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Identifying and Controlling Metabolic Skin Disorders

Eczema, Psoriasis, and Exercise-Induced Urticaria

Erik S. Adams, MD, PhD

Sports Dermatology Series Editor:
William Dexter, MD


In Brief: Inflammatory skin conditions can present obstacles that affect athletic participation. In eczema and psoriasis, cutaneous lesions can lead to skin breakdown, which may disqualify an athlete from participation and may also contribute to secondary infection. Adequate control of chronic skin conditions can, therefore, ensure more consistent athletic participation, and successful treatment may improve social functioning, as well. Clinicians treating athletes who have exercise-induced urticaria should be aware of the need for close observation and continual reassessment to distinguish between cholinergic urticaria and exercise-induced anaphylaxis.

The severity of skin conditions in athletes can range from merely annoying to life-threatening anaphylaxis with cutaneous findings. Clinicians need a working knowledge of commonly seen dermatologic conditions that pertain to exercise, and they must be able to recognize serious conditions when they arise. As with nondermatologic conditions in athletes, goals of evaluation and treatment include accurate diagnosis, recognition of the potential for worsening disease, and safe and successful return to play. Certain metabolic skin conditions, such as eczema, psoriasis, and exercise-induced urticaria, may make exercise or sports participation more difficult. These conditions share an inflammatory origin, although their pathophysiologic mechanisms differ.


The term "eczema" is often used synonymously with atopic dermatitis, although eczematous reactions occur in individuals with and without other atopic findings, such as bronchial hyperreactivity, allergic rhinitis, conjunctivitis, and positive skin-prick tests to allergens or foods. Approximately 10% to 25% of eczema probably arises from a nonallergic source, and most is associated with atopy. The umbrella term "atopic eczema/dermatitis syndrome" (AEDS) was recently introduced to cover the different subtypes of atopic dermatitis that have certain clinical characteristics in common.1

Because up to 10% of US school children have eczema,2 the probability that any given sports team will include athletes who have eczema is fairly high. In the United Kingdom, approximately 80% of patients are mildly affected.3 Among those more severely affected in the United States, 60% report a disruption of their daily activities, 80% have problems with sleep, and 55% are embarrassed about their condition.4

Diagnosis. Eczema should be viewed as a skin manifestation stemming from a wide variety of disorders. An approach to the differential diagnosis should take into account the ability of the clinician to determine that the skin lesion is indeed eczematous. Disorders known to cause eczema as well as a variety of noneczematous skin lesions that may resemble eczema (table 1) should be included. Because eczema may appear as just an erythematous or papular and pruritic skin lesion, the initial differential diagnosis should be fairly extensive. Diagnosis is aided by a history of eczema in infancy or childhood, other atopic findings in the patient or an atopic family history, the distribution of the rash, a skin biopsy with evaluation by a dermatopathologist, an elevated serum immunoglobulin (IgE) level in patients who have atopic eczema, and a negative potassium hydroxide (KOH) prep test if a dermatophyte infection is suspected.

TABLE 1. Differential Diagnosis of Eczema
Noneczematous Disorders
That May Mimic Eczema
Eczematous Disorders
Bacterial skin infection
Dermatophyte infection
Drug eruption
Eczema herpeticum
Guttate psoriasis
Mycosis fungoides
Pityriasis lychenoides
Pityriasis rosea
Scabies infestation
Secondary syphilis
Staphylococcal scalded
   skin syndrome
Allergic contact dermatitis
Atopic dermatitis
Asteatotic eczema
Dyshidrotic eczema
Irritant contact dermatitis
Keratosis pilaris
Nummular eczema
Photocontact dermatitis
Pityriasis alba
Seborrheic dermatitis

The appearance of eczema varies with its severity (figure 1). Milder lesions may be only erythematous and macular. Papules and microvesicles also occur in milder cases, but more severe outbreaks are characterized by weeping and exudation with crusting. Chronic cases result in dryness and thickening of the skin (ie, lichenification). The common feature, regardless of severity, is pruritus, which can be intense and is typically paroxysmal, leading to frenzies of scratching and subsequent excoriation. In adolescents and adults, the most typical locations for eczematous lesions are the flexor surfaces of arms and legs, especially flexor creases; hands; genitalia; and, occasionally, the face. However, distribution in more severe cases can be considerably more extensive. Several online dermatologic sites show the wide variety of eczema presentations.5

Treatment. For mild eczema, appropriate treatment ranges from moisturizing lotions to topical steroids; however, chronic topical steroid use carries a risk of skin atrophy, striae, and pigmentation abnormalities. Treatment of lesions around the eyes and on the face with corticosteroids should be avoided. Other traditional therapies include wet occlusive dressings to preserve skin moisture, antihistamines to control pruritus, and phototherapy. Immunosuppressant therapy with cyclosporine has also been employed.6

Despite the wide range of therapies available, 32% of patients with eczema report that their treatment regimen is ineffective.4 Pimecrolimus is a new topical nonsteroidal inhibitor of inflammatory cytokines that is marketed as first-line therapy for mild to moderate eczema.6,7 However, clinicians should take into account how easily a patient's eczema appears to be controlled with emollients and the sparing use of topical corticosteroids before recommending pimecrolimus. Because it suppresses T-cell function, pimecrolimus should not be applied to areas of active cutaneous viral infection.

Return to play. The athlete's skin integrity, the likelihood of damage to affected skin from athletic gear, and the possibility that a contagious infectious agent is present should be considered. A primary infective agent, such as in eczema herpeticum, could be causing the eczematous eruption. Bacterial infection, or secondary impetiginization, of eczematous skin is common, usually caused by Staphylococcus aureus or group A beta-hemolytic streptococci. However, infections near mucous membranes and body orifices can be caused by bacteria from those sources, such as gram-negative enterics, when the proximal thighs or buttocks are involved. In one study,8 44% of infected eczematous lesions yielded mixed anaerobic and aerobic organisms. A culture may be indicated before beginning antibiotic therapy if the lesion is near an orifice or mucous membrane.

Secondary bacterial infection in eczema may require withholding the patient from sports participation, especially in sports that involve skin-to-skin contact between athletes. Return-to-play decisions need to be individualized, based on several factors, including likelihood of skin-to-skin contact between athletes (open lesions typically preclude any swimming), the location of a lesion and its ease of being adequately occluded, the duration of antibiotic treatment, evidence of clinical improvement with antibiotics, and suspicion of another nonbacterial infectious disease. Automatic return to play after 24 hours of oral antibiotics should be discouraged, because the possibility exists for selection of an ineffective antibiotic or misdiagnosis of a viral infection, such as herpes simplex.

Recent intriguing studies9 on individuals who have eczema have disclosed that sweating during exercise is decreased by about two-thirds, compared with noneczematous controls. Decreased perspiration raises the possibility of inadequate cooling during exercise in the heat. Evaporative cooling through sweating is the primary mode of heat loss in hot weather, highlighting the importance of the skin in thermoregulation. No studies have yet documented an increased incidence of heat illness in athletes with eczema, but heat illness is potentially life-threatening. An increased index of suspicion is probably wise when athletes who have eczema become ill while exercising in heat or high humidity. Team physicians and athletic trainers should know in advance if any of the athletes under their care have eczema.


Psoriasis is an autoimmune disorder manifested by scaly, erythematous plaques. Patches may be large and confluent, as in plaque psoriasis (figure 2), or discrete and separate, as in guttate psoriasis. Other types of psoriasis include pustular and erythrodermic. Guttate psoriasis is a common variant, especially in children,10 and may arise as a poststreptococcal rash or as a drug eruption. Milder cases of plaque psoriasis may involve lesions around hair follicles or on the extensor surfaces of extremities. The severity of pruritus, if present, varies with the severity of disease. As with eczema, secondary bacterial skin infections can occur.

Diagnosis. Characteristic skin lesions in psoriasis are key for proper diagnosis. The differential diagnosis of psoriatic lesions may include dermatophyte infection, lichen planus, lupus erythematosus, mycosis fungoides, nummular eczema, parapsoriasis, pityriasis rosea, psoriasis, secondary syphilis, seborrheic dermatitis, and small plaque parapsoriasis.

Psoriatic lesions are covered with a silver-colored scale, whereas the lesions of lichen planus have a purple hue. Pityriasis rosea can be mistaken for psoriasis, but the herald patch in pityriasis rosea, an oval patch larger than the other lesions present, is helpful in diagnosis. A positive family history is also helpful—and a number of genetic markers for the condition have been identified—but it is by no means a prerequisite.

Athletes who have psoriasis are at risk for Koebner's phenomenon, in which psoriatic lesions appear on previously uninvolved skin as a consequence of trauma. On the plantar foot, plaques tend to occur along the weight-bearing surfaces during gait and may wax and wane with athletic activity.11 Any skin examination should include the plantar surface of the feet. Usual sites of involvement include the scalp and eyebrows, knees, elbows, ears, genitalia, and nails. Nail involvement usually involves pitting and yellowing (figure 3) and may be mistaken for onychomycosis or the nail pitting of alopecia areata.

Psoriatic arthritis is a disabling aspect that is rarely seen in childhood but occurs in up to 10% of adult cases, depending on the population studied.12 Characteristically, the metacarpophalangeal and proximal interphalangeal joints of the hands as well as the axial skeleton are affected. Radiographic changes demonstrate erosion of articular surfaces, similar to rheumatoid arthritis.

Treatment. New agents that target the biologic cause of plaque formation have revolutionized the treatment of psoriasis. Traditional therapy involves the use of combinations of drugs and treatments, sometimes on a rotating basis. Rotation allows patients to use more intensive therapies for a short time to control flares or to minimize long-term exposure to a noxious medication. Table 2 lists both traditional treatments and some of the new biologic agents available.13-15 Combination therapy allows dosages of individual agents to be lowered, thereby reducing side effects, while relying on the synergistic effects of multiple treatment modalities. Of course, when psoriasis results from a drug eruption, removal of the offending agent is advised.

TABLE 2. Available Therapies for Psoriasis Treatment
Coal tar preparations
PTH (1-34)1515
UVB phototherapy

Psoralen plus UVA (PUVA)
Oral retinoids


PTH = parathyroid hormone
UVA = ultraviolet A
UVB = ultraviolet B

Infliximab and etanercept are tumor necrosis factor-alpha antagonists, also used for rheumatoid arthritis and Crohn's disease, and alefacept reduces counts of a subpopulation of T cells. Although alefacept administration does not appear to increase infection rates, a report16 of 180 patients taking etanercept revealed a number of serious infections, including septic joints and psoas abscess with Mycobacterium avium-intracellulare.

Mild psoriasis may be successfully treated with selenium formulations, topical corticosteroids, or coal tar extracts. Use of more aggressive treatment modalities should not be undertaken lightly. Many of the agents used (see table 2) are immunosuppressive or carcinogenic, and certain combinations are hazardous. For example, cyclosporine combined with psoralen-ultraviolet-light treatment (PUVA) increases the risk of squamous cell carcinoma, and methotrexate sodium is known for its hepatotoxicity and interaction with a number of medications, including nonsteroidal anti-inflammatory drugs. The oral retinoids, such as acitretin and etretinate, are highly teratogenic, relegated to pregnancy category X by the US Food and Drug Administration. Co-ingestion of acitretin and ethanol results in esterification of acitretin to produce etretinate, which has a half-life of 120 days, considerably longer than the 5-day half-life of acitretin.13 Clearly, many of these treatments require extensive specialized knowledge before prescribing them.

Two studies16,17 have highlighted the negative social effects of psoriasis. Patients who have this disorder frequently report a sense of social isolation and stigmatization, and they tend to be less likely to be involved in sports. The beneficial effects of participation in sports and exercise are well established. Successful treatment of psoriatic plaques may lead to increased involvement in an active lifestyle, and, therefore, improved overall health.

Patients who have pustular psoriasis of the palms and soles have lower bone mineral density than controls.18 This finding may be attributed in part to decreased weight-bearing exercise, but the affected group in this study were four times as likely to smoke as controls, and the effect of prolonged corticosteroid use could also play a role.

Return to play. As with eczema, secondary bacterial skin infections can occur that may affect return to play. The same precautions should be observed for both conditions.

Exercise-Induced Urticaria and Anaphylaxis

Clinicians who treat athletes should be familiar with exercise-induced urticaria and anaphylaxis. In evaluating an athlete who has urticarial lesions or hives that occur during exercise, accurate classification of the type of urticaria is important (table 3).

TABLE 3. Categories of Exercise-Induced Urticaria and Their Features

TypeSize of  
PrecipitantPotentially Life-  
Hypotension  Bronchospasm  Laryngeal

2-4 mmIncreased
core body
No2-4 hrRareCommonNo

> 1 cmTrigger food
plus exercise   
YesUp to 4 hr*  CommonNoCommon

> 1 cmExercise onlyYesUp to 4 hr*CommonNoCommon

4-5 mmExercise onlyYesUp to 4 hr*CommonNoCommon

> 1 cmExercise onlyYesUp to 4 hr*CommonNoCommon

*Headache may persist for up to 4 days.

Cholinergic urticaria is usually distinguished from the other causes, because it arises in response to a rapid increase in core body temperature. Individuals who have this disorder may also experience urticaria in a hot tub or hot shower or with a fever.19,20 The urticarial wheals tend to be smaller in cholinergic urticaria than in most other varieties, and vascular collapse is not a typical coincident finding. Other signs of parasympathetic activation, such as lacrimation, diarrhea, and salivation, are uncommonly seen but can be diagnostically helpful.21 Onset between the ages of 10 and 30 is common, and the incidence is highest in the mid-to-late 20s.19

Cold-induced urticaria is also described in the literature, with punctate hives similar to urticaria induced by elevated body temperature.22 Cold and cholinergic urticaria can coexist in the same individual.23 Cholinergic urticaria produces smaller wheals of about 2- to 4-mm diameter (figure 4). In exercise-induced anaphylaxis, wheals are at least 1 cm in diameter and can become confluent.

Exercise-induced anaphylaxis showed a 2:1 female predominance in a 1989 study24 of individuals with age of onset ranging from 4 to 74 years (mean age, 24.7 years). The most common pattern of occurrence was twice weekly. A wide variety of exercise was implicated. Most joggers required a medium-to-fast pace to elicit symptoms, but some had symptoms even with mild exertion. Generalized pruritus was experienced by 92% of subjects, urticaria in 83%, angioedema in 78%, respiratory symptoms in 59%, and syncope in 32%. Flushing, profuse sweating, headache, and gastrointestinal symptoms were also common. Atopy is common in such individuals, manifested as allergic rhinitis or eczema. Exercise-induced anaphylaxis can show a familial pattern, leading to the designation of the subtype of familial exercise-induced anaphylaxis. No suggestion is made that this changes the evaluation or management, other than to inquire about its occurrence in other family members.21

Food-dependent exercise-induced anaphylaxis is an unusual subtype in which exercise will precipitate symptoms only if certain food items have been ingested. A wide variety of foods and some medications have been implicated (table 4).25-27 Many foods that are not commonly implicated as allergens may act as triggers. Sometimes the precipitating foods are highly specific, as in the case of a 16-year-old girl who developed exercise-induced anaphylaxis only after ingesting pizza or a cheese sandwich, and not from a wide variety of other foods to which she demonstrated positive skin test results, including wheat.28 This case also demonstrates the potential severity of episodes, as treadmill testing after eating the cheese sandwich resulted in hives, chest pain, hypotension, and electrocardiographic (ECG) evidence of myocardial ischemia. Clearly, a detailed history is paramount in the successful diagnosis of food-dependent exercise-induced anaphylaxis.

TABLE 4. Ingested Substances Implicated in Food-Dependent Exercise-Induced Anaphylaxis
Beta-lactam antibiotics
Vegetable oil

NSAIDs = nonsteroidal anti-inflammatory drugs

As the severity of food-dependent exercise-induced anaphylaxis can vary from urticaria with flushing to vascular collapse and airway compromise, the thoroughness of the evaluation should be tailored to the patient's presentation and the clinician's confidence that the patient actually has exercise-induced anaphylaxis and not merely food-dependent urticaria. One literature recommendation25 includes a detailed history and physical exam, ECG, echocardiogram, pulmonary function tests, skin-prick allergen testing, serum IgE level test, radioallergosorbent test (RAST) assays for specific food-related IgE, baseline stress test, and then separate stress testing after ingestion of each suspected food. A less intensive approach would include RAST testing only for those patients whose skin testing would be unreliable, such as when dermatographism is present; cardiac and pulmonary testing only when symptoms dictate; and a trial of eliminating foods to which the patient tested positive.26 The more intensive approach is recommended when a patient's reactions are severe, increasing the level of danger if they were allowed to occur without medical supervision.

It is generally recommended that offending foods be avoided for about 4 to 6 hours before exercise, and for this reason, exercise before breakfast is often convenient. However, because food-dependent exercise-induced anaphylaxis is such a common subtype, it may be advisable for affected athletes to avoid any postprandial exercise. Athletes should only exercise in the company of someone capable of rendering emergency assistance, and self-injectable epinephrine should be readily available.27

Diagnosis is guided largely by the size of the wheals, the presence of bronchospasm or laryngeal edema, knowledge of the precipitant factors, and other signs (see table 3).

Whereas cholinergic urticaria is not considered life threatening, exercise-induced anaphylaxis, in which urticaria is a prominent feature, must be recognized and treated immediately. Laryngeal edema and vascular collapse can occur, although only one death from exercise-induced anaphylaxis has been described in the literature.29 Fortunately, exercise-induced anaphylaxis is rare in comparison to other varieties of cholinergic urticaria.

In exercise-induced anaphylaxis, respiratory compromise occurring from laryngeal edema should be distinguished from dyspnea caused by bronchospasm, which occurs in cholinergic urticaria. The former causes inspiratory stridor, heard best at the larynx, and the latter is characterized by expiratory wheezing in the lung fields, secondary to small, peripheral airway constriction. In the emergency evaluation and management of exercise-induced anaphylaxis (table 5), note that the principal task should be to distinguish between cholinergic urticaria and exercise-induced anaphylaxis, as the latter can be life-threatening. Because symptoms and signs can overlap, an initial diagnosis of cholinergic urticaria should continually be reassessed during treatment, in case the patient actually has exercise-induced anaphylaxis. Development of vascular collapse, laryngeal edema, or angioedema should prompt an immediate change of diagnosis and therapy.

TABLE 5. Emergency Evaluation and Management of Exercise-Induced Anaphylaxis
Evaluation    Important FindingsInterventionRationale

HistoryPrior occurrence, food allergy, nausea or vomitingAdminister subcutaneous epinephrineOnly medication known to reverse anaphylaxis

Mental statusConfusion, stupor, or loss of consciousnessMaintain airway, supply oxygenLaryngeal edema can cause obstruction

Vital signs*Hypotension, tachycardiaSupply IV fluids (normal saline)Volume expansion to counteract vasodilation and to secure IV access

Respiratory signsStridor, labored breathingGive antihistaminesExercise-induced anaphylaxis is histamine mediated

Skin signsUrticaria (note size)Transfer to emergency facilityAdequate resources are needed to treat life-threatening condition

*A complete set of vital signs, including core body temperature, is required in any emergency situation to aid in excluding other conditions that may cause mental status changes, such as cardiogenic shock and heatstroke.

IV = intravenous

Treatment and prevention of exercise-induced anaphylaxis episodes may be aided by antihistamines, such as hydroxyzine. This antihistamine seems to be more universally recommended, although its dosing schedule is somewhat prohibitive, at four times daily. A once- or twice-daily antihistamine would be a reasonable alternative, provided that an adequate response to treatment is obtained. The mast-cell stabilizer cromolyn sodium has shown variable results in treating exercise-induced anaphylaxis. The rationale for its use is that histamine release in exercise-induced anaphylaxis results from mast-cell degranulation, though it may not achieve appreciable systemic concentrations.30 Consistent exercise may raise the threshold for an anaphylactic attack, so athletes who have this disorder should place themselves on a regular exercise schedule.20

Return to play is allowed as long as the athlete feels well enough to play.

Take-Home Points

Of the dermatologic conditions reviewed, only exercise-induced anaphylaxis is potentially life-threatening, but the clinician should appreciate the negative impact that eczema, psoriasis, and cholinergic urticaria can have on a patient's healthy, active lifestyle. Newly available medications for the treatment of eczema and psoriasis should be employed when needed, but milder cases may respond adequately to less aggressive measures. Recent findings regarding diminished rates of sweating in patients with eczema should heighten our index of suspicion for heat illness in these patients.

The life-threatening nature of exercise-induced anaphylaxis mandates aggressive treatment when signs of vascular collapse and airway compromise are present, and preventive strategies are likewise important. The triggers in food-dependent exercise-induced anaphylaxis may be difficult to identify, but they are important. In difficult cases, when the triggers are unclear, it may be reasonable to recommend that the athlete avoid postprandial exercise altogether.


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Dr Adams is a sports medicine physician at the Midwest Institute of Sports Medicine in Middleton, Wisconsin. Address correspondence to Erik S. Adams, MD, PhD, Midwest Institute of Sports Medicine, 2521 Allen Blvd, Middleton, WI 53562; e-mail to [email protected].

Disclosure information: Dr Adams discloses no significant relationship with any manufacturer of any commercial product mentioned in this article. No drug is mentioned in this article for an unlabeled use.