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Allergen-Mediated Disease

Keeping Patients Active

John W. O'Kane, MD; Ginger A. Woodford, PharmD

THE PHYSICIAN AND SPORTSMEDICINE - VOL 27 - NO. 9 - SEPTEMBER 1999


Correction: In "Allergen-Mediated Disease: Keeping Patients Active" (September, page 49), two dosages were listed incorrectly and two drugs were mislabeled as sedating in table 1 (page 54) because of errors introduced in editing. The correct dosage for cetirizine hydrochloride is 5 or 10 mg orally once a day. The correct dosage for budesonide is 2 sprays twice a day or 4 sprays once a day. In addition, cetirizine and fexofenadine hydrochloride should be listed as causing little or no sedation. The corrected version of this table is available on this page.


In Brief: A nasal corticosteroid is the most effective treatment for allergic rhinitis, but delayed improvement can reduce compliance. Topical vasoconstrictors, cromolyn, and NSAIDs are recommended for allergic conjunctivitis. Some athletes who have exercise-induced or exercise-exacerbated asthma may have a refractory period, which, along with short- and long-term beta-2 agonists, inhaled corticosteroids, and leukotriene antagonists, may be used to manage symptoms. Topical steroids are the main treatment for atopic dermatitis. Drug restrictions by sports governing bodies can limit therapies for competitive athletes.

Allergic disease is common among athletes and the general public, accounting for many healthcare visits annually. Allergic disorders can be particularly debilitating for athletes and exercisers because they may compromise upper airway and pulmonary function, skin integrity, and, consequently, performance. Four common allergen-mediated diseases are allergic rhinitis and conjunctivitis, atopic dermatitis, and asthma. Identifying their triggers and physiologic pathways can help physicians and athletes manage these disorders through nonpharmacologic and pharmacologic therapies.

Physiologic Mechanisms

Allergic rhinitis, conjunctivitis, atopic dermatitis, and asthma can occur alone or together in allergic (atopic) individuals. Not surprisingly, the diseases share common pathophysiologic mechanisms. Typical allergens include plant pollens, animal dander, dust mites, and certain foods. Atopic individuals may or may not have elevated serum immunoglobulin E (IgE) specific for these or other allergens. When allergen exposure occurs, IgE associated with mast cells or basophils binds the allergen, and subsequent cell degranulation releases histamine, leukotrienes, and other inflammatory mediators. This immediate hypersensitivity has effects on target tissue, including increased vascular permeability and capillary leak, vasodilation, bronchoconstriction, and sensory stimulation, resulting in itching and sneezing.

In the 4 to 8 hours following allergen exposure, cytokines, acting as chemoattractants, mediate the late-phase response, causing an influx of multiple inflammatory cells, including T-lymphocytes, macrophages, and additional eosinophils and basophils. The T-lymphocytes (TH2) and macrophages are primarily responsible for inflammatory changes resulting in allergen-mediated chronic tissue damage. Eosinophils and basophils are responsible for the priming response that makes the target tissue more susceptible to subsequent episodes of immediate hypersensitivity.

An understanding of this pathophysiologic cascade can guide the planning of an optimal treatment regimen. In difficult cases, treatment should target as many steps in the cascade as possible. Measures include allergen avoidance if possible, desensitization to the allergen, and medications that block the immediate hypersensitivity and the chronic inflammatory response. Because of the priming effect, susceptible persons should be pretreated to minimize symptoms.

Allergic Rhinitis

Symptoms and susceptibility. Allergic rhinitis affects 10% to 30% of adults (1). It is caused by allergen-induced inflammation of the nasal mucosa, resulting in rhinorrhea, sneezing, itching, and nasal congestion. Fatigue, headache, and malaise are also common. Allergic conjunctivitis may also accompany rhinitis. Seasonal allergic rhinitis ("hay fever") is caused by pollens or molds, and perennial allergic rhinitis is caused by animals, dust mites, occupational allergens, or molds and pollens that are present year-round. A positive family history of allergies, particularly in both parents, increases the risk of developing allergic rhinitis. The risk increases with age into early adulthood.

Athletes in any sport may be affected, depending on the allergens involved. Those with pollen allergies are often most symptomatic during outdoor spring or fall sports. Athletes who play on natural turf may have significant symptoms after the grass has been mowed.

College-age athletes attending school away from home may develop seasonal allergic rhinitis because of a new environmental exposure. Perennial allergies to mold or dust mites may also be exacerbated by poorly ventilated or infrequently cleaned dorm rooms.

History. To help identify potential allergens, a history should include potential exposures during sports and other activities, exposures to animals, and the timing of symptoms. A family history and a history of favorable response to antihistamines are also important. Concomitant allergic disease such as atopic dermatitis, conjunctivitis, or asthma should also be investigated because successful treatment should address each manifestation of allergen-mediated disease (2). The history should also explore other causes of rhinorrhea and congestion, including viral upper respiratory tract infection (URTI), acute and chronic sinusitis, and the use of oral contraceptives, excessive topical nasal decongestants, and cocaine.

Physical exam. The physical examination should include an examination of the nares, which can be aided by a nasal speculum. Pale, edematous, bluish-gray mucosa is common in allergic rhinitis, while erythema is more common in URTI. The turbinates should be inspected, since regional mucopurulent exudate may indicate sinusitis. Polyps and septal deviation, if present, may account for nasal obstruction. An examination of the tympanic membrane may reveal serous otitis media from chronic eustachian-tube dysfunction. Patients should also be evaluated for other manifestations of allergic disease discussed below.

Diagnostic tests. Skin-prick testing for common allergens can help identify an offending allergen that patients can attempt to avoid or to which they can be desensitized. If nasal airway obstruction or anatomic variation is thought to be a contributing factor, fiber-optic nasal endoscopy can be useful. Limited computed tomography of the sinuses is a cost-effective, accurate way to evaluate for chronic sinusitis.

Minimizing exposure. Avoiding allergens is one means of nonpharmacologic treatment that can be aided by skin-prick testing. To avoid seasonal allergens, an athlete can limit outdoor training during certain times of the year or wear a filter mask. Tree pollens usually cause problems throughout the spring, and grasses produce allergens during the summer. Weed pollens tend to be elevated in the fall and perennially in warmer climates. Pollen levels drop after a rainfall, offering an opportunity for outdoor training.

Avoiding perennial allergens is more difficult. In general, molds favor damp outdoor environments but may be abundant in older homes and buildings and in damp indoor areas. Indoor allergens can be minimized by cleaning damp areas with disinfectants or bleach, increasing ventilation, limiting carpeting and old upholstered furniture, eliminating indoor standing water, and avoiding excessive humidity and humidifiers. Controlling humidity can also help control dust mites, since they favor humid environments. The effects of dust mites can also be reduced by washing bedding regularly in hot water, having a nonallergic person vacuum and make beds, and covering all pillows and mattresses with an allergen barrier (1).

Medication. The selection of medication should be based on the pathophysiology of the disease. If feasible, prophylactic treatment should be used to prevent the onset of significant symptoms. Once an allergic response is primed, treatment becomes more difficult.

Five types of pharmacologic agents are commonly prescribed for the treatment of allergic rhinitis: antihistamines, decongestants, anticholinergics, cromolyn, and corticosteroids (table 1). A nasal corticosteroid is the most effective treatment for congestion and rhinorrhea, but significant improvement in symptoms may take a number of days and requires good compliance. Oral antihistamines, used as first-line therapy, do not work as well for congestion but reduce itching, sneezing, and rhinorrhea (3). "First generation" antihistamines, though less expensive than newer antihistamines, are less desirable in active persons because of their sedative effects.


Table 1. A Profile of Common Medications for Allergic Rhinitis

Drug Class and Name Additional Indications Common Trade Name Adult Dosage Comments

Antihistamines

Cetirizine HCl Urticaria Zyrtec 5 or 10 mg qd orally Causes little or no sedation

Chlorpheniramine maleate Pruritus, urticaria Chlor-Trimeton 4 mg qid orally Sedating

Diphenhydramine HCl Pruritus, urticaria Benadryl 25-50 mg qid orally Sedating

Fexofenadine HCl Urticaria Allegra 60 mg bid orally Causes little or no sedation

Hydroxyzine HCl Pruritus Atarax 25 mg tid-qid Sedating

Loratadine Urticaria Claritin 10 mg/day orally Causes little or no sedation
Cromolyn

Cromolyn sodium Nasalcrom 1 spray 3-6 times/day Onset of effects, 1-2 weeks
Corticosteroids

Beclomethasone dipropionate Polyp prevention Beconase, Vancenase 1 spray bid-qid Onset of effects, 3 days to weeks

Budesonide Polyp prevention Rhinocort 2 sprays bid or 4 sprays qd Onset of effects, 3 days to weeks

Flunisolide Polyp prevention Nasalide 2 sprays bid Onset of effects, 3 days to weeks

Fluticasone propionate Polyp prevention Flonase 2 sprays daily Onset of effects, 3 days to weeks

Triamcinolone acetonide Polyp prevention Nasacort 2 sprays daily Onset of effects, 3 days to weeks
Decongestants

Oxymetazoline HCl Congestion Afrin 0.05% solution, 2 sprays bid 3-4 days maximum use; may cause rebound congestion

Phenylephrine HCl Congestion Neo-Synephrine 0.25% solution, 2-3 sprays every 3-4 hours 3-4 days maximum use; may cause rebound congestion

Phenylpropanolamine HCl Congestion, drainage promotion Rhindecon 25 mg orally every 3-4 hours May cause anxiety and/or insomnia

Pseudoephedrine HCl Congestion, drainage promotion Sudafed 60 mg orally every 4-6 hours May cause anxiety and/or insomnia

Decongestants decrease congestion through intranasal vasoconstriction but do not have any effect on other allergy symptoms. Sympathomimetic side effects are common with oral preparations, and the use of topical preparations is limited to less than 5 days because of rebound congestion. Intranasal cromolyn is useful as an additional treatment in highly allergic individuals, particularly as a prophylaxis before a predicted allergen exposure or during the allergy season. Intranasal anticholinergic spray (eg, ipratropium bromide, 0.03%) is a useful second-line treatment for rhinorrhea that is not controlled with oral antihistamines or nasal corticosteroids.

The use of several classes of pharmacologic agents, which act on different phases of the inflammatory response, may control symptoms more effectively than a single agent (4).

Desensitization is often useful in a patient who requires multidrug treatment or in whom side effects are unacceptable, particularly if he or she has significant sensitivity to few allergens.

Allergic Conjunctivitis

Allergic conjunctivitis, which often accompanies allergic rhinitis but may also occur alone, includes acute, seasonal, and perennial conjunctivitis. Acute conjunctivitis occurs with direct exposure of the eye to an antigen, resulting in rapid and significant swelling of the conjunctiva. Seasonal and perennial forms of conjunctivitis are caused by the same allergens as seasonal and perennial rhinitis and therefore follow similar temporal patterns (5).

Signs and symptoms of allergic conjunctivitis include watery, itchy eyes and mild conjunctival erythema and edema. The physical exam requires eversion of the eyelid to observe the extent of conjunctival involvement, since the palpebral and bulbar conjunctiva, normally concealed by the lids, may be the only areas significantly affected. Patients who have perennial symptoms generally have positive skin-prick tests, most often for dust mites, and eosinophils are often present in a conjunctival smear (6).

The symptoms of allergic conjunctivitis can be alleviated by some of the same classes of agents used for symptomatic treatment of allergic rhinitis, including antihistamines and mast-cell stabilizers such as cromolyn sodium (4) and by topical nonsteroidal anti-inflammatory agents and topical vasoconstrictors (table 2) (7). Ophthalmic glucocorticoid solutions may provide dramatic relief of immune-mediated forms of conjunctivitis, but long-term use is not recommended. Patients who use opthalmic glucocorticoids run the risk of cataract formation and increased intraocular pressure that may lead to glaucoma. Further, the immunosuppressive actions of these agents set the stage for the onset or acceleration of secondary ocular infections. Thus, an ophthalmology consultation is recommended if a topical glucocorticoid is considered for treating allergic conjunctivitis.


Table 2. A Profile of Common Medications for Allergic Conjunctivitis

Drug Class and Name Additional Indications Common Trade Name Adult Dosage Comments

Cromolyn
Cromolyn sodium Rhinitis, pruritus Crolom 4% solution, 1-2 drops 4-6 times/day
Topical Glucocorticoids

Dexamethasone sodium phosphate Congestion, rhinitis, pruritus Decadron 0.05% ointment, bid-qid; 0.1% solution, 1 drop every 1-6 hr Prolonged use increases intraocular pressure

Prednisolone Congestion, rhinitis, pruritus Pred Forte 0.125% and 1% solution, 0.12% and 1% suspension, 1 drop every 1-6 hr Prolonged use increases intraocular pressure
Topical NSAIDs

Diclofenac sodium Rhinitis, pruritus Voltaren 0.1% solution,
1 drop qid

Ketorolac tromethamine Rhinitis, pruritus Acular 0.5% solution,
1 drop qid

Topical Vasoconstrictors

Lodoxamide tromethamine Congestion, rhinitis, pruritus Alomide 0.1% solution,
1-2 drops qid
3-5 day maximum use; may cause rebound congestion

Naphazoline HCl Congestion, pruritus Naphcon 0.1% solution,
1 drop, bid-qid
3-5 day maximum use; may cause rebound congestion

Naphazoline HCl + pheniramine maleate Congestion, rhinitis, pruritus Naphcon-A 0.1% solution,
1 drop, bid-qid
3-5 day maximum use; may cause rebound congestion

Asthma

Asthma is characterized by reversible airway obstruction signaled by a reversible decrease in forced expiratory volume in one second (FEV1) of more than 15% in response to a trigger such as an allergen, respiratory irritant, or exercise. While the airway obstruction is intermittent, the underlying inflammatory process in patients who have persistent symptoms is ongoing and may result in airway remodeling.

Allergies and exercise. Asthma is included in the discussion of allergic disease because allergies are a significant trigger in 50% of asthmatic adults (2). Furthermore, exercise-induced asthma (EIA), which affects 10% to 20% of all athletes, may affect up to 40% of athletes who have allergies (8). Food eaten before exercise may also aggravate bronchospasm for several days following exposure (9).

Many athletes who have EIA complain of symptoms only with exercise, while 50% to 80% of patients who have persistent asthma have exercise-induced bronchospasm (8). In most cases, airway obstruction induced only by exercise represents a mild form of asthma, while airway obstruction triggered by multiple factors with more persistent symptoms indicates more severe disease. The risk of chronic inflammatory changes increases with the severity and persistence of symptoms.

The prevalence of asthma is increasing in the general population and in athletes. In fact, it increased from 11% to 20% in Olympic athletes between the 1984 and 1996 Summer Olympics (10). With appropriate treatment, however, asthmatic Olympic athletes were as likely to win medals as nonasthmatic athletes. Winter Olympians may be even more susceptible to bronchospasm than their summer counterparts, possibly because of the exacerbating effects of cold, dry air. One study of cross-country skiers in Sweden demonstrated a 70% prevalence of EIA (11).

Signs and symptoms. Typical signs and symptoms include a minimally productive or nonproductive cough, wheezing, shortness of breath, chest pain or tightness, inability to take a full breath, or difficulty in exhaling fully. Asthma is more likely in those who have a family or personal history of allergic disease.

EIA symptoms tend to occur about 5 to 8 minutes after the onset of intense exercise (80% of VO2 max), are the most intense over the next 7 to 10 minutes, and begin to improve over the next 20 minutes (9). Despite similar levels of exertion, certain activities seem more asthmogenic than others. Outdoor running is the most asthmogenic, followed by indoor running, cycling, swimming, and walking. Cold, dry air is also more asthmogenic, and, not surprisingly, airborne pollutants aggravate bronchoconstriction in susceptible individuals. Clinicians must try to distinguish athletes who have persistent asthma from those who have EIA only, because the former require chronic anti-inflammatory treatment.

Lung auscultation in a patient who has persistent asthma and active bronchoconstriction is generally abnormal, while the office exam of a person who has EIA only is usually normal. Typical pulmonary findings in acute asthma include wheezing, rhonchi, a prolonged expiratory phase, hyperinflation, and decreased breath sounds. The absence of wheezing during an acute attack should not be reassuring; it may be a sign that the airflow has diminished so much that it no longer generates sound. Signs of upper or lower respiratory tract infection or physical signs of other allergic disease should be noted.

Diagnosic tests. If a patient has normal baseline spirometry, the diagnosis can be made by demonstrating a 15% drop in FEV1 following inhalation of a bronchial irritant, such as methacholine, or following an exercise challenge in those suspected of having EIA. Asthma is also diagnosed by demonstrating a 15% increase over baseline in FEV1 after administration of an inhaled beta-adrenergic agonist. Normal baseline FEV1 may not accurately identify or exclude asthma. Highly trained athletes may have a normal resting FEV1 or forced vital capacity and attain a 15% supranormal effect after using a bronchodilator. In a patient who has a history of asthma following exercise, a diagnosis of EIA can be made if the patient's postexercise symptoms fail to occur after he or she has been treated with an inhaled beta-adrenergic agonist before an exercise challenge.

Airway obstruction can also be quantified by peak flow testing, but because this is more effort-dependent than spirometry, it is a less reliable diagnostic tool. However, peak flow can be very useful for monitoring the response to therapy in patients who have chronic symptoms.

Athletes who have suspected allergic triggers and recalcitrant asthma should undergo skin-prick testing. The findings can help these athletes to avoid specific allergens and can suggest whether desensitization should be tried.

Treatment. The goals of asthma treatment are to prevent chronic asthma symptoms and exacerbations; maintain normal daily activities, including exercise and other physical activities; maintain normal or near-normal lung function; and minimize or eliminate the side effects of medication (12).

Nonpharmacologic. Nonpharmacologic treatment includes avoiding allergens, respiratory irritants, and other triggers as much as possible. Patients who have EIA should try to breathe through the nose rather than the mouth and should avoid exertion in excessively cold, dry, or polluted air.

In addition, many athletes with EIA have a refractory period, in which symptoms decrease by 50% or more following an initial bout of exercise-induced bronchospasm. By provoking symptoms through exertion and then recovering before competition, 50% of athletes who have EIA are refractory for 60 minutes, and some may be refractory for up to 3 hours (13).

Medications. Asthma medications can control symptoms in the short and long term. Long-term-control medications are taken daily to achieve and maintain control of persistent asthma (12,14). The most effective medications reduce inflammation, and the most potent anti-inflammatory medications are inhaled corticosteroids. Patients who have persistent asthma, whether mild, moderate, or severe, require daily anti-inflammatory medication for long-term control.

Quick-relief medications, on the other hand, promptly alleviate acute airflow obstruction and its accompanying symptoms of cough, chest tightness, shortness of breath, and wheezing. These medications include short-acting inhaled beta-2 agonists and, in some cases, anticholinergics (table 3) (4). All asthma and EIA patients must have such a medication to take as needed.


Table 3. A Profile of Common Asthma Medications

Drug Class and Name Common Trade Name Adult Dosage Side Effects and Comments
Anticholinergic

Ipratropium bromide Atrovent Inhaler, 2-3 puffs qid; nebulizer, 500 micrograms every 6-8 hr
Beta-Adrenergic Agonists

Albuterol Ventolin, Proventil Inhaler, 2 puffs qid, as needed; 2-4 mg orally tid-qid; nebulizer every
6 hr, as needed
Palpitations, insomnia; acute therapy

Pirbuterol acetate Maxair Inhaler, 1-2 puffs every 4-6 hr Palpitations, insomnia

Salmeterol Serevent Inhaler, 2 puffs bid Use according to schedule

Terbutaline sulfate Breathaire, Brethine Inhaler, 2 puffs every 4-6 hr; 5 mg orally tid or 0.25 mg subcutaneously, as needed (may be repeated after 15 min) Palpitations, insomnia; acute therapy
Inhaled Corticosteroids

Beclomethasone dipropionate Beclovent, Vanceril Inhaler, 2-4 puffs tid-qid Not for acute therapy; oral candidiasis risk, so rinse mouth after use

Flunisolide Aerobid Inhaler, 2-4 puffs bid Not for acute therapy; oral candidiasis risk, so rinse mouth after use

Fluticasone propionate Flovent 88-440 micrograms bid (44, 110, and 220 micrograms/puff MDIs) Not for acute therapy; oral candidiasis risk, so rinse mouth after use

Triamcinolone acetonide Azmacort 2 puffs tid-qid or 4 puffs bid Not for acute therapy; oral candidiasis risk, so rinse mouth after use
Leukotriene Antagonists

Montelukast sodium Singulair 10 mg/day orally No laboratory monitoring; currently preferred leukotriene antagonist

Zafirlukast Accolate 20 mg/day orally or 20 mg 2 hr before exercise Monitor AST, ALT, CBC; drug interactions; potential compliance problems
Methylxanthine

Theophylline Slo-Bid, Theo-Dur 13 mg/kg/day maximum, up to 900 mg/day Drug interactions; CNS and GI toxicity; requires blood-level monitoring

Abbreviations: MDI = metered dose inhaler; AST = aspartate aminotransferase; ALT = alanine aminotransferase; CBC = complete blood count; CNS = central nervous system; GI = gastrointestinal


A new group of medications—the leukotriene antagonists—inhibit the bronchospastic and inflammatory effects of leukotrienes, which play a significant role in asthma induced by exercise, aspirin, or allergens (14-16). Though the specific indications for these drugs are still being established, patients who have aspirin- or exercise-induced asthma have benefited from their use (15). These medications are currently recommended as an add-on therapy for all asthmatics.

For the use of these medications in patients who have EIA, see "Controlling Exercise-Induced Asthma," below.

Atopic Dermatitis

Atopic dermatitis may be an IgE-mediated chronic inflammatory skin condition. It often occurs with other allergic syndromes and is frequently the first manifestation of allergic disease in children. Triggers include a variety of food and airborne allergens, skin infection, skin irritants, emotional stress, and environmental factors, including cold, dry air. Food sensitivity is common in children, while adults are generally more sensitive to airborne allergens or other irritants. In athletes, allergic dermatitis can be exacerbated by skin irritation from protective equipment, excessive sweating, or physical trauma. Outdoor winter sports enthusiasts are particularly susceptible because of skin dehydration from cold, dry air.

Diagnosis. Patients generally complain of pruritus and a rash involving the antecubital and popliteal fossae as well as the face, hands, and feet. Physical examination may demonstrate acute pruritic lesions, with skin erythema, papules, and vesicles. Subacute lesions progress to scaling, with early evidence of excoriation, while chronic lesions appear as thickened plaques, lichenification, and prurigo nodularis (17). Patients are susceptible to bacterial and viral superinfection, which can result in acute erythema, tenderness, discharge, crusting, or vesiculation overlying chronic changes. A family and/or personal history of atopy is common.

Patients often have elevated serum IgE, but the diagnosis is made clinically, and determining the serum level is not usually necessary or cost-effective. Positive skin-prick testing can document atopy. Identifying the offending agent, though, requires controlled elimination of suspected allergens, since the skin disease usually is the result of sensitivity to only a few of the allergens for which the patient tests positive. Correct identification of problematic foods is particularly important for athletes, since they should avoid an overly restricted diet (17).

Treatment. Treatment involves a combination of preventive measures and an individualized therapeutic regimen. Patients should generally avoid the excessive use of soap while bathing and afterwards should use emollients, ideally petrolatum. They should also avoid irritants such as detergents, solvents, wool, and lanolin. Topical steroids of the lowest effective potency are the mainstay of therapy for atopic dermatitis (table 4) and may be used in conjunction with topical antibiotics such as mupirocin ointment and emollients (18,19). Topical coal tar may help some patients, though its messiness often results in poor compliance.


Table 4. Common Atopic Dermatitis Medications: Preparations and Strength

Drug and Potency Available Preparations Strength
Low Potency
Dexamethasone Gel 0.10%
Dexamethasone sodium phosphate Cream 0.10%
Fluocinolone acetonide Cream, solution 0.01%
Hydrocortisone Cream, lotion, ointment, solution 0.25%, 0.50%, 1.0%, 2.50%
Hydrocortisone acetate Cream, lotion, ointment, gel, foam 0.50%, 1.0%
Medium Potency
Betamethasone benzoate Cream, lotion, gel 0.03%
Betamethasone dipropionate Lotion 0.05%
Betamethasone valerate Cream 0.10%
Fluocinolone acetonide Cream, ointment 0.03%
Fluticasone propionate Cream, ointment 0.05%
Hydrocortisone butyrate Cream 0.10%
Hydrocortisone valerate Cream, ointment 0.20%
Mometasone furoate Cream, lotion, ointment 0.10%
Triamcinolone acetonide Cream, lotion, ointment 0.03%, 0.10%, 0.50%
High Potency
Augmented betamethasone dipropionate Cream 0.05%
Betamethasone dipropionate Cream, ointment 0.05%
Betamethasone valerate Ointment 0.10%
Diflorasone diacetate (emollient base) Cream, ointment 0.05%
Fluocinolone acetonide Cream 0.20%
Fluocinonide Cream, ointment, gel 0.05%
Triamcinolone acetonide (with propylene glycol) Ointment 0.10%
Very High Potency
Augmented betamethasone dipropionate Ointment 0.05%
Clobetasol propionate Lotion, ointment 0.05%
Diflorasone diacetate Ointment 0.05%
Halobetasol propionate Cream, ointment 0.05%

Oral antibiotics are used to treat secondary staphylococcal colonization or infection, and oral antihistamines may decrease pruritus. Systemic corticosteroids are extremely effective for severe, acute flairs of atopic dermatitis, but adverse effects limit prolonged use. Phototherapy that combines ultraviolet A and B rays of various frequencies may be used to treat atopic dermatitis that does not respond to topical therapy (19).

Restricted Medications

Because some medications are banned by sports governing bodies, certain therapies may not be available for competitive athletes. Current listings of the National Collegiate Athletic Association's (NCAA's) banned substances can be found on the World Wide Web at https://www.ncaa.org/sports_sciences/drugtesting, and inquiries regarding the International Olympic Committee's (IOC) banned substances can be made by calling the Olympic Drug Reference Line (1-800-233-0393).

None of the previously discussed treatments is included on the 1998-99 NCAA Banned-Drug Classes. However, several are either restricted or prohibited under current IOC regulations:

  • Certain inhaled corticosteroids (beclomethasone dipropionate, budesonide, flunisolide, fluticasone propionate, triamcinolone acetonide) are permitted for asthma treatment only when written notification is provided.
  • Topical corticosteroids (anal, aural, dermatologic, nasal, opthalmologic) are permitted without notification.
  • Systemic corticosteroids (oral, rectal, and injected) are prohibited.
  • Albuterol, salmeterol, albuterol/ipratropium bromide, and terbutaline sulfate are permitted by inhaler only, and only when notification is submitted by a respiratory or team physician.
  • Metaproterenol sulfate and pirbuterol acetate are prohibited.
  • Other medications are permitted as long as the urinary concentrations are not above established levels. IOC-accredited laboratories must report findings for levels of specific substances (ephedrine, more than 5 micrograms/mL, and phenylpropanolamine and pseudoephedrine, more than 10 micrograms/mL).

Management for Performance

Allergen-mediated diseases affect millions of active persons and athletes. Fortunately, current treatments can relieve most symptoms sufficiently to permit active patients to continue exercising and athletes to compete at the highest levels. Physicians who care for these individuals must maintain a high index of suspicion for these conditions and manage them aggressively to maximize patients' quality of life and athletic performance.

References

  1. Dykewicz MS, Fineman S, Skoner DP, et al: Diagnosis and management of rhinitis: complete guidelines of the Joint Task Force on Practice Parameters in Allergy, Asthma and Immunology. Ann Allergy Asthma Immunol 1998;81(5 pt 2):478-518
  2. Li J, Pearlman DS, Nicklas RA, et al: Algorithm for the diagnosis and management of asthma: a practice parameter update: Joint Task Force on Practice Parameters. Ann Allergy Asthma Immunol 1998;81(5 pt 1):415-420
  3. Dykewicz M, Fineman S: Executive summary of Joint Task Force Practice Parameters on Diagnosis and Management of Rhinitis. Ann Allergy Asthma Immunol 1998;81(5 pt 2):463-468
  4. Meltzer E: Pharmacological treatment options for allergic rhinitis and asthma. Clin Exp Allergy 1998;28(suppl 2):27-36
  5. Buckley R: Allergic eye disease: a clinical challenge. Clin Exp Allergy 1998;28(suppl 6):39-43
  6. Dart JK, Buckley RJ, Monnickendan M, et al: Perennial allergic conjunctivitis: definition, clinical characteristics and prevalence: a comparison with seasonal allergic conjunctivitis. Trans Ophthalmol Soc U K 1986;105(pt 5):513-520
  7. Fauci A, Braunwald E, Isselbacher K, et al: Diseases of immediate type hypersensitivity, in Fauci AS, et al (eds): Harrison's Principles of Internal Medicine, ed 14. New York City, McGraw-Hill Health Professions Division, 1998, pp 1860-1869
  8. Kawabori I, Pierson WE, Conquest LL, et al: Incidence of exercise-induced asthma in children. J Allergy Clin Immunol 1976;58(4):447-455
  9. Katz R: Management of the elite athlete who has exercise-induced asthma, in Weiler JM (ed): Allergic and Respiratory Disease in Sports Medicine. New York City, Marcel Dekker, Inc, 1997, pp 367-375
  10. Weiler J, Layton T, Hunt M: Asthma in United States Olympic athletes who participated in the 1996 Summer Games. J Allergy Clin Immunol 1998;102(5):722-726
  11. Larsson K, Ohlsen P, Larsson L, et al: High prevalence of asthma in cross country skiers. BMJ 1993;307(6915):1326-1329
  12. National Asthma Education and Prevention Program (National Heart, Lung, and Blood Institute): Guidelines for the Diagnosis and Management of Asthma: Expert Panel Report 2. Bethesda, MD, US Dept of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute, 1997, pp 1-52
  13. Randolph C: Exercise-induced asthma: update on pathophysiology, clinical diagnosis, and treatment. Curr Probl Pediatr 1997;27(2):53-77
  14. Staton G, Ingram R: Asthma. Sci Am 1998;14:1-15
  15. Leff J, Busse WW, Pearlman D, et al: Montelukast, a leukotriene-receptor antagonist, for the treatment of mild asthma and exercise-induced bronchoconstriction. N Engl J Med 1998;339(3):147-152
  16. Drazen JM, Israel E, O'Byrne PM: Treatment of asthma with drugs modifying the leukotriene pathway. N Engl J Med 1999;340(3):197-206
  17. Leung DY, Hanifin JM, Charlesworth EN: Disease management of atopic dermatitis: a practice parameter: Joint Task Force on Practice Parameters. Ann Allergy Asthma Immunol 1997;79(3):197-211
  18. Habif TP: Dermatology: Clinical Dermatology: A Color Guide to Diagnosis and Therapy. St Louis, CV Mosby, 1990, pp 86-90
  19. Rudikoff D, Lebwohl M: Atopic dermatitis. Lancet 1998;351(9117):1715-1721


Controlling Exercise-Induced Asthma

Patients who have exercise-induced asthma (EIA) alone or who have chronic asthma that is exacerbated by exercise have the best chance of controlling symptoms during exercise through careful timing of and/or combining medications.

For control of EIA, patients usually begin by using a short-acting beta-agonist, taking two to four puffs 5 to 60 minutes before exercise. The effects should last 2 to 3 hours.

A long-acting medication is an alternative if prolonged exertion is anticipated and repeated dosing of a short-acting medication is impractical. The effects of a long-acting beta-2 agonist taken at least 30 minutes before exercise will last 10 to 12 hours; however, recent evidence suggests that these protective effects decrease when the medications are used regularly for as little as 14 days (1,2).

Cromolyn or nedocromil may also be used before exertion; the effect lasts 1 to 2 hours. The combination of cromolyn and albuterol has been shown to be more potent than either alone (1).

If exercise-induced symptoms persist in a patient who has lone EIA despite these treatments, regular treatment with inhaled corticosteroids and/or leukotriene antagonists often provides benefits (3). Athletes who require regular anti-inflammatory therapy to control EIA may, in fact, have chronic asthma and should be evaluated further. Chronic asthmatics who already receive regular anti-inflammatory medication may benefit from increased dosages or a combination of a leukotriene antagonist and an inhaled corticosteroid.

Concomitant allergic rhinitis or sinusitis should always be addressed to optimize symptom control.

References

  1. McFadden ER, Jr, Gilbert IA: Exercise-induced asthma. N Engl J Med 1994;330(19):1362-1367
  2. Nelson JA, Strauss L, Skowronski M, et al: Effect of long-term salmeterol treatment on exercise-induced asthma. N Engl J Med 1998;339(3):141-146
  3. National Asthma Education and Prevention Program (National Heart, Lung, and Blood Institute): Guidelines for the Diagnosis and Management of Asthma: Expert Panel Report 2. Bethesda, MD, US Dept of Health and Human Services, Public Health Service, National Institutes of Health, National Heart, Lung, and Blood Institute, 1997, pp 1-52


Dr O'Kane is an assistant professor of orthopedics and family medicine and a team physician at the University of Washington in Seattle; he is a member of the American Medical Society for Sports Medicine. Dr Woodford is a pharmacy resident in family medicine at the University of Washington. Address correspondence to John W. O'Kane, MD, Dept of Orthopaedics, University of Washington, Box 354060, Seattle, WA 98195-4060; address e-mail to [email protected].


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