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- Introduction
- Skin infections
- Fungal infections
- Tinea curis
- Tinea versicolour
- Tinea incognita
- Bacterial infections
- Impetigo
- Pitted keratolysis
- Viral infections
- Herpes simplex virus
- Herpes gladiatorum
- Molluscum contagiosum
- Common warts
- Sports-related allergic and irritant dermatitis
- Urticaria
- Contact dermatitis
- Dermatological manifestations of physical, cold, and electromagnetic injury
- Acne mechanica
- Trauma - induced skin disease
- Athlete’s nodules
- Heat and cold related skin disease
- Intertrigo
- Miliaria, (‘prickly heat’)
- Erythema ab igne
- Ultraviolet-related skin disease
- Exacerbation of pre-existing skin disease
- Dermatological effects of anabolic-androgenic steroids
Introduction
The skin plays an important role in protecting the body from noxious external stimuli such as mechanical forces, temperature changes, and harmful chemicals. It is no surprise, therefore, that cutaneous disorders are an important factor in every athletic specialty. Sports dermatology is concerned with skin disorders related to athletic activity, manifesting either as a primary disorder or as an exacerbation of a pre existing dermatological dermatosis. Sports dermatology is an enlarging field and this chapter summarizes some of the more commonly encountered problems.
Skin infections
Fungal infections
Dermatophytic fungi live in the stratum corneum (most superficial epidermal layer) and can cause superficial infections. Tinea pedis or ‘athlete’s foot’ affects the interdigital and lateral areas of the feet and is characterized by pruritis, scaling, and occasional soreness. The classic ‘wet form’ presents with white macerated scale, fissures, and occasionally with vesicles and bullae. Less commonly a ‘dry form’ or ‘moccasin foot’ is seen as a dry, rough, diffuse white scale affecting the sole. The problem is often bilateral and the toenails may also be involved (manifest by discolouration, thickening, crumbling and Subungual scale of one or more toenails). Tinea pedis is a chronic disorder and patients may be afflicted for decades. Infection occurs by person-to-person or by contact with infected fomites such as a towel or floormat. It is undoubtedly influenced by the microenvironment of the clad foot, and factors which exacerbate the condition include a moist, warm environment; a sweaty foot enclosed in a non-absorbent sock and occlusive shoe such as a ‘trainer’ is a likely target for tinea pedis. Secondary bacterial infection is sometimes seen and may present as cellulitis, lymphangitis, or inguinal lymphadenopathy. The diagnosis of tinea pedis is confirmed by examining scrapings of keratinous debris in a 10% potassium hydroxide (KOH) preparation and observing the characteristic hyphae. Culture permits identification of the causative fungus (usually Trichophyton rubrum, T. mentagrophytes, or Epidermophyton floccosum). The differential diagnosis includes pompholyx, pustular psoriasis, pitted keratolysis and allergic contact dermatitis to shoes; a positive skin scraping however does not necessarily exclude these dermatoses, as a superficial dermatophyte infection may be superimposed upon an area of already broken skin.
Treatment Acutely inflamed ‘wet’ forms of superficial fungal infections should be treated with a combination of shooting antiseptic soaks or paints (e.g. Castellan’s) and topical antifungals. Soaks should be lukewarm and contain potassium permanganate 1 in 10 000 and the feet immersed in the solution for 15 minutes three times daily. Effective topical antifungals include the newer imidaoles such as miconazole, econazole or clotrimoxazole in a cream or tincture base; these should be applied twice daily for approximately two weeks. Careful attention should be given to avoidance of exacerbating factors such as sweat, heat, and occlusion. Socks should be cotton or wool, and preferably changed once or twice during the day. Footwear such as thongs or clogs should be worn while using communal showers or change rooms. Athletes should alternate pairs of sneakers or shoes if possible to allow airing in between periods of wear. Infection of the nails is an indication for oral antifungal therapy as dermatophyte in the nail are relatively resistant to topical agents. A new allylamine drug, terbinafine, can achieve a mycological cure of toenail onychomycosis in 70-80% of patients following twelve weeks of therapy1. Other oral agents used include griseofulvin, ketoconazole and intermittent itraconazole. Although generally safe agents, ketoconazole is contraindicated in patients with hepatic disorders and can interact with other medications, for example, warfarin. Itraconazole has fewer hepatic side effects but is considerably more expensive than other oral antifungals. Amorolfine 5% nail lacquer can be applied to affected nails once or twice per week and has shown to cure approximately 40-55% of patients with toenail onychomycosis 2.
1. Tosti A, Piraccini BM, Stinchi C, Venturo N, Bardazzi F, Colombo MD. 1996 Treatment of dermatophyte nail infections: An open randomized study comparing intermittent terbinafine therapy with continuous terbinafine treatment and intermittent itraconazole therapy. Journal of the American Academy of Dermatology, 34, 595-600.
2. Haria M and Bryson HM. Amorolfine. 1995 A review of its pharmacological properties and therapeutic potential in the treatment of onychomycosis and other superficial fungal infections. Drugs, 49 (1): 103-20.
Other fungal infections include tinea cruris, tinea versicolour and tinea incognita.
Tinea curis (‘jock itch’)
Commences in the groin folds and extends out in an annular or circular fashion with a scaly, inflamed border. Hyphae can also be identified on KOH preparation of scale taken from the active advancing border. Treatment of tinea cruris is with oral griseofulvin and concomitant topical treatment with one of the newer imidazole creams.
Tinea versicolour
Not actually a dermatophyte infection but is due to the saprophytic yeast Pityrosporum orbicular which develops into is parasitic fungal form Malasezia furfur. This transformation may be provoked by humidity, ambient heat, as a result of exercise, secondary to diabetes mellitus or iatrogenic immunosuppression e.g. systemic corticosteroid treatment or immunosuppressives for solid organ transplants.
Tinea versicolour infection produces hyper-or hypopigmented macules on the torso and proximal limbs with fine bran like scale. Infection can be chronic and recurrent with exacerbations following climatic changes in humidity. Organisms can be detected in a KOH preparation of skin scrapings. Treatment of pityriasis versicolour has traditionally been with selenium sulphide (Selsun® shampoo) applied as a cream to the affected areas twice daily or more recently with imidazole creams or foaming washes.
Treatment needs to be applied to skin beyond the disappearance of the eruption, however, relapses are common with topical therapies. A course of oral ketoconazole or itraconazole for seven days is effective in eliminating the reservoir of Pityriasis organisms and helps prevent further relapses.
Tinea incognita
Refers to the specific clinical picture seen when a potent topical corticosteroid preparation is mistakenly applied to a tinea infection. Inflammatory features such as erythema may be absent; typically a mild, pink, scaly annular macule with central clearing is seen. Skin scrapings stained with KOH show abundant hyphae and permit the correct diagnosis.
Bacterial infections
Impetigo
A superficial bacterial infection characterized by honey-coloured crusts or vesicles on a moist erythematous base. Impetigo is highly infectious and is spread by direct contact or fomites and can infect intact skin. The organism(s) responsible are usually streptococcus or staphylococcus aureus. High ambient temperatures, humidity, low altitude and poor hygiene may favour development and transmission of impetigo. Streptococcal impetigo has spread amongst footballers and those playing North American football1.
Treatment consists of topical or systemic antibiotics directed against both streptococcus and staphylococcus. Removal of crusts by gentle soaking with warm compresses of potassium permanganate (1 in 10 000) dilution followed by a topical antibiotic such as mupirocin or fusidic acid, for approximately seven to ten days is effective. The entire skin, scalp included, should be washed with an antiseptic soap daily for ten days. Alternatively, a ten day course of broad spectrum oral antibiotics active against ß-lactamase producing staphylococci is also efficacious.
The patient should be isolated until clearance of crusts and not allowed to compete in contact sports. In particular, sportsmen such as wrestlers should be free of new lesions for at least 48 hours prior to competition and should have no moist, exudative or draining lesions prior to tournament participation.
. Bartlett P, Martin R, Cahill B. 1982 Furunculosis in a high school football team (1982). American Journal of Sports Medicine, 10: 371-4.
Pitted keratolysis
A bacterial infection of the palmar surface of the feet due to superficial infection with corynebacterium species. It characteristically appears as shallow white pits or dents in the stratum corneum. Increased sweating (hyperhidrosis) is thought to play an aetiological role in the condition and thus may be seen with increased frequency in athletes. Maceration and malodour may be associated findings. Treatment consists of general preventative measures to control hyperhidrosis (absorbent socks, leather shoes, ‘shoe-free’ intervals), topical application of antiperspirants containing 20% aluminium chloride, an topical antibiotics such as 1-2% erythromycin or clindamycin solution.
Viral infections
Herpes simplex virus (HSV)
HSV is a double stranded DNA virus which typically causes recurrent infections of the mucous an periorifical membranes. However, it can infect any skin surface and remain latent in the ganglia of peripheral nerves.
Herpes gladiatorum
Herpes gladiatorum has been described in participants in close contact sports such as wrestling and rugby (also known in the latter as ‘scrumpox’) and in a recent study of American college wrestlers 7.6% were reported to have had a herpes skin infection in the preceding 12 months1. Herpes gladiatorum is transmitted primarily by direct skin to skin contact, and abrasions in the skin may allow a pathway of infection. The majority of lesions occur on the head or face, followed by the trunk and/or extremities. A prodromal itching or burning sensation is followed by clustered vesicular lesions on an erythematous base which heal with crusts over about one to three weeks. Less commonly headache, malaise, sore throat and fever may accompany the primary infection. Recurrent episodes may occur following the initial infection and may precipitated by sunburn, illness, and emotional stress. HSV antibodies, acquired from previous cold sores, may be protective from acquiring herpes gladiatoraum eruptions. Because of its unexpected location on the cutaneous surface, herpes gladiatorum any be confused with impetigo, varicella, staphylococcal furunculosis, or allergic or irritant contact dermatitis. Adequate treatment, counseling and public health strategies depend on making an accurate diagnosis, hence viral immuno fluorescence and cultures should be obtained by gently breaking an intact vesicle and firmly rubbing the swab tip across the base of the erosion.
Treatment of herpes gladiatorum is ideally with oral acyclovir (200mg five times a day for the five days) and is most effective if commenced at the first symptoms of an outbreak. Topical acyclovir is available but is probably less effective. Concomitant secondary impetiginisation should also be treated. HSV can survive for hours to days outside the host if environmental conditions are appropriate2 hence all contaminated surfaces should be cleaned with antiseptic solution. In the vesicular phase and until the crusts have separated, patients should avoid sports which could involve physical contact.
1. Becker TM. Herpes Gladiatorum: 1992 A Growing Problem in Sports Medicine (1992). Cutis 50: 150-2
2. Nerurkar LS, West F, May M et al. Survival of herpes simplex virus in water specimens collected from hot tubs in spa facilities and on plastic surfaces (1983). Journal of the American Medical Association 250: 3081-3.
Molluscum contagiosum
A highly infectious pox virus which can also be spread by human contact. The organism appears to be easily spread in an aqueous medium, for example, in communal baths, spas and pools. Amongst athletes, swimmers and cross country runners have the highest incidence of mollusca. Their incidence may be increased in patients with underlying active atopic dermatitis. They typically appear as solitary or multiple flesh-coloured dome shaped papules with a central umbilication. The differential diagnosis includes multiple basal cell carcinomata, cryptococcosis and appendageal tumours such as trichoepitheliomas. They can be treated by gently breaking the surface of the lesion and extracting the central keratinous plug. Other treatments employed are cryosurgery with liquid nitrogen, electrodessication and topical trichloroacetic acid or tretinoin. Athletes may resume contact sports 48 to 72 hours after the lesions have cleared.
Common warts
Are epidermal growths caused by infection by the human papillomavirus group (HPV). Infection can occur if infected debris from warts comes in contact with abraded skin and can result in either autoinoculation or transmission to susceptible individuals. However, it is not generally thought to be highly infective and thus not limit participation in contact sports. Plantar warts can cause pain with ambulation, thereby limiting performance in sporting activities. Warts may also be more common in callouses which develop in sport1. Paring of plantar warts with a #15 blade reveals small black spots corresponding to thrombosed capillaries within papillae, thus distinguishing the lesions from callouses or corns, which lack these dots and have a central hyaline core.
Treatment of plantar warts is challenging and may cause as much inconvenience to the athlete as the presence of the wart itself. Daily application of salicylic and lactic acid preparations under occlusion with concomitant paring with an emery board may be effective, as may repeated cryosurgery and paring at two or three week intervals. For resistant warts, intralesional bleomycin injections or carbon dioxide ablation can be used. Oral high dose Cimetidine therapy (30-40mg/kg/day) has reportedly been successful in childhood warts; however other studies have shown no advantage in Cimetidine over placebo in adults2.
1 Kantor G and Bergfeld W. 1988 Common and uncommon Dermatologic diseases related to sports activities. Exercise and Sports Science Reviews 16: 215-53
2 Yilmaz E, Alpsoy E, Basaran E. 1996 Cimetidine therapy for warts: A placebo-controlled, double-blind study. Journal of the American Academy of Dermatology 34: 1005-7.
Sports-related allergic and irritant dermatitis
Urticaria
Urticaria or hives, is relatively common disorder and its incidence is highest in young adults. It can be defined as a transient red and/or oedematous swelling of the dermis or subcutaneous tissues. Some factors which can provoke urticaria include medications such as analgesics and non-steroidal anti inflammatory agents, which may be ingested by athletes from time to time. Of particular interest are the physical urticarias. These are triggered by a variety of physical causes such pressure, cold, heat, water (aquagenic), and solar irradiation. Most patients suffer from idiopathic urticaria as well; that is, physical factors may not always contribute to urticarial lesions. Athletes may develop pressure urticaria from tight fitting belts, clothing, or on the soles of feet following running. Cold induced urticaria can be precipitated by food, drinks, and changes in the ambient temperature. If the whole body is cooled suddenly, as when diving into a swimming pool, an episode of urticaria could lead to circulatory collapse. It is thus very important to recognize this uncommon condition and instruct patients to avoid such triggers. Exposure to the sun or artificial light sources may rarely be followed by itching, erythema and wheals. Cholinergic urticaria is a type of eruption associated with sweating. The weals are characteristically small and surrounded by large red halos, and last less than an hour following the trigger. Flushing, faintness, asthma, nausea, vomiting, and diarrhoea may occasionally occur as a result of systemic histamine released by mast cells. Water-induced urticaria presents in a similar fashion. The treatment of the physical urticarias is firstly to eliminate the triggers as far as is possible. An episode of Cholinergic urticaria may be followed by a refractory period of up to 24 hours; athletes may therefore wish to ‘warm up’ a few hours prior to a specific event where the unpleasant effects of weals may be undesirable. Non-sedating antihistamine agents such as loratadine or cetirizine are usually effective treatment.
Contact dermatitis
Many natural and synthetic substances can induce dermatitis or inflammation of the skin upon physical contact. Sports enthusiasts may be particularly vulnerable to irritant dermatitis from equipment and medicaments. In addition, sweat and local heat and humidity may enhance a substance’s allergenic or irritating potential by interfering with the normal barrier function of the skin. An irritant reaction will result in dermatitis independently of a specific immunological reaction and will tend to produce a similar reaction in all persons exposed to the irritant. For example, chronic exposure to water and detergents may result in irritant contact hand dermatitis.
An allergic contact dermatitis, however, is a delayed (type IV) immunological reaction involving specifically sensitized T lymphocytes in a susceptible individual. Some of detective work may be required to identify the offending allergen; for example, a linear abdominal eruption in a surfer may be attributable to allergic contact dermatitis to nickel contained in the zip fastener of a wet suit. A spectrum of clinical presentations may be seen in both irritant and allergic contact dermatitis. Classically, contact with an allergenic plant (e.g. Rhus iv, grevillea, primula obconica) in a sensitized individual results in a bullous, intensely itchy, linear eruption of the forearms. These reactions may be seen in outdoor athletes. Rubber is a known sensitizer and may produce either a delayed type contact dermatitis (usually due to accelerants or antioxidants used in rubber manufacture) or an urticarial type immediate reaction (due to latex allergy). Bathing caps, nose clips, ear plugs, fins and finstraps, swimming goggles, diving suits, and underwater masks and mouthpieces are all capable of producing potentially serious cutaneous reactions in swimmers or divers. Of particular concern would be a patient with type 1 allergy to rubber latex who dived with a rubber mouthpiece and experienced an urticarial reaction while diving. Allergic contact dermatitis to shoes (tanning agents used in leather, rubber, glues, inner soles) may result in a symmetrical bilateral dermatitis affecting the feet, in a distribution reminiscent of actual contact with the allergen (for example, a rash on the lateral aspect of the soles may correlate with allergy to inner soles). Sports participants may develop allergic contact dermatitis to topically applied medicaments (salicylates, linaments, tea tree ail, antibiotics, antiseptics, and any fragrances or preservatives contained therein) or tapes and plasters (colophony, para-tertiary-butylphenol-resin).
PABA - containing sunscreens used by athletes may also result in allergic contact dermatitis, often involving sun exposed skin only. Identification of the offending allergen may be difficult and patients should be referred to specialist dermatology centres for detailed patch testing should allergic contact dermatitis be suspected. Topical corticosteroids with wet dressings, and occasionally oral corticosteroids, along with withdrawal of the offending substance, are used to treat allergic contact dermatitis.
Dermatological manifestations of physical, cold, and electromagnetic injury
Acne mechanica
Acne mechanica is a papulopustular eruption caused by the physical factors of pressure, occlusion, friction, and heat acting upon the skin1 . It is believed that these mechanical stresses, rather than follicular infection by normal skin commensals (as in common acne) play a primary causative role in sports-related acne. Pre-existent acne vulgaris is therefore not necessarily a precursor of acne mechanica, although the mechanical stresses mentioned above certainly aggravate common acne. Acne mechanica is one of the more prevalent dermatoses among athletes. Heavy protective padding, headgear, occlusive synthetic garments such as leotards, and golfers carrying heavy bags can precipitate acne mechanica. It has thus been observed in American football players, hockey players, aerobics participants and golfers. An unusual example of acne mechanica has been described on the neck of a shot putter at the position where the shot is rested against the neck before being thrown.
Acne keloidalis is a specific chronic pilosebaceous disorder affecting the posterior occipital scalp of predominantly black skinned individuals; it has reportedly developed in helmet-wearing football players with no prior history of the disorder2. Prevention of the condition is important in management and wearing a clean, absorbent cotton T shirt under uniforms and equipment may be useful. Early removal of clothing and showering after sport will also alleviate aggravating factors. Thorough cleansing followed by keratolytics such as salicylic acid in ethanol, or tretinoin cream. Topical antibiotics such as clindamycin or erythromycin in an astringent base are helpful in visibly infected cases. Systemic antibiotics, used with success in common acne, seem to be of less benefit in acne mechanica. The eruption invariably settles down during seasonal breaks from participation in sports activities.
1 Basler RSW. 1992 Acne Mechanica in Athletes (1992). Cutis 50: 125-128
2 Harris H. Acne Keloidalis Aggravated by Football Helmets (1992). Cutis 50: 154-156.
Trauma - induced skin disease
Foot blisters may result from heat and humidity combined with unaccustomed localized friction. Improperly fitting shoes and sporadic training may contribute to their development. They are best treated by sterile aspiration, leaving the overlying skin intact to form a natural dressing. The area can then be treated with an antibiotic ointment or antiseptic and covered with a simple dressing. Newer hydrophilic dressings are comfortable and absorbent and may allow the athlete to resume participation. Prevention is the key to successful treatment; shoes should be properly fitting and worn with two pairs of cotton socks. Foot powders may help to absorb moisture and thus reduce skin shearing forces. Anecdotal evidence suggests that application of Friar’s Balsam Amy ‘toughen’ skin and reduce the incidence of blisters.
Black heel or talon noir are petechiae occurring over the posterior aspect of the heel. They are common in sports such as basketball, squash, or football, where frequent changes in direction occur, resulting in a shearing effect on the skin. The colour of the eruption may alarm the athlete and cause them to present. No treatment is required apart from reassurance.
Jogger’s nipple is a painful and often fissured dermatitis eruption over the nipples produced by friction from unyielding vests or T shirts and may also occur in women who do not wear undergarments while jogging. Treatment is with anemollient such as emulsifying ointment or white soft paraffin, or a mild topical corticosteroid, and elimination of the underlying trigger.
‘ Tennis toe’, actually observed in a variety of activities including cricket, jogging and skiing , is due to haemorrhage under the nail plate of the great toe caused by impact between the distal end of the nail plate and the shoe. This may result in an acutely painful subungual haematoma which may require drainage. The injury may be prevented in some cases by excising away a small portion of the toe of the shoe, thus reducing the impact effect on the toe.
Repeated low grade trauma or pressure to the skin surface will result in a protective hyperkeratotic response to prevent injury to underlying structures; eventually a callus will form. The type of sport will determine the location and shape of the callus; for example, the hands of a rower or weightlifter, or the soles of a jogger. Corns (clavi) are callosities over bony prominences. Athletes with long second or third toes (Morton’s toe) may develop buckling of the second toe which forces the second metatarsal head into the ground and results in clavus formation in this position. Clavi are exquisitely tender to lateral pressure or squeezing. Treatment of callosities and clavi begins with correction of the abnormal mechanical stresses and consultation with a podiatrist may help to identify these. The lesions can be pared with a scalpel blade and keratolytics applied to help remove excess keratin. Cryotherapy of clavi requires relatively long freezing times (approximately 90 seconds); the resultant crust is shaved in three or four weeks, and often one treatment can abolish the clavus1
Athlete’s nodules
Athlete’s nodules are connective tissue naevi (collagenomas) at sites of recurrent trauma and friction. They may appear in knuckles, pretibial areas or dorsal aspects of the feet, in an area directly related to the particular sport.
‘Nike nodules’ appear on the dorsal foot from repetitive trauma associated with jogging2
Surfer’s nodules develop on the dorsal foot from trauma associated with surfboards. Piezogenic papules are small, painful herniations of fat through areas of damaged dermis, often appearing on the mediolateral aspects of the feet. They may only be apparent when the foot is in a weightbearing position. Support stockings may afford some symptomatic relief.
1 Sheard C. Simple Management of Plantar Clavi (1992). Cutis 50: 138.
2 Basler RSW and Jacobs Senior Lecturer Orthopaedic Surgery. Athlete’s nodule. Reply (letter) (1991). Journal of the American Academy of Dermatology 20: 318.
Heat and cold related skin disease
Intertrigo
An inflammatory dermatosis affecting the body folds, in particular the submammary and genitocrural areas. Obesity, sweat and friction predispose to its development, and the clinical appearances can range from mild erythema to frank dermatitis with secondary bacterial or candidal infection. In refractory cases, diabetes mellitus should be excluded. Avoidance of tight clothing, carefully applied wet dressings in the acute phase, and the application of one of the imidazole preparations alone, or with a topical corticosteroid, may help control the condition. It is important to remember that fleural psoriasis occasionally presents a similar clinical picture and may lack the characteristic silvery scale in the moist flexural region. Flexural psoriasis is generally more erythematous with a well defined border, and there is often evidence of psoriasis elsewhere on the body such as the scalp, elbows or knees.
Miliaria, (‘prickly heat’)
Occurs in a hot and humid environment when sweat becomes trapped within ducts before it reaches the epidermal surface. It mainly affects the torso. Three types of miliaria are seen depending on the level of obstruction with the skin. Miliaria crystalline occurs when obstruction is very superficial in the epidermis, resulting in fragile vesicles. Miliaria rubra is the most common type and is due to obstruction in the intraepidermal sweat duct, and presents as erythematous papules associated with pruritus and stinging. Miliaria profunda is rarely seen outside of the tropics and is due to obstruction of deeper dermal sweat ducts. Treatment of miliaria consists of reducing environmental heat and humidity, use of mildly astringent lotions to help relieve ductal obstruction, and mild topical corticosteroids to reduce inflammation. Miliaria may be followed by a period of hypohidrosis or defective sweating, and may put athletes at risk for overheating injury for several weeks.
Erythema ab igne
Is a characteristic cutaneous eruption consisting of a well demarcated area of livedoid erythema and pigmentation, most commonly seen on the lower legs of older women who sit too close to a heater in winter. Vascular injury secondary to heat damage is thought to play a role. Similar eruptions may be seen in athletes who apply heat packs to the skin for musculoskeletal injuries. Cold compressions are also used for such injuries and cryogenic damage to skin following their correct usage has been reported 1. The eruption consisted of bullae and erythema 24 hours following a 25 minute exposure time to the cold compress. The degree of hypothermia delivered by such cold compresses may be potentiated by applying an elastic bandage and/or actually sitting on the cold compress thus firmly immobilizing it against the skin. This method of application should therefore be avoided.
1 Cipollaro V. Cryogenic Injury Due to Local Application of a Reusable Cold Compress (1992). Cutis 50: 111-112.
Ultraviolet-related skin disease
Sunburn
Sunburn is a preventable skin injury which has acute and chronic effects on the skin. Acute effects include erythema, oedema and desquamation. Chronic effects comprise increased incidence of cutaneous tumours (including malignant melanoma, squamous and basal cell carcinomata, keratoacanthoma), photoaging and atrophy. Malignant melanoma is of particular concern because of its aggressive behaviour and strong correlations between frequency of sunburns in youth and the development of melanoma. Prevention of sunburn and excessive photoexposure in sports participants is an area of preventative medicine which should be endorsed by all sports enthusiasts - spectator, athlete, and official alike. Sporting activities should ideally be timed for early morning or mid to late afternoon in order to avoid the harsher midday ultraviolet rays. Broad spectrum sunscreen agents (which block out UVB, UVA and infrared rays) with a sun protection factor (SPF) of at least 15 times normal should be applied and reapplied frequently during outdoor exposure. Use of hats and protective clothing, preferably also with good UV blocking abilities, should also be endorsed.
Ultraviolet light exposure may also result in phototoxic reactions to substances either orally ingested, for example, non-steroidal antiinflammatory agents , or applied topically, for instance perfumes and essential oils. Even brief exposure to ultraviolet light may cause intense reactions in persons who have used photosensitizing agents, and this can persist long after cessation of the offending agent.
Exacerbation of pre-existing skin disease
A variety of dermatological conditions may become exacerbated by sport activity. Although acne may arise de novo following trauma from sport, it is also a common condition of young people and may worsen with activity. It is important to remember that treatments for acne such as isotretinoin (oral synthetic vitamin A derivative) may give rise to side effects such as photosensitivity, skin fragility, and myalgias, which can interfere with sporting performance. Minomycin, a commonly used oral antibiotic for acne, can also result in photosensitivity.
Psoriasis is a common skin disorder with quite varied clinical manifestations. Psoriasis is often exacerbated by trauma (the Koebner or isomorphic response) and palmoplantar psoriasis may also be influenced by chronic mechanical pressure. Retinoids and tar preparations may result in photosensitivity.
Many patients with atopic dermatitis find that sweating aggravates their condition. Seasonal exacerbations in spring and autumn are also frequent. Chlorinated, as opposed to saltwater, pools can be very drying for atopic individuals, and frequent showering may also exacerbate eczema. Exposure of the skin to irritant chemicals or physical trauma should thus be avoided as far as possible.
Dermatological effects of anabolic-androgenic steroids
The use of self-administered anabolic-androgenic steroids by athletes and body builders may be widespread and under recognized. Anabolic steroids are synthetic derivatives of testosterone. High doses may stimulate the production of sebum by sebaceous glands and increase the numbers of normal follicular bacteria. Acne, oily hair and skin, sebaceous cysts, hirsutism, and rogenetic alopecia, striae (stretch marks), seborrheic dermatitis, and secondary bacterial infections occur with increased frequency in this group of athletes. Cutaneous side effects are often the initial clinical manifestations of anabolic steroid usage1 .
1 Scott MJ and Scott AM. Effects of Anabolic-Androgenic Steroids on the Pilosebaceous Unit (1992). Cutis 50: 113-117. | |
