the lung to a more global distribution in the lung during exercise. This change in the distribution of ventilation would be brought about by bronchoconstriction, especially in the lung bases. This is possibly where the higher incidence of diagnosis of asthma in sport is coming from, especially if we use the eucapnic voluntary hyperventilation (EVH) test rather than the resting pulmonary function tests with a bronchodilator or the exercise or methacholine challenge tests.

Some respiratory physicians comment that the exercise-induced bronchoconstriction, with no clinical symptoms during the day or at night time, is not a currently-recognised form of asthma, as there may be no chronic inflammation. I would recommend we say this is for an expert panel opinion and we await evidence-based clinical articles on the subject.

There is a definite ‘advantage’ for swimmers to having asthma. More medals are won by asthmatic swimmers than swimmers with normal lungs.9,10

Case report 3

GH is a 36-year-old ex-swimmer who had asthma as a competing athlete in his teens and 20s, with exercise challenge test showing a greater than 10 per cent drop in FEV-1 when he was training. He complained of exercise-induced dyspnoea. He was treated with a beta-2 sympathomimetic before training and competition.

He continued to use a bronchodilator intermittently. His resting FEV-1 was normal, at 118 per cent predicted without a bronchoconstrictor effect of exercise. His methacholine challenge test was negative. On discontinuation of vigorous training for swimming in his mid 20s, he has had no symptoms of asthma and a negative exercise challenge test. All anti-asthma medication was stopped.

Why do asthmatic athletes perform so well at the Olympic Games?

Many possible explanations have been put forward for this objective finding:

  1. They were elite athletes who then developed asthma.
  2. Asthma drugs are possibly ergogenic (not proven).
  3. Asthma and high performance have a common gene pool. This association with the gene for asthma (important in about 33 per cent of asthmatics) and a gene for endurance performance is unproven.
  4. Asthma represents a ‘training stimulus’, in that they are breathing against resistance of bronchospasm. This training against obstructive airflow improves the muscles of ventilation so that in competition, they have an advantage.

Swimming has the highest incidence of asthma than any sport.7 It has been documented that when swimmers stop training vigorously, up to 66 per cent reverse their asthma.8,9 This may be the explanation for Case Report 2. We have known for a long time that asthma may wax and wane clinically.

Of course, he might never have had asthma. This would then need an explanation.

We have been saying since 1999 that asthma has been over-diagnosed in sport. This was because patients/athletes wanted to use beta-2 stimulants to possibly enhance their performance (not proven). Case 3 illustrates exercise-induced bronchospasm in a patient with normal lung function at rest. He had a negative methacholine test. His clinical file was negative and without symptoms of asthma, except after exercise when competing.

Diagnostic criteria4

Bronchodilator test (spirometry) after a sympathomimetic bronchial challenge test giving bronchoconstriction.

  • Pharmacological
  • Methacholine, saline 4.5 per cent, mannitol 4.5 per cent.
  • Histamine is obsolete.

  • Physiological
  • Eucapnic voluntary hyperventilation.
  • Exercise challenge test.

  • Resting pulmonary function tests: 12 per cent bronchodilation above the athlete’s resting forced expiratory volume in one second (FEV-1).

  • Non-pharmacological challenge: 10 per cent bronchoconstriction in FEV-1. This includes exercise and eucapnic voluntary hyperventilation.

  • Pharmacological stimulation tests: 20 per cent bronchoconstriction in FEV-1 at a methacholine dose of 1mg/ml or less (or 4mg/ml if the patient used corticosteroid by inhalation in the previous four months).

Other pharmacological challenge tests include 4.5 per cent saline and mannitol (a 15 per cent drop in FEV-1 is a positive test).

  • Clinical file should include:
  • Consultations with their physicians.
  • Hospital emergency department attendance or admissions for acute exacerbations of asthma or treatment with oral corticosteroids.
  • Age of onset of asthma.
  • Symptom description day and night.
  • Trigger factors.
  • Medication use.
  • Past history of atopy or childhood asthma.
  • Physical examination.
  • Skin-prick test or RAST showing allergic hypersensitivity.

References

  1. Carlsen KH, Anderson SD, Bjermer L, Bonini S, Brusasco V, Canonica W, Cummiskey J, Delgado L, Del Giacco SR, Drobnic F, Haahtela T, Larsson K, Palange P, Popov T, van Cauwenberge P. Treatment of exercise-induced asthma, respiratory and allergic disorders in elite athletes: Epidemiology, mechanisms and diagnosis: Part I of the report from the Joint Task Force of the European Respiratory Society and the European Academy of Allergy and Clinical Immunology. J Allergy (63) 2008.
  2. Carlsen KH, Anderson SD, Bjermer L, Bonini S, Brusasco V, Canonica W, Cummiskey J, Delgado L, Del Giacco SR, Drobnic F, Haahtela T, Larsson K, Palange P, Popov T, van Cauwenberge P. Treatment of exercise-induced asthma, respiratory and allergic disorders in sport and the relationship to doping: Part II of the report from the Joint Task Force of European Respiratory Society and European Academy of Allergy and Clinical Immunology. J Allergy (63) 2008.
  3. KH Carlsen et al. European Respiratory Journal, 2005, Monograph 33. Diagnosis, prevention and treatment of exercise-related asthma. ‘Respiratory and allergic disorders in sport.’
  4. Fitch K, Sue-Chu M, Anderson S, Boulet LP, Hancox R, McKenzie D, Backer V, Rundell K, Alonso JM, Kippelen P, Cummiskey J, Garnier A, Ljungqvist A. Asthma and the elite athlete: Summary of the IOC Consensus Conference Lausanne, Switzerland, January 22-24, 2008. J Allergy & Clinical Immunology 122(2) 2008.
  5. Fitch K, Sue-Chu M, Anderson S, Boulet LP, Hancox R, McKenzie D, Backer V, Rundell K, Alonso JM, Kippelen P, Cummiskey J, Garnier A, Ljungqvist A. Why inhaled Beta2 agonists are prohibited and why the IOC has introduced its policy on inhaled beta2 agonists. J Allergy & Clinical Immunology 122(2) 2008.
  6. Anderson, SD, Kippelen P. Airway injury as a mechanism for exercise-induced bronchoconstriction in elite athletes. J Allergy and Clinical Immunology 2008; 122:225-35.
  7. Lemiere C, Malo JL, Boutet M. Reactive airways dysfunction syndrome due to chlorine: Sequential bronchial biopsies and functional assessment. Eur Respir J. 1997;10:241-4.
  8. Helenius I, Rytilä P, Sarna S, et al. Effect of continuing or finishing high-level sports on airway inflammation, bronchial hyperresponsiveness, and asthma: A five-year prospective follow-up study of 42 highly-trained swimmers. J Allergy Clin Immunol. 2002;109:962-8.
  9. Bougault V, Turmel J, Boulet LP. Airway hyper-responsiveness in elite swimmers: Is it a transient phenomenon? J Allergy Clin Immunol. 2011;127:892-8.
  10. McKenzie DC, Fitch KD. The asthmatic athlete: Inhaled Beta-2 agonists, sport performance, and doping. Clin J Sport Med 2011; 21:46-50.
  11. Couto M, Horta L, Delgado L, et al. Impact of changes in anti-doping regulations (WADA Guidelines) on asthma care in athletes. Clin J Sport Med. 2013;23 (1):74-7.
  12. Eder W, Ege MJ, von Mutius E. The asthma epidemic. N Engl J Med. 2006 Nov 23;355(21):2226-35.
  13. Tiffany Sharples, study: Is Asthma overdiagnosed? Time Magazine. Nov 18, 2008.
  14. WADA. Medical information to support the decisions of TUECs for asthma. Internal document, Version 4, 12.2011.

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