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International Symposium on Special Problems of Allergic Athletes
Summary tnternational Symposium of AItergic Athletes Sheldon
C. Siegel,
M.D. LOS Angeles,
This most stimulating, informative, and provocative symposium deals in depth with the special problems and management of allergic athletes. It will serve to emphasize to our allergist-immunologist colleagues that sports medicine no longer lies solely in the domain of the orthopedists and surgeons, but encompasses many medical aspects of sports unrelated to trauma and requires the expertise of many specialists inciuding our own. In a summary of this symposium it would be inappropriate for me to attempt to paraphrase the content of all contributions, each of which has been so eiegantly presented. What I hope to do is highlight some of those areas covered and emphasize those that I believe will require additional attention in the future. One of the major problems confronting the allergic athlete is exercise-induced asthma (EIA). Although it has been recognized for centuries that exercise can provoke an attack of asthma, only in the last 20 years has there been renewed and intense interest in the subject. In the past couple of years great strides have been made in our understanding of the underlying pathophysioiogic mechanisms involved in EIA. Many of these advances in our knowledge of the many factors that influence the severity of the reaction were made by the investigators who are part of this symposium. A recent hypothesis invoked the concept that the primary precipitating event in EIA is cooling of the airways, which results from the humidification of the inspired air. Drs. Sheppard and Anderson very nicely review the evidence previously presented to support the hypothesis that respiratory heat loss is the cause of EIA, and then present their findings and give their reasons why this theory is untenable as the full explanation for the induction of bronchospasm. They conclude from their elegant studies, which used hy-
From the Department of Pediatrics, Division of Allergy-lmmunology. University of California School of Medicine. Los Angeles. Calif.
on
Calif.
perosmolar, hypoosmolar, and isoosmoiar aerosols, that the loss of water per se, not heat loss, is the major stimulus for triggering EIA, possibly via a transient increase in osmolarity of the surface airway. Whether the latter induces bronchoconstriction via irritant receptors of the parasympathetic system, as suggested by the observations that the bronchoconstrictor response can be partly inhibited with atropine, or whether mediators are released from airway mast cells has not been fully settled. In support of the latter, Dr. Lee and associates found that neutrophil chemotactic factor (NCF) is released during exercise and that cromoiyn prevents both EIA and the release of NCF. In concert with this latter concept are the studies cited by Dr. Eggleston in his discussion of the papers. He and his asociates have demonstrated that both basophils and human lung mast ceils spontaneously secrete mediators at the osmolarities found in airway surface fluid. Although I believe we are close to adopting a unified hypothesis for EIA, some pieces of the puzzle do not seem to fit. For example, Dr. Lee and his colleagues mention the inability to find NCF and the delayed appearance of histamine after hyperventiiationinduced asthma. They postulate that an exercise “X” factor accounts for this discrepancy. Even more puzzling is the fact that one can make an asthmatic refractory to further EIA by having him exercise while breathing warm humid air, which does not in itself produce EIA. Furthermore, about SO% of patients made refractory to exercise challenge, presumably from release of stored mediators, will develop bronchospasm to a specific inhaled allergen. Dr. Nadei addresses the broader issue of hyperreactivity of the airways as it retates to the athlete. He reminds us that cough, increased mucus production, and edema of the airways as well as bronchospasm often handicap the athlete. I believe it is importent to reemphasize a point stressed throughout this presentation, namely, that a number of diverse factors undoubtedly contribute to the airways hyperreactivity 745
746
Siegel
to a wide variety of stimuli. Cells other than the mast cells in the airways, like the epithelial cells, and mediators such as the leukotrienes and prostaglandins. as well as histamine and NCF, must certainly play some role in the production of hyperreactivity of the airways. I liked the comment that the key to our understanding of the problem is to learn how all of the various cells are involved in producing the hyperir&ability and how they talk to one another. Despite the recent advances made in our understanding of the mechanisms responsible for producing airway hyperreactivity, which is partly reviewed by Dr. Nadel, 1 believe it is still safe to say that they are complex and poorly understood. Dr. Middleton presents a very intriguing and enticing concept of how calcium ion migration or mobilization might play a central role in the development of hyperreactivity of the airways in asthma. He points out that the function of most of the cell types (smooth muscle, mast cells, mucous glands, vagus nerve, inflammatory cells) that have some effect on airway caliber and reactivity is dependent upon Ca++ ions, which serve as a coupling agent between excitation and contraction and stimulations and secretion. For example, migration of Ca + + ions into smooth muscle causes contraction; entrance into mast cells will prevent mediator release; migration into goblet cells causes mucus secretion; and Ca++ ions affect vagus nerve impulse initiation and conduction and migration of leukocytes. Dr. Middleton reminds us, as does Dr. Furukawa, that calcium channel blockers such as nifedipine, verapamil, and others do abrogate EIA and histamine contraction of smooth muscle in vitro, but do not act as bronchodilators. Although calcium channel blocking drugs might possibly find some use in the treatment of asthma, particularly in preventing EIA, given the existing evidence it seems unlikely that present agents will play a major role in the treatment of asthma. Dr. Bierman reminds us that some patients may experience a delayed bronchospastic response after exercise, comparable to that observed after allergen challenge. It is surprising that this biphasic response to exercise went unrecognized until Dr. Bierman and coworkers outlined it just 3 years ago, especially as it may occur in approximately a third of patients exhibiting EIA. It is specially interesting that cromolyn blocks this delayed reaction, as it does after antigen challenge, and that NCF has also been observed to be released in a biphasic manner only in those patients with a delayed response to exercise. Drs. Eggleston, Shapiro, and Rosenthal present three excellent papers detailing three bronchial challenge methods of assessing asthma. In addition to
J. ALLERGY
CLIN.
IMMUNOL. MAY 1984
reviewing the standard EIA protocol to be done in the laboratory, Dr. Eggleston also reviews a technique of evaluating EIA in athletes under field conditions. He advises us to remember some of the precautions that are necessary in carrying out an EIA test, including the necessity of taking a good medical history: performing a physical examination; if indicated, using a “stepped” protocol; monitoring by ECG; and hnally, having cardiopulmonary resuscitation equipment available at all times. One little pearl that he mentioned, which I felt worth repeating, was that a series of short sprints performed by the patient is a useful technique for inducing a refractory period to EIA. Dr. Shapiro’s article on methacholine challenge provides evidence that this test might be extremely useful in those athletes who cough or complain of tightness in their chests or shortness of breath, but who do not wheeze. Those patients with a positive challenge will frequently respond to a bronchodilator and/or cromolyn. I agree with her contention that a methacholine challenge may be a safer and better test than exercise to screen for hyperreactivity of the airways. Dr. Rosenthal presents an innovative and simplified method of inducing bronchospasm via a eucapnic voluntary hyperventilation challenge. The method does not invoke the use of any cold air or the monitoring of end-expiratory CO,. It should prove to be another practical and useful tool by which the effects of hyperventilation on the airways can be assessed. Perhaps the most important point to be made with regard to managing patients with EIA is to tell patients it can be controlled and they should not refrain from normal physical activity, and to encourage them to participate in sports activities. This point was not emphasized enough throughout the symposium even though I am certain all of the participants agree with that adage. From four good reviews on the pharmacologic agents that can be used in managing EIA, 1 gathered that there was a consensus that the B-adrenergic agonists, especially the newer B,-selective agents such as albuterol, terbutaline, fenoterol, etc., administered by aerosol were the most effective. Some investigators have felt that oral adrenergic preparations are less effective than the aerosols. There is also some agreement that cromolyn and theophylline, although effective in preventing EIA, are less effective than B-adrenergic aerosols. On the other hand, cromolyn has the advantage of preventing both the immediate and the delayed type of response and it produces no adverse effects on the cardiovascular system. Dr. Ellis makes a couple of salient and interesting comments when discussing theophylline. He believes there might be a minor advantage to use of the sus-
VOLllME NUMBER
73 5. PART 2
tained-acting over the short-acting theophylline preparations.Onepoint he makes, and with which I wholeheartedly agree, is that there is not always a direct relationship between serum levels of theophylline and the amount of bronchodilatation obtained. Most of the effect occurs at lower levels; at higher levels there is a diminishing response and of course, an increased likelihood of toxic reactions. The upper limit of the so-called “therapeutic range” of 10 to 20 kg/ml has been set primarily by the fact that the frequency of side effects increases beyond the 20 p,g/ml level. On the other hand, the lower limit is less well defined and we have found that many children will get good bronchodilatation with levels below 10 kg/ml.’ A recent report from National Jewish Hospital in Denver also supports the contention that there is not always continuous improvement with increasing serum levels of theophylline in patients with mild asthma.’ These authors found little improvement in lung function when serum theophylline levels were increased. Dr. Ellis also mentions the possibility that theophylline could aid the competitive athlete in that methylxanthines are known to strengthen the contractility of striated muscle and could conceivably combat fatigue. Dr. Furukawa ably covers other pharmacologic agents that might have some potential for the management of EIA. The cromolyn-like drugs have, to date, been disappointing and many have associated seriousunwanted properties. Atropine and its isomer ipratropium appearto be effective in selectedpatients, especially in those with chronic bronchitis; thesemay have a place for treatment of those patients unresponsive to p-agonists, but are unlikely to be useful for the athlete with EIA. Two articles concern other types of adverse reactions that occur from exercise. Drs. Sheffer and Austen very nicely review their experience with exerciseinduced anaphylaxis. 1 am astonishedthat they are already aware of 500 individuals who have exhibited this unusual phenomenon. I was further surprisedto learn that none of the patients, who were carefully studiedin their laboratories, manifestedclinically any signsof wheezing or had changesin their pulmonary function findings. This syndrome is especially intriguing in that symptoms are more likely to develop after eating, especially if a food contains specific allergen to which the patient is sensitive. The reasonsfor this are not clear and further studiesare being performed to clarify this relationship. Someof the subjectsstudied experienced an increasein blood histamine levels. It seemslikely that other mediators might also be identified in the future. Treatment of exercise-induced anaphylaxis has been unsatisfactory. Dr. Kaplan addressesthe subjects of exercise-
induced hives, and cholinergic and cold-induced urticaria, all of which can affect the athtetc. Hr very eloquently outlines what is known of the pathogenesis of both of th’esesyndromes and makes iecommendations for treating them. My associate, Dr. Katz. reviews thr‘ pathophysiology and analomy of the nose. He alsr~presentssome interesting data on two gold medal contendersin the upcoming Olympics. Both of these patients. in contrast to what IS normally observed. had noted nasal congestion during warm-ups and during track events, and these observations were confirmed in our laboratory. This brought to mind that when I exercise. on the rare occasions that I do. 1 also CieCelopnasal congestion and rhinorrhea. Obviously, additional studieswill be necessaryto contirm thcsc preliminao observations. Dr. SIavin presentsa thorough and cucellent discussionof the problem of sinusitis as it relatesto the managementof the allergic athlete. He makes;~JI important point. which should be emphasized: that the symptomsand signsof the sinusitismay not be readily apparentand that one shouldalways ha!;c a high index ot’ suspicion of this diagnosis. i agree that an s-ray view of the sinusesis the most reliable means of diagnosing sinusitis. My associatesand I feel that in children, a Waters view of the maxillae is 4Iicient in most casesI:Oconfirm the diagnoslh. Dr. Pierson and associatesbeautifulI:\ review the subject of air pollutants and their effect on bronchial hyperreactivity, a problem that will undoubtedly be encountered in Los Angeles during the forthcoming Olympic Games.They presentevidence that both sulfur dioxide and.ozone lead in a dose-responsemanner to bronchial constriction and that exercise along with other factors may enhancethis responhr Dr. Fitch presentsa comprehensive re\ieu of all factors that ma.y contribute to the health problemsof the allergic athlete during an OLympiad. I am surprised to learn that 20% of recent Australian Olympic athietes have allergic disorders;Dr. Fitch cxpreksessomeconcern that these athletes might suffer more adverse effects than oiher nonallergic compernors from air pollution in the forthcoming Olympic Gameb. He points out that the present antidopinp rules do not permit the use of any oral or topical decongestants. ln a very well organized and comprehensive presentation, Kathleen Mahan reviews the guidelinesfor the nutritional care of the athlete. She provides many practical suggestionsasto the type of diet that should be given to the athlete and in addition. presentsa fairly detailed discussion of food intolerances along with some approachesfor the diagnosis and treatment of such.
748
J. ALLERGY
Siegel
Dr. Oseid along with his Norwegian committee members are to be congratulated for the excellent program they have developed and implemented to control doping among their Olympiad athletes. They emphasize the need for changes in rules so that a-adrenergic agents can be used for the treatment of allergic rhinitis and upper respiratory infections. Finally, Dr. Clarke details the drug-monitoring problem in the United States and clarifies the goveming bodies of the Olympic athletes in the States. As the Director of Sports Medicine Division of the U.S. Olympic Committee, I would hope that some of the problems and suggestions made in this symposium
CLIN. IMMUNOL. MAY 1984
might be considered by the Olympic governing bodies concerned with drugs permissible for use by elite athletes. REFERENCES I. Katz RM, Rachelefsky GS, Siegel SC, Mickey MR: Theophylline administration in children with asthma: Optimal pulmonary function and possible tolerance to chronic administration. Ann Allergy 50:23-6. 1983 2. Klein JJ, Letlcowitz MS, Spector SL, Chemiak RM: Relationship between serum theophylline levels and pulmonary function before and after inhaled beta-agonist in “stable” asthmatics. Am Rev Respir Dis 127:413-6. 1983
C. Siegel,
M.D. LOS Angeles,
This most stimulating, informative, and provocative symposium deals in depth with the special problems and management of allergic athletes. It will serve to emphasize to our allergist-immunologist colleagues that sports medicine no longer lies solely in the domain of the orthopedists and surgeons, but encompasses many medical aspects of sports unrelated to trauma and requires the expertise of many specialists inciuding our own. In a summary of this symposium it would be inappropriate for me to attempt to paraphrase the content of all contributions, each of which has been so eiegantly presented. What I hope to do is highlight some of those areas covered and emphasize those that I believe will require additional attention in the future. One of the major problems confronting the allergic athlete is exercise-induced asthma (EIA). Although it has been recognized for centuries that exercise can provoke an attack of asthma, only in the last 20 years has there been renewed and intense interest in the subject. In the past couple of years great strides have been made in our understanding of the underlying pathophysioiogic mechanisms involved in EIA. Many of these advances in our knowledge of the many factors that influence the severity of the reaction were made by the investigators who are part of this symposium. A recent hypothesis invoked the concept that the primary precipitating event in EIA is cooling of the airways, which results from the humidification of the inspired air. Drs. Sheppard and Anderson very nicely review the evidence previously presented to support the hypothesis that respiratory heat loss is the cause of EIA, and then present their findings and give their reasons why this theory is untenable as the full explanation for the induction of bronchospasm. They conclude from their elegant studies, which used hy-
From the Department of Pediatrics, Division of Allergy-lmmunology. University of California School of Medicine. Los Angeles. Calif.
on
Calif.
perosmolar, hypoosmolar, and isoosmoiar aerosols, that the loss of water per se, not heat loss, is the major stimulus for triggering EIA, possibly via a transient increase in osmolarity of the surface airway. Whether the latter induces bronchoconstriction via irritant receptors of the parasympathetic system, as suggested by the observations that the bronchoconstrictor response can be partly inhibited with atropine, or whether mediators are released from airway mast cells has not been fully settled. In support of the latter, Dr. Lee and associates found that neutrophil chemotactic factor (NCF) is released during exercise and that cromoiyn prevents both EIA and the release of NCF. In concert with this latter concept are the studies cited by Dr. Eggleston in his discussion of the papers. He and his asociates have demonstrated that both basophils and human lung mast ceils spontaneously secrete mediators at the osmolarities found in airway surface fluid. Although I believe we are close to adopting a unified hypothesis for EIA, some pieces of the puzzle do not seem to fit. For example, Dr. Lee and his colleagues mention the inability to find NCF and the delayed appearance of histamine after hyperventiiationinduced asthma. They postulate that an exercise “X” factor accounts for this discrepancy. Even more puzzling is the fact that one can make an asthmatic refractory to further EIA by having him exercise while breathing warm humid air, which does not in itself produce EIA. Furthermore, about SO% of patients made refractory to exercise challenge, presumably from release of stored mediators, will develop bronchospasm to a specific inhaled allergen. Dr. Nadei addresses the broader issue of hyperreactivity of the airways as it retates to the athlete. He reminds us that cough, increased mucus production, and edema of the airways as well as bronchospasm often handicap the athlete. I believe it is importent to reemphasize a point stressed throughout this presentation, namely, that a number of diverse factors undoubtedly contribute to the airways hyperreactivity 745
746
Siegel
to a wide variety of stimuli. Cells other than the mast cells in the airways, like the epithelial cells, and mediators such as the leukotrienes and prostaglandins. as well as histamine and NCF, must certainly play some role in the production of hyperreactivity of the airways. I liked the comment that the key to our understanding of the problem is to learn how all of the various cells are involved in producing the hyperir&ability and how they talk to one another. Despite the recent advances made in our understanding of the mechanisms responsible for producing airway hyperreactivity, which is partly reviewed by Dr. Nadel, 1 believe it is still safe to say that they are complex and poorly understood. Dr. Middleton presents a very intriguing and enticing concept of how calcium ion migration or mobilization might play a central role in the development of hyperreactivity of the airways in asthma. He points out that the function of most of the cell types (smooth muscle, mast cells, mucous glands, vagus nerve, inflammatory cells) that have some effect on airway caliber and reactivity is dependent upon Ca++ ions, which serve as a coupling agent between excitation and contraction and stimulations and secretion. For example, migration of Ca + + ions into smooth muscle causes contraction; entrance into mast cells will prevent mediator release; migration into goblet cells causes mucus secretion; and Ca++ ions affect vagus nerve impulse initiation and conduction and migration of leukocytes. Dr. Middleton reminds us, as does Dr. Furukawa, that calcium channel blockers such as nifedipine, verapamil, and others do abrogate EIA and histamine contraction of smooth muscle in vitro, but do not act as bronchodilators. Although calcium channel blocking drugs might possibly find some use in the treatment of asthma, particularly in preventing EIA, given the existing evidence it seems unlikely that present agents will play a major role in the treatment of asthma. Dr. Bierman reminds us that some patients may experience a delayed bronchospastic response after exercise, comparable to that observed after allergen challenge. It is surprising that this biphasic response to exercise went unrecognized until Dr. Bierman and coworkers outlined it just 3 years ago, especially as it may occur in approximately a third of patients exhibiting EIA. It is specially interesting that cromolyn blocks this delayed reaction, as it does after antigen challenge, and that NCF has also been observed to be released in a biphasic manner only in those patients with a delayed response to exercise. Drs. Eggleston, Shapiro, and Rosenthal present three excellent papers detailing three bronchial challenge methods of assessing asthma. In addition to
J. ALLERGY
CLIN.
IMMUNOL. MAY 1984
reviewing the standard EIA protocol to be done in the laboratory, Dr. Eggleston also reviews a technique of evaluating EIA in athletes under field conditions. He advises us to remember some of the precautions that are necessary in carrying out an EIA test, including the necessity of taking a good medical history: performing a physical examination; if indicated, using a “stepped” protocol; monitoring by ECG; and hnally, having cardiopulmonary resuscitation equipment available at all times. One little pearl that he mentioned, which I felt worth repeating, was that a series of short sprints performed by the patient is a useful technique for inducing a refractory period to EIA. Dr. Shapiro’s article on methacholine challenge provides evidence that this test might be extremely useful in those athletes who cough or complain of tightness in their chests or shortness of breath, but who do not wheeze. Those patients with a positive challenge will frequently respond to a bronchodilator and/or cromolyn. I agree with her contention that a methacholine challenge may be a safer and better test than exercise to screen for hyperreactivity of the airways. Dr. Rosenthal presents an innovative and simplified method of inducing bronchospasm via a eucapnic voluntary hyperventilation challenge. The method does not invoke the use of any cold air or the monitoring of end-expiratory CO,. It should prove to be another practical and useful tool by which the effects of hyperventilation on the airways can be assessed. Perhaps the most important point to be made with regard to managing patients with EIA is to tell patients it can be controlled and they should not refrain from normal physical activity, and to encourage them to participate in sports activities. This point was not emphasized enough throughout the symposium even though I am certain all of the participants agree with that adage. From four good reviews on the pharmacologic agents that can be used in managing EIA, 1 gathered that there was a consensus that the B-adrenergic agonists, especially the newer B,-selective agents such as albuterol, terbutaline, fenoterol, etc., administered by aerosol were the most effective. Some investigators have felt that oral adrenergic preparations are less effective than the aerosols. There is also some agreement that cromolyn and theophylline, although effective in preventing EIA, are less effective than B-adrenergic aerosols. On the other hand, cromolyn has the advantage of preventing both the immediate and the delayed type of response and it produces no adverse effects on the cardiovascular system. Dr. Ellis makes a couple of salient and interesting comments when discussing theophylline. He believes there might be a minor advantage to use of the sus-
VOLllME NUMBER
73 5. PART 2
tained-acting over the short-acting theophylline preparations.Onepoint he makes, and with which I wholeheartedly agree, is that there is not always a direct relationship between serum levels of theophylline and the amount of bronchodilatation obtained. Most of the effect occurs at lower levels; at higher levels there is a diminishing response and of course, an increased likelihood of toxic reactions. The upper limit of the so-called “therapeutic range” of 10 to 20 kg/ml has been set primarily by the fact that the frequency of side effects increases beyond the 20 p,g/ml level. On the other hand, the lower limit is less well defined and we have found that many children will get good bronchodilatation with levels below 10 kg/ml.’ A recent report from National Jewish Hospital in Denver also supports the contention that there is not always continuous improvement with increasing serum levels of theophylline in patients with mild asthma.’ These authors found little improvement in lung function when serum theophylline levels were increased. Dr. Ellis also mentions the possibility that theophylline could aid the competitive athlete in that methylxanthines are known to strengthen the contractility of striated muscle and could conceivably combat fatigue. Dr. Furukawa ably covers other pharmacologic agents that might have some potential for the management of EIA. The cromolyn-like drugs have, to date, been disappointing and many have associated seriousunwanted properties. Atropine and its isomer ipratropium appearto be effective in selectedpatients, especially in those with chronic bronchitis; thesemay have a place for treatment of those patients unresponsive to p-agonists, but are unlikely to be useful for the athlete with EIA. Two articles concern other types of adverse reactions that occur from exercise. Drs. Sheffer and Austen very nicely review their experience with exerciseinduced anaphylaxis. 1 am astonishedthat they are already aware of 500 individuals who have exhibited this unusual phenomenon. I was further surprisedto learn that none of the patients, who were carefully studiedin their laboratories, manifestedclinically any signsof wheezing or had changesin their pulmonary function findings. This syndrome is especially intriguing in that symptoms are more likely to develop after eating, especially if a food contains specific allergen to which the patient is sensitive. The reasonsfor this are not clear and further studiesare being performed to clarify this relationship. Someof the subjectsstudied experienced an increasein blood histamine levels. It seemslikely that other mediators might also be identified in the future. Treatment of exercise-induced anaphylaxis has been unsatisfactory. Dr. Kaplan addressesthe subjects of exercise-
induced hives, and cholinergic and cold-induced urticaria, all of which can affect the athtetc. Hr very eloquently outlines what is known of the pathogenesis of both of th’esesyndromes and makes iecommendations for treating them. My associate, Dr. Katz. reviews thr‘ pathophysiology and analomy of the nose. He alsr~presentssome interesting data on two gold medal contendersin the upcoming Olympics. Both of these patients. in contrast to what IS normally observed. had noted nasal congestion during warm-ups and during track events, and these observations were confirmed in our laboratory. This brought to mind that when I exercise. on the rare occasions that I do. 1 also CieCelopnasal congestion and rhinorrhea. Obviously, additional studieswill be necessaryto contirm thcsc preliminao observations. Dr. SIavin presentsa thorough and cucellent discussionof the problem of sinusitis as it relatesto the managementof the allergic athlete. He makes;~JI important point. which should be emphasized: that the symptomsand signsof the sinusitismay not be readily apparentand that one shouldalways ha!;c a high index ot’ suspicion of this diagnosis. i agree that an s-ray view of the sinusesis the most reliable means of diagnosing sinusitis. My associatesand I feel that in children, a Waters view of the maxillae is 4Iicient in most casesI:Oconfirm the diagnoslh. Dr. Pierson and associatesbeautifulI:\ review the subject of air pollutants and their effect on bronchial hyperreactivity, a problem that will undoubtedly be encountered in Los Angeles during the forthcoming Olympic Games.They presentevidence that both sulfur dioxide and.ozone lead in a dose-responsemanner to bronchial constriction and that exercise along with other factors may enhancethis responhr Dr. Fitch presentsa comprehensive re\ieu of all factors that ma.y contribute to the health problemsof the allergic athlete during an OLympiad. I am surprised to learn that 20% of recent Australian Olympic athietes have allergic disorders;Dr. Fitch cxpreksessomeconcern that these athletes might suffer more adverse effects than oiher nonallergic compernors from air pollution in the forthcoming Olympic Gameb. He points out that the present antidopinp rules do not permit the use of any oral or topical decongestants. ln a very well organized and comprehensive presentation, Kathleen Mahan reviews the guidelinesfor the nutritional care of the athlete. She provides many practical suggestionsasto the type of diet that should be given to the athlete and in addition. presentsa fairly detailed discussion of food intolerances along with some approachesfor the diagnosis and treatment of such.
748
J. ALLERGY
Siegel
Dr. Oseid along with his Norwegian committee members are to be congratulated for the excellent program they have developed and implemented to control doping among their Olympiad athletes. They emphasize the need for changes in rules so that a-adrenergic agents can be used for the treatment of allergic rhinitis and upper respiratory infections. Finally, Dr. Clarke details the drug-monitoring problem in the United States and clarifies the goveming bodies of the Olympic athletes in the States. As the Director of Sports Medicine Division of the U.S. Olympic Committee, I would hope that some of the problems and suggestions made in this symposium
CLIN. IMMUNOL. MAY 1984
might be considered by the Olympic governing bodies concerned with drugs permissible for use by elite athletes. REFERENCES I. Katz RM, Rachelefsky GS, Siegel SC, Mickey MR: Theophylline administration in children with asthma: Optimal pulmonary function and possible tolerance to chronic administration. Ann Allergy 50:23-6. 1983 2. Klein JJ, Letlcowitz MS, Spector SL, Chemiak RM: Relationship between serum theophylline levels and pulmonary function before and after inhaled beta-agonist in “stable” asthmatics. Am Rev Respir Dis 127:413-6. 1983