Adolescent Health Care: A Practical Guide
Miscellaneous Dermatological Disorders
Mei-Lin T. Pang
Lawrence F. Eichenfield
Although acne is the most prevalent skin disorder during adolescence, other diseases such as seborrhea, eczematous dermatitis, fungal infections, warts, and several other conditions are also very common. These disorders while variable in severity, may assume the importance of a serious illness in an adolescent concerned about body image and popularity. Effective therapy and understanding of the adolescent's feelings may lead to a strong alliance between the patient and health care provider. Acne is discussed in Chapter 19; this chapter describes other skin problems commonly encountered during adolescence.
Eczematous dermatitis is an inflammatory response of the skin to multiple exogenous and endogenous factors and includes a group of problems whose etiology is often either multifactorial or unknown. The two major groups of dermatitis affecting adolescents are contact dermatitis and atopic dermatitis. In a review of the most common dermatological problems seen by internists, dermatitis was the most common diagnosis, making up 15.8% of them (Feldman et al., 1998).
- Distribution: Areas that have been exposed to the inciting agent, often including the hands, eyelids, genitalia, and legs.
- Lesions: Pruritic, vesicular, erythematous and/or edematous lesions in a well-demarcated area, often corresponding to the distribution of contact. Erythema, edema, and crusting are often present. If chronic, lichenification, scaling, and pigmentary changes are also seen.
Approximately 80% of contact dermatitis is irritant and 20% allergic. Contact and irritant dermatitis may be indistinguishable clinically, but irritant dermatitis usually occurs on the hands. Photoallergic dermatitis usually occurs on sun-exposed areas such as face and neck in response to photosensitization by ingested drugs. Patch testing may be helpful in confirming allergic contact dermatitis if a specific antigen is suspected.
- Irritant dermatitis: A nonimmunologically mediated dermatitis that can occur in individuals exposed to the agent when exposed to adequate doses. Prior exposure is not required. Common agents include the following:
- Alkalis: Soaps, detergents, bleaches, and cleansers
- Acids: Hydrochloric acid, nitric acid, oxalic acid, carbolic acid, acetic acid, and salicylic acid
- Hydrocarbons: Oils and tars
- Physical irritation or friction
- Allergic contact dermatitis: A type IV, delayed-type hypersensitivity reaction occurring in patients sensitive to a specific agent (usually an environmental chemical). Prior exposure is required for a reaction. Examples include the following:
- Rhus (poison ivy, oak, or sumac)
- Nickel and other metals, particularly mercury and chromium
- Rubber compounds (latex)
- Dichromate: A common cause of shoe dermatitis; also found in metals, paint, cement, and photographic chemicals
- Fabric dyes or chemical finishes (e.g., formaldehyde resin)
- Adhesives: The rubber component or the glue
- Cosmetics: Hair dyes, hair sprays, artificial nails, nail hardeners, lipsticks, eye makeup, preservatives, sunscreens, perfumes, and mouthwashes
- Atopic dermatitis
- Tinea corporis
- Seborrheic dermatitis
- Keratosis pilaris
- Icthyosis vulgaris
- Identify and avoid the offending agent.
- Topical corticosteroid creams are applied twice a day to affected areas. Moderate to high potency steroids may be necessary.
- Antihistamines may help decrease the associated pruritus.
- Widespread, severe contact dermatitis may require a course of systemic corticosteroids (40–60 mg/day for 7 days, tapered over 2–3 weeks).
Atopic dermatitis is a common, chronic, pruritic dermatitis also known as atopic eczema and allergic eczema. Onset typically occurs in childhood and may improve or continue in adolescence. It appears in approximately 17% of children, with 90% presenting before the first year of life.
There are many features that may be used for clinical diagnosis.
- Essential features (must be present)
- Eczematous dermatitis (acute, subacute, or chronic)
- Typical morphology and age-specific patterns. In adolescence, the morphology resembles the adult pattern of flexural lichenification and involvement of the face, neck, and hands. Lesions consist of pruritic, slightly elevated, flat-topped papules that tend to coalesce to form lichenified, scaly plaques. The plaques may become excoriated, exudative, or crusted.
- Chronic or relapsing history
- Important features (seen in most cases, adding support to diagnosis)
- Early age of onset
- Personal and/or family history. Approximately 50% of individuals concurrently have either asthma or allergic rhinitis. A positive family history of atopy (asthma, allergic rhinitis, and atopic dermatitis) is present in two thirds of individuals.
- Immunoglobulin E (IgE) reactivity
- Associated features (suggestive of a diagnosis of atopic dermatitis but are too nonspecific for use in defining or detecting atopic dermatitis for research or epidemiological studies)
- Atypical vascular responses (e.g., facial pallor, white dermatographism, delayed blanch response)
- Keratosis pilaris/hyperlinear palms/icthyosis
- Keratosis pilaris: Follicular hyperkeratosis on the lateral upper arms and thighs
- Ocular/periorbital changes (e.g., Dennie-Morgan lines)
- Other regional findings (e.g., perioral changes/periauricular lesions)
- Pityriasis alba: Ill-defined, scaly, hypopigmented patches typically on the face, neck, trunk, and extremities of children and adolescents between the ages of 3 and 16. It is thought to represent a low-grade eczematous dermatitis and is a minor feature of atopic dermatitis. It is typically asymptomatic, however teenagers may complain of pruritus.
- Perifollicular accentuation/lichenification/prurigo lesions
- Infections: Increased susceptibility to infections with herpes simplex virus, Staphylococcus aureus, Trichophyton rubrum, warts, and molluscum contagiosum
- Eye: Increased prevalence of cataracts, keratoconus, recurrent conjunctivitis, periorbital darkening, and retinal detachment
- Skin: Exfoliative dermatitis
- Seborrheic dermatitis: Greasy, scaly scalp; distribution more likely to include scalp, eyebrows, and ears
- Contact dermatitis: History of contact with an offending agent and patterned distribution of the eruption
- Tinea corporis or pedis: Sharp margins; confirmed by positive findings from potassium hydroxide examination
- Scabies: Distribution usually includes web spaces of hands, groin, buttocks, and axilla; skin scraping positive for mites or eggs
- Psoriasis: Well-demarcated erythematous plaques with silvery scale; predilection for extensor surfaces; nail pitting common, but not specific
- Keratosis pilaris
- Education: Health care providers should discuss the chronic, recurrent course of atopic dermatitis with patients and their families. They should also review common, exacerbating factors. Written and verbal information as well as treatment plans may be helpful.
- Hydration: Patients with atopic dermatitis have increased transepidermal water loss secondary to impaired function of the water permeability barrier, and decreased ceramide levels in the skin. Many advocate the “soak and seal” method, consisting of lukewarm to warm baths or showers lasting no more than 10 to 20 minutes using a gentle, nonsoap cleanser. The patient should then moisturize within a few minutes of bathing.
- Moisturizers: Moisturizers help preserve the stratum corneum barrier and maintain hydration of the skin. Ointments are the most moisturizing but may be too occlusive in hot or humid environments, leading to sterile folliculitis or increased pruritus. Creams and lotions have higher water content than ointments, making them easier to apply. Additives such as fragrances or preservatives can be irritating and should therefore be avoided. Moisturizers can dilute the effect of topical medications and should be applied at least 20 minutes after topical medications.
- Avoidance of irritants: Patients with atopic dermatitis have increased responsiveness to irritants. Loose fitting, noncoarse clothing is recommended. Patients with severe atopic dermatitis may find using cotton gloves or socks can protect the skin from potential irritants and reduce trauma from scratching. Cleansers with minimal defattening activity and neutral pH are recommended. Products labeled for “sensitive skin” may be better tolerated in patients with atopic dermatitis. Environmental factors such as temperature, humidity, and fabric texture can also contribute to skin irritation. Patients tend to fare better in air-conditioned or temperate environments where sweating is minimized. Sun exposure can also lead to overheating, evaporation, and perspiration.
- Avoidance of allergens: Some adolescents may be sensitive to dust mites, animal dander, or other airborne triggers. Although food allergies are more common in atopic patients, eczematous flares caused by specific foods occur only in few adolescents.
- Addressing psychosocial issues: Atopic dermatitis can have a profound effect on the patient and family. Sleep disturbance secondary to pruritus can impact work and school function leading to more missed days at school, increased work absenteeism, household stress, and economic burden of the disease. Sedating antihistamines may be useful in this setting. Behavior modification (e.g., reward system for not scratching) to break the itch-scratch cycle is also recommended.
- Topical corticosteroids: Topical corticosteroids are a mainstay of therapy in treating acute disease. They range in potency from very mild (1%–2.5% hydrocortisone) to superpotent (clobetasol). They are typically applied twice daily to affected areas.
- Topical calcineurin inhibitors: Tacrolimus (Protopic) 0.03% ointment is approved for use in patients 2 to 15 years of age, and 0.03% and 0.1% are approved for short-term and intermittent long-term use in adults with moderate-severe atopic dermatitis. Pimecrolimus (Elidel) 1% cream is approved for use in patients at least 2 years of age with mild-moderate atopic dermatitis.
- Antibacterial therapy: Patients with atopic dermatitis are more prone to secondary skin infections. Systemic antibiotics such as a first- or second-generation cephalosporin (e.g., cephalexin 25–50 mg/kg/day divided b.i.d. to t.i.d., with 2 g maximum total daily dose) for 7 to 10 days are usually recommended. Long-term antibiotic therapy is discouraged as this may select for resistant organisms. Topical antibiotics such as mupirocin (Bactroban, Centany) applied t.i.d. for 7 to 10 days may be used to treat localized infections. Intranasal application of mupirocin twice daily for 5 days can reduce nasal carriage of S. aureus. Patients with eczema herpiticum usually require systemic acyclovir in a hospital setting. Bleach baths (cup bleach mixed in a full bath two to three times a week) decrease bacterial colonization and may be useful as adjunctive therapy in patients with recurrent staphylococcal infections.
- Antihistamine and anxiolytic therapy: Pruritus is one of the most troublesome features of atopic dermatitis. Scratching can lead to excoriation, secondary infection, bleeding, lichenification, or nodular changes. Patients often complain of sleep disturbance, impacting the patient and caregiver's quality of life. Systemic antihistamines such as diphenhydramine and hydroxyzine can be used for their sedating effects when given at bedtime. Doxepin is a tricyclic antidepressant with histamine-blocking properties. It should be used in patients with severe disease.
Other Types of Eczematous Dermatitis
- Lichen simplex chronicus: One or more lichenified plaques, probably secondary to repeated local trauma such as rubbing or scratching
- Dyshidrotic eczema (pompholyx): Recurrent crops of vesicles on palms and soles and sides of fingers and toes; exacerbated by stress and frequent exposure to water
- Seborrheic dermatitis: Greasy scaling patches on scalp, eyebrows, nasolabial area, intertriginous areas, and chest
- Nummular atopic dermatitis: Minute vesicles and papules that enlarge to form discrete, erythematous, coin-shaped patches.
- Acne: See Chapter 19 for discussion.
- Folliculitis: Infection of a hair follicle is common and usually involves S. aureusor streptococci. Other causes include fungi (Candida and Pityrosporum), viruses (herpes simplex virus and molluscum), and drugs (corticosteroids, lithium, halogenated compounds). The infection is usually superficial and characterized by tiny pustules near affected hair follicles, surrounded by an area of erythema. Common locations include the scalp, extremities, buttocks, and perioral and perinasal areas. Other areas include the groin or pubic area in patients who shave or wax, especially if the patient does not exfoliate the area on a regular basis. Treatment involves local hygiene with antibacterial soaps or cleansers and a topical antibiotic ointment, solution, or foam (e.g., clindamycin). The differential diagnosis includes culture-negative (normal flora) folliculitis, eosinophilic folliculitis, acne vulgaris, rosacea, keratosis pilaris, and pseudofollicultis barbae.
Pseudofolliculitis barbae is a noninfectious, inflammatory condition occurring in men with darkly pigmented skin and tightly curled hair, caused by reentry of curved hairs after shaving. Curative therapy includes avoidance of shaving and letting the beard grow. Although this will eliminate the condition, this is not always practical. Steps to improve the condition include the following:
- Pretrim hair with clippers, leaving 1 to 2 mm stubble.
- Wash with a nonabrasive acne soap and rough washcloth, dislodging ingrown hairs with a soft toothbrush. Rinse with warm water and apply warm compresses to the area for at least 2 minutes.
- Massage a moderate amount of lather and shave in the direction of hair growth with a sharp razor using short, even strokes.
- Rinse with cool to cold tap water and apply cold compresses for at least 5 minutes.
- Dislodge any remaining ingrown hairs with a sterile needle or toothpick.
- Aftershave should be a gentle, moisturizing type. Topical 1% hydrocortisone cream may be used for 1 to 2 weeks if there is any itching or burning. Topical retinoids may also be beneficial.
- Impetigo: Although most common in children, impetigo does occur in adolescents. Impetigo consists of discrete and coalescent vesicles that quickly become pustular, then rupture, leaving a thick yellowish crust. The lesions are usually related to group A β-hemolytic streptococci or S. aureus. Localized infection can be treated with topical mupirocin (Bactroban), but more extensive or recurrent disease requires treatment with systemic antibiotics. Resistance to erythromycin and penicillin is very common. Methicillin-resistantStaphylococcus aureus(MRSA) is increasing in frequency. Antibiotics should be prescribed on the basis of community resistance patterns.
- Pseudomonas folliculitis or hot tub dermatitis: Pruritic papulopustular eruptions appear typically 1 to 2 days after exposure to a whirlpool, hot tub, or swimming pool, with a predilection for areas covered by a swimsuit, the axillae, and the upper arms. Usually self-limited and resolves in 7 to 14 days, is rarely associated with constitutional symptoms or systemic infection.
- Furuncles: Staphylococcal abscesses develop around hair follicles, typically in areas of friction. Multiple lesions may coalesce and extend into the subcutaneous tissue, forming carbuncles. Treatment includes warm compresses, antistaphylococcal antibiotics, and incision and drainage of fluctuant lesions. Recurrent or chronic furunculosis requires eradication of the staphylococcal carrier state. MRSA should be considered if the patient fails standard antibiotic therapy. Recurrent furuncles in the groin may be secondary to anaerobic bacteria.
Eruptions consisting of scaly patches and plaques that occur with some frequency during adolescence include psoriasis, pityriasis rosea, seborrheic dermatitis, fungal infections, drug eruptions, and secondary syphilis (for a discussion of syphilis, see Chapter 64).
Psoriasis affects between 1% and 3% of the population, with the age at onset being between 10 and 20 years in approximately 25% of the cases. Psoriasis is a chronic, genetically influenced, and immunologically-based inflammatory disease of the skin and joints.
The cause of psoriasis is unknown; however, heredity seems to play an ever-increasing role. Several human leukocyte antigens (HLA) located on the short arm of chromosome 6 are associated with psoriasis: HLA-B13, HLA-Bw16, HLA-B17, and HLA-B37. White patients who are HLA-Bw16 positive are 13 times more likely to develop psoriasis. Japanese patients are 25 times more likely to develop psoriasis if they are HLA-Bw16 positive (Svejgaard et al., 1975). One study found HLA-Bw16 expressed in 90% of patients with early-onset disease and in 50% of patients with late-onset disease compared to 7.4% in a control group (Schmitt-Egenolf et al., 1996).
Precipitating factors of psoriasis include the following:
- Certain infections including streptococcal pharyngitis
- Cold weather and low humidity
- Administration of certain medications
Psoriasis leads to hyperkeratosis and thickening of the epidermis, as well as increased vascularity and infiltration of the dermis with inflammatory cells. The symptoms of psoriasis are highly variable.
- Appearance: Round, circumscribed erythematous plaques with a silvery “micaceous” scale. The plaques are usually well demarcated and pinpoint bleeding can occur when a scale is removed. Small teardrop-size or guttate lesions are often associated with streptococcal pharyngitis.
- Distribution: Scalp, trunk, elbows, and knees are common sites. Usually the condition is mild and affects <20% of the skin. In some individuals, local skin trauma (such as tattoo or burn) will precipitate psoriatic lesions in that area (Köbner phenomenon). Inverse psoriasis is limited to the umbilicus and intertriginous areas.
- Nails may show pitting, onycholysis, and oil spots in approximately 10% of individuals with psoriasis.
- Psoriatic arthritis: A seronegative oligoarthritis that may present as acute monoarticular disease in childhood, and is fortunately uncommon in adolescence.
- Depression may be present secondary to the significant skin lesions.
Diagnosis of psoriasis is based on typical appearance, location of lesions, or rarely skin biopsy results.
Psoriasis may remit spontaneously or as a result of therapy, but recurrences are almost certain. There is no cure for psoriasis and treatment is oriented to suppress or ameliorate the disease. Treatment depends on the severity, duration, and site of disease, as well as the emotional state and treatment preference of the adolescent. Many individuals will need some continuing maintenance therapy that includes the following:
- Evaluation and avoidance of precipitating factors.
- Topical therapyshould be tried first. Topical therapies are convenient and lack serious side effects of systemic therapy. Their efficacy is debatable.
- Topical corticosteroids: A first choice among most dermatologists. A higher strength preparation is usually used for acute flares and areas with thickened plaques, and medium-potency preparations are used for maintenance. Used alone, topical corticosteroids are most appropriate for lesions limited to isolated small areas of the body. Potent steroids should be avoided in thinner areas of the skin such as face, groin, and genital regions. Use of more potent topical steroids should be limited to approximately 2 weeks, at which time a lower potency topical agent should be used. In addition, once the plaques have flattened out, the application can be reduced in frequency (e.g., every 12 hours for three doses, once a week). The health care provider must remember that the topical corticosteroid preparation can vary widely in potency depending on the vehicle. For example, betamethasone dipropionate at a given concentration can vary from midpotent to superpotent depending on the vehicle (Table 20.1). Adverse effects include epidermal atrophy (reversible), dermal atrophy with development of striae especially in intertriginous areas, perioral dermatitis, and rosacea. Allergic contact dermatitis and pituitary-adrenal axis suppression may be seen with prolonged use of potent (class I) corticosteroids.
- Calcipotriene (Dovonex) ointment: A synthetic vitamin D3analog useful in treating mild to moderate plaque-type psoriasis. The medication can be an effective first- or second-line topical agent for chronic plaque psoriasis. Although not as effective as superpotent topical corticosteroids, it does not have their side effects. In clinical trials, calcipotriene 0.005% ointment was as effective as fluocinonide 0.05% ointment and
betamethasone valerate 0.1% ointment in decreasing plaque and disease severity (Linden and Weinstein, 1999). The most common adverse side effect was irritant dermatitis (in 10%–15% of individuals).
- Tazarotene (Tazorac) gel or cream: A synthetic retinoid effective for mild to moderate psoriasis. It may be used as a second-line agent either as monotherapy or in combination with other topical medications. Adverse effects may include local irritation such as pruritus, burning, and erythema in up to 30% of individuals and is increased with higher concentrations of medication. Efficacy may be increased and irritation reduced when used with a mid- to high-potency topical corticosteroid. Tazarotene is used as a once-daily topical gel or cream. It is contraindicated in unstable plaque psoriasis in progress, erythrodermic psoriasis, patients with a history of allergic contact dermatitis to tarazotene, and pregnant or lactating females.
- Tars: Extremely effective but unpopular agents due to messiness and staining. However, they are inexpensive and mostly free of side effects. Tars are particularly effective for pruritic psoriasis. Some preparations may be more cosmetically pleasing to the adolescent. The most widely used preparation is tar shampoo for scalp psoriasis.
- Anthralin: Anthralin inhibits enzymes involved in epidermal proliferation. It is useful as a second-line
agent as monotherapy or in combination with other agents for moderate to severe psoriasis. It should not be used in plaque, pustular, or erythrodermic psoriasis. Anthralin is often used for short periods such as 15 to 30 minutes/day. Anthralin also can stain skin and clothing. Healthy skin should be avoided.
- Keratolytics: Ointments with salicylic acid (2%–10%) can help soften plaques and can be used with topical corticosteroids or coal tar to improve penetration.
- Intralesional corticosteroids: Useful for localized psoriatic plaques; potential side effects include atrophy and hypopigmentation.
- Systemic therapyis rarely indicated in adolescents because of the potential long-term side effects. Cases with severe disease should be referred to a specialist and treatment may involve the following:
- Phototherapy: Two types of phototherapy are available: ultraviolet B (UVB) and psoralen plus ultraviolet A (UVA). UVA combined with oral or topical psoralens is reserved for severe, recalcitrant psoriasis, because of the increased risk of developing skin cancer.
- Systemic therapy can include methotrexate, acitretin (a systemic retinoid), cyclosporine A, and biological agents such as tumor necrosis factor α (TNF-α) inhibitors. All should be used under the care of a specialist.
Pityriasis rosea is a self-limited disorder of unknown cause frequently occurring during adolescence.
- Lesions: Oval, salmon-colored papular and macular, 1- to 2-cm scaly lesions, whose long axes follow the body's lines of cleavage in a “Christmas tree” distribution. The lesions typically have a fine cigarette paper–like scale peripherally.
- Herald or mother patch: A large, 2- to 6-cm single lesion that typically precedes the rash by 2 to 21 days.
- Distribution: Symmetrical, occurring mainly on the trunk, upper arms, and lower neck, with occasional involvement of face, scalp, hands, and feet.
- Pruritus: Ranges from very mild to severe.
- Other systemic symptoms: Constitutional symptoms are rare.
- Tinea corporis
- Secondary syphilis
- Seborrheic dermatitis
- Reassurance: Condition spontaneously resolves within 6 to 8 weeks.
- Antihistamines or topical corticosteroids: Use if pruritus is significant.
- Erythromycin for 14 days resulted in complete response in one study (Sharma et al., 2000).
Seborrheic dermatitis is a chronic inflammatory disease of the skin, limited to areas of excessive sebaceous gland activity.
- Distribution: Usually involves the scalp, eyebrows, forehead, lips, ears, nasolabial creases, axilla, chest, inframammary folds, umbilicus, and groin.
- Appearance: Dry, moist, or greasy scales often crusted with yellow patches of various sizes.
- Pruritus: May or may not be present.
- Course: Marked by many remissions and exacerbations.
- Tinea corporis
- Pityriasis rosea
- Atopic and contact dermatitis
- Scalp should be shampooed two to three times a week with products based on tar, selenium sulfide, sulfur, or zinc, ketoconazole 2% shampoo, or combination scalp treatments.
- Hydrocortisone 1% to 2.5% or, if necessary, low-potency nonfluorinated topical corticosteroids may be used sparingly for short periods on the face. However, it is best to avoid topical corticosteroids on the face and a trial of ketoconazole 2% cream may be worthwhile. Many topical corticosteroids are available in solutions, shampoos, or foams for the scalp. Topical corticosteroids such as fluocinolone acetonide 0.01%, clobetasol propionate, and betamethasone valerate are some examples.
The dermatophytoses are the most common fungal diseases of the skin. The three principal genera responsible are Trichophyton, Microsporum,and Epidermophyton. These are responsible for tinea capitis, tinea corporis, tinea pedis, tinea barbae, tinea cruris, and tinea unguium (onychomycosis). Other common superficial fungal infections in adolescents include tinea or pityriasis versicolor caused by Pityrosporum orbiculare and Candida albicans, which is the causative agent in many cases of intertrigo, paronychia, vaginitis, and pruritus ani.
Tinea capitis is a dermatophyte infection of the scalp and hair follicles, most commonly caused in the United States by Trichophyton tonsurans. It usually presents as an enlarging scaly patch of alopecia, often consisting of broken hairs (black dots). However, there may be a noninflammatory presentation consisting of dandruff-like scale, minimal pruritus and subtle hair loss which may be mistaken for seborrheic dermatitis. A granulomatous mass, or kerion, can develop in response to the infection. Some of these fungi are spread by contact with objects such as combs, brushes, and hats, and others from cats and dogs.
The diagnosis can be made by either fluorescence of the infected hairs with a Wood's lamp, examination of the hairs with potassium hydroxide, or culture of infected hairs. Some studies show that only one third of individuals will have positive results from examination of a potassium hydroxide specimen, so one cannot necessarily rely on the
potassium hydroxide examination alone. If the diagnosis is in question, a culture can be taken.
Treatment is with systemic griseofulvin, microsize 20 to 25 mg/kg/day or ultramicrosize 10 to 15 mg/kg/day for 6 to 8 weeks or until there is clinical and mycological cure (up to 12–16 weeks.) Terbinafine 250 mg/day for 2 to 4 weeks has been used as an alternative in resistant cases or in patients who cannot tolerate griseofulvin. Itraconazole capsules may be administered 5 mg/kg/day or oral solution 3 mg/kg/day for 4 weeks as continuous therapy or 5 mg/kg/day for 1 week per month for 2 to 4 months as pulse therapy. In addition, topical selenium sulfide 2.5% or ketoconazole 2% shampoo should be used twice weekly to reduce the shedding of spores. Table 20.2 summarizes antifungal agents used in the treatment of common superficial fungal infections.
This is a dermatophyte infection involving the bearded area. It is more common in adolescents living in rural areas who work with farm animals. There is usually unilateral involvement of the neck or face and results in either deep nodular suppurative lesions or superficial, crusted, partially bald patches. Treatment is with griseofulvin (500 mg daily for 4–6 weeks).
The skin examination is significant for pruritic, annular lesions that spread centrifugally with central clearing involving any area of the body except the hair, nails, palms, and soles. Scales and pruritic vesicles may be present. The condition is commonly seen in wrestlers.
The diagnosis is confirmed by potassium hydroxide examination of a skin scraping or fungal culture. The differential diagnosis includes other papulosquamous eruptions such as dermatoses (nummular eczema, atopic dermatitis, contact dermatitis), pityriasis versicolor, annular psoriasis, and pityriasis rosea.
If the lesions are localized, topical therapy can be chosen from various agents (Table 20.3). If the lesions are widespread or resist local therapy, griseofulvin microsize 500 mg daily for 4 weeks is effective. Systemic fluconazole, itraconazole, and terbinafine are alternative choices but are not approved for the treatment of dermatophytosis. Huang et al. (2004)reviewed oral therapy of common superficial fungal infections of the skin. Treat sources of infection such as pets, infected family members, or other close contacts (including those that occur during sports such as wrestling).
Commonly called jock itch or crotch rot, this is a common dermatophyte infection of the groin in male adolescents, particularly during summer months. Typical lesions are bilateral or unilateral, crescent shaped, reddish, and scaly, with sharply defined, raised borders on the upper and inner surfaces of the thighs. The scrotum is usually unaffected.
The diagnosis is generally made on the basis of clinical appearance, negative findings from Wood's lamp examination, and the presence of branching hyphae on potassium hydroxide wet mount. Cultures of the scales can be performed, if necessary, for diagnosis.
Differential diagnoses of common groin eruptions include the following:
- Candidiasis: Eruptions are more inflammatory with less discrete margins and individual satellite papules or pustules outside the confluent area. The scrotum is commonly affected. A potassium hydroxide preparation reveals budding yeast and pseudohyphae. Candidiasis can be treated with topical nystatin, ketoconazole, or miconazole cream two times a day.
- Erythrasma: A superficial bacterial skin infection of intertriginous sites caused by Corynebacterium minutissimum(short gram-positive diphtheroid). The rash appears as a well-defined pinkish or brownish patch that may be smooth or covered by a fine scale resembling a cutaneous dermatophytosis. The rash fluoresces a coral red color under a Wood's lamp, caused by porphyrin production. Potassium hydroxide preparation may show negative results, but Gram stain may show gram-positive filamentous rods ( minutissimum). Erythromycin is the treatment of choice and can be used either orally or topically. One gram in divided doses can be given orally for 5 to 7 days or topical erythromycin twice a day can be used. Alternative therapies have included topical 10% to 20% aluminum chloride, 2% clindamycin hydrochloride solution, and miconazole cream. In addition, a single 1-g dose of clarithromycin has been reported to be effective (Wharton et al., 1998).
- Psoriasis: Often accompanied by psoriatic lesions elsewhere. Potassium hydroxide preparation and Wood's lamp examination are usually negative. Biopsy may be helpful. Topical corticosteroids are the initial treatment of choice.
- Intertrigo: This skin condition is more common in obese patients, and consists of well-demarcated, red, macerated, foul-smelling skin with a nonraised border in inguinal creases. Findings are negative for potassium hydroxide wet mount and Wood's lamp examination. Patients are advised to keep the affected area dry.
- Seborrheic dermatitis: Treatment includes low potency (class VI–VII) topical corticosteroids, ketoconazole 2% cream.
- Neurodermatitis: Characterized by leathery, lichenified, mottled eruption with ill-defined borders. Potassium hydroxide preparation and Wood's lamp examination are negative. Low-potency topical corticosteroids may be used for treatment.
- Irritant dermatitis: There is usually a history of use of sprays, soaps, detergents, or medication.
- Other pruritic groin rashes include scabies, pediculosis pubis, and miliaria.
Treatment of tinea cruris includes loose clothing, drying skin thoroughly after bathing, weight reduction if obese, laundering contaminated clothing and linens, and topical powders. Elimination of coexisting tinea pedis is also important. Topical antifungal creams or oral griseofulvin microsize 500 mg daily for 4 weeks is an effective antifungal regimen.
A dermatophyte infection involving soles of the feet and toe webs. Early signs include scaling, maceration, and fissuring of the toe webs that can extend to scaling, redness, and vesicular eruptions on the soles. Tight-fitting occlusive footwear and warm humid weather are predisposing factors. The infection is often transmitted through shared bath and shower facilities.
Tinea pedis is typically diagnosed clinically. Potassium hydroxide examination will reveal branching hyphae.
Tinea pedis can be confused with pitted keratolysis, juvenile plantar dermatosis, dyshidrosis, psoriasis, and contact dermatitis.
Treatment for tinea pedis consists of the following:
- Employ a regimen of soaks or wet compresses with Burow or Domeboro solution for 15 to 30 minutes two to four times daily.
- Secondary bacterial infection should be treated with topical or oral antibiotics depending on severity.
- A topical antifungal agent can be helpful. If infection is severe or unresponsive, a course of griseofulvin microsize 500 mg/day or ultramicrosize 660 to 750 mg/day for 4 to 8 weeks may be helpful. Oral antifungals should be considered in patients with diabetes, immunocompromised state, or moccasin tinea pedis.
- If there is a severe inflammatory response or an “id” reaction (see “Dermatophytid” section), a short 1-week course of topical or systemic steroids is helpful.
- Keep feet dry and well aerated; sandals should be worn if possible or white cotton socks with shoes.
- Follow a prophylactic program of drying the feet thoroughly after baths, and then use a medicated powder such as Tinactin or Zeasorb-AF, or Lotrimin AF spray once the infection has resolved.
Tinea unguium is a dermatophyte infection of the nail plate. Onychomycosis includes all infections of the nail caused by any fungus, including dermatophytes and yeast. The infection begins with a white or yellow discoloration of the distal part of the nail. The nail subsequently becomes thickened, brittle, elevated, and deformed. Identification of the causative organism is essential for therapy. It is important to sample the subungual debris near the nail bed for culture as various nail dystrophies, including psoriasis, may be confused with onychomycosis.
The following drugs essentially replaced the use of griseofulvin for this condition. Terbinafine (250 mg/day for 3 months) has been approved to treat toenail infections, but only 6 weeks of treatment is necessary for the fingernails. Itraconazole (100 mg twice daily for 3 months) has been approved or it can be given in a pulsed regimen of 200 mg twice daily for 1 week per month repeated for 3 months to treat toenail involvement. The pulsed regimen may be preferable due to shorter treatment duration and rare association of adverse reactions. Treatment for fingernails is shorter, with only 6 weeks of daily therapy or 2 months of the pulsed regimen recommended. When prescribing these newer medications, one must consider potential drug interactions, side effects, and appropriate monitoring. Alternatives to systemic therapy include topical ciclopirox 8% topical solution (Penlac nail lacquer) or avulsion of the nail plate followed by topical therapy.
An “id” reaction is a cutaneous or systemic reaction to the fungal antigen borne through the bloodstream from the primary fungal focus to sensitized areas of the skin. The condition is often associated with dermatophytoses of the scalp and feet and rarely causes systemic problems including fever, anorexia, adenopathy, and leukocytosis. The reaction may consist of a widespread follicular scaly eruption or may be limited to a vesiculobullous or scaly eruption of the hands. The former is more commonly associated with tinea capitis and the latter with tinea pedis.
Tinea (Pityriasis) Versicolor
- Clinical manifestations: Scaly tan, brown, or hypopigmented macules or patches typically located over the
upper trunk and arms, and occasionally on the face and neck, caused by P. orbiculare. The lesions are usually asymptomatic.
- Predisposing factors: Humidity, hyperhidrosis, heredity, diabetes, and systemic corticosteroids.
- Diagnosis: Made by observation of hyphae and spores (spaghetti and meatballs) on potassium hydroxide wet mount. Wood's lamp examination is helpful in showing yellowish or brownish fluorescence.
- Differential diagnosis: Pityriasis alba, vitiligo, pityriasis rosea, seborrheic dermatitis, and syphilis.
- Topicals: A study by Lange et al. (1998) found that ketoconazole shampoo used as a single application or applied daily for 3 days was effective in eliminating tinea versicolor. Other agents include selenium sulfide 2.5% shampoo, ketoconazole 2% shampoo, zinc pyrithione shampoo or soap, sulfosalicylic acid, Tinver lotion (25% sodium thiosulfate, 1% salicylic acid, and 10% alcohol), or terbinafine 1% (Lamisil) spray. Usually these agents are used in the shower or overnight as tolerated daily for 2 weeks, then several times a month for maintenance. Topical antifungals of the imidazole class are effective but expensive for large areas of involvement.
- Systemic fluconazole and itraconazole: Fluconazole (400 mg as a single dose) and itraconazole (200 mg/day for 5–7 days) have been shown to be effective in the treatment of tinea versicolor. These medications are not U.S. Food and Drug Administration approved for use in the treatment of tinea versicolor.
Drug-associated skin eruptions are very common and mediated by a variety of immunological mechanisms. Hypersensitivity reactions are classified by the Gell and Coombs classification: types I to IV.
- Type I reactions are due to antigen-induced cell activation of mast cells and basophils leading to urticaria or angioedema. A common example is urticaria or anaphylaxis due to penicillin. Anaphylactoid or pseudoallergic reactions mimic type I reactions but are caused by pharmacologic release of histamine from mast cells. Antigen sensitization is not required for these reactions and may therefore occur with first exposure.
- Type II reactions result from interaction of antigen-specific IgG or IgM antibodies with drug antigens on cell membranes. Examples include antibiotic-induced hemolytic anemia or thrombocytopenia.
- Type III reactions occur secondary to circulating soluble drug–antigen–antibody complexes that deposit into tissues. The most common example is serum sickness.
- Type IV delayed-type hypersensitivity reactions are mediated by activated T cells that recognize specific antigens. Reactions include allergic contact dermatitis and fixed drug reactions.
Most drug reactions occur within 1 to 3 weeks of exposure to a new medication and resolve when the offending agent is fully excreted or metabolized.
The following are various common drug eruptions and implicated agents, organized by morphology.
Maculopapular or Morbilliform Rash
These rashes are usually bilateral and symmetrical, starting on the trunk then spreading to the extremities. Exanthematous drug eruptions can mimic viral exanthems with flat and raised “blotchy” areas with maculopapular rashes and “measles-like” pattern for morbilliform eruptions. Common drugs include:
Pruritic, erythematous edematous papules and plaques, also called wheals, can occur anywhere on the body. Lesions usually blanch with pressure, although a dusky appearance or areas of central pallor may be seen. Individual lesions typically resolve in <24 hours, although a course of urticaria can last weeks to months.
Examples of drugs associated with non-IgE–mediated urticaria include:
Examples of drugs associated with IgE-mediated urticaria include:
Generalized erythematous macules, plaques or bullae, often with targetoid lesions. Mucosae may be involved and fever may accompany more severe reactions. Drugs implicated include the following:
Deep pink to purple, painful nodules; classically on the anterior tibial surfaces.
Drugs implicated include the following:
Generalized erythematous eruption with diffuse scaling.
Drugs implicated include the following:
Comedones and inflammatory papules or pustules.
Drugs implicated include the following:
Rashes of many types with accentuation in photoexposed areas, predominantly on the face and upper extremities.
Drugs implicated include the following:
Fixed Drug Eruptions
One or a few erythematous, hyperpigmented, or gray-blue ovoid lesions with occasional bullae on the hands, face, lips, feet, and genitalia. They occur in the same location with repeated exposure to the inciting drug.
Drugs implicated include the following:
For a discussion, see Chapter 64.
- Etiology: Caused by human papillomavirus (HPV), a DNA virus of Papovaviridae family. Numerous HPV types have been identified (>70). Although there is some association between HPV type and the clinical type of wart, this is not a 100% correlation. HPV types 1, 2, and 4 are associated with common warts and plantar warts. Flat warts appear more related to HPV types 3 and 10.
- Age: Ten percent of 2- to 12-year-old children are affected. Peak prevalence is between the ages of 10 and 19; thereafter, the prevalence decreases.
- Prevalence: Seven percent to 10% of the general population.
- Transmission: Inoculation occurs by direct or indirect contact from one person to another; autoinoculation is common. Local trauma promotes inoculation.
- Incubation: 1 to 6 months.
- Clinical manifestations: The clinical classification and appearance of a wart is dependent on the wart's location on the skin.
- Verruca vulgaris
- Single or multiple in occurrence
- Most frequently occurs on hands, fingers, and periungually but can occur anywhere
- Usually sharply circumscribed, firm hyperkeratotic papules 1 to 5 mm or larger in diameter
- Filiform warts with projecting thread-like structures often appear on the neck and face
- Verruca plana (flat warts)
- Flat skin-colored or pink lesions, 1 to 3 mm, smooth and slightly raised with a tendency to coalesce
- Commonly occur on the face, dorsa of hands, wrists, and knees
- Often numerous and may occur in a linear pattern as a result of trauma (e.g., scratching or shaving) causing viral spread
- Verruca plantaris (plantar warts)
- Occur on the plantar surface of the feet, usually at pressure points
- Typically, do not extend above the skin surface; covered by hyperkeratotic material
- May occur as an isolated lesion or in groups (mosaic warts)
- May appear as multiple small black points representing thrombosed blood vessels
- Condylomata acuminata (venereal warts):Moist, polypoid warts located in the genital area and may be transmitted venereally. These are discussed in Chapter 66.
- Treatment: Warts vary in natural history. Most regress spontaneously within 1 to 2 years. Some warts remain unchanged or spread. The recurrence rate is high regardless of the choice of therapy. There are no specific antiviral therapies for curing HPV infection, although vaccines for genital herpes viruses are available. Existing treatments for warts aim to destroy visible lesions or induce an immune response to verrucae without causing scarring. Flat warts tend to be resistant to therapy and should be treated minimally to avoid scarring. Light freezing with liquid nitrogen is of value. Topical tretinoin can also be used to treat flat warts.
- Home therapywith 17% salicylic acid with or without occlusion for up to 12 weeks is effective in treating one half to two thirds of patients. One method of use is as follows:
- Soak the affected area in hot water for 10 to 20 minutes
- File away as much skin as possible using a pumice stone or nail file without causing skin irritation
- Apply salicylic acid to warts, avoiding healthy skin
- Cover warts with occlusive dressing such as duct tape
- Remove tape in the morning
- Repeat nightly
- Cryotherapy: Application of liquid nitrogen is an effective method of treating most warts and usually causes less skin scarring than electrodesiccation.
Commercial over-the-counter cryotherapy products are not as strong as liquid nitrogen. Liquid nitrogen may be administered with spray units (cryostats) or with cotton-tipped applicators. Multiple treatments may be necessary.
- Liquid nitrogen should be applied to the wart tissue long enough to create a white rim of 1 to 2 mm, usually approximately 10 to 15 seconds.
- Avoid freezing surrounding tissue, especially near digital vessels and nerves at the sides of fingers.
- Over days to weeks, a blister forms and may be hemorrhagic, and peels off with part or all of the wart.
- Electrodesiccation and curettage: This treatment requires expert skill due to increased destruction and scarring.
- Podophyllin: Condylomata acuminatum can effectively be treated with 20% to 25% podophyllin in benzoin, podophyllotoxin (0.5% solution), or trichloroacetic acid solution (various concentrations).
- Imiquimod 5% (Aldara) isa cell-mediated immunological response modifier and has been approved to treat genital warts.
- Carbon dioxide laser surgery, flash-lamp pulsed dye laser therapy, bleomycin, tretinoin, 5-fluorouracil, and immunotherapy have been used to treat recalcitrant warts.
Molluscum contagiosum is a common condition caused by a poxvirus infection. (For more information, see Chapter 67.)
Parasitic Skin Infections
- Pediculosis: See Chapter 67 for more information.
- Scabies: See Chapter 67 for more information.
Miscellaneous Skin Conditions
Vitiligo is an acquired, disfiguring disease characterized by well-circumscribed, depigmented plaques. Depigmentation is caused by destruction of melanocytes by an unknown mechanism. It may be associated with autoantibodies, thyroid disease, and leukotrichia (depigmentation of the hair).
- Age at onset: Fifty percent of cases experience some pigment loss before age 20.
- Prevalence: Vitiligo occurs in approximately 1% to 2% of the population.
The cause is unknown, but autoimmune mechanisms are speculated.
- Depigmented, well-circumscribed macules, several millimeters to several centimeters, appear on the skin. In lighter-skinned individuals, this may be first noticed during the summer as involved skin contrasts with tanned skin.
- Any area can be affected, but the face and extremities are most common. Areas subjected to repeated trauma, pressure, or friction are often affected.
- Usually the distribution is bilateral and symmetrical but may be segmental. Segmental vitiligo is usually not associated with other autoimmune diseases.
- Wood's lamp examination is helpful in identifying early lesions.
Morphea (localized scleroderma), postinflammatory hypopigmentation, pityriasis alba, and tinea versicolor may be confused with vitiligo.
Treatment is only partially satisfactory. Spontaneous repigmentation rarely occurs. Treatment includes the following:
- Use of sunscreens for photoprotection and avoidance of sun
- Use of a cover-up cosmetic such as Dermablend or Covermark
- Mid to high-potency topical corticosteroid or topical calcineurin inhibitor (tacrolimus, pimecrolimus)
- Ultraviolet B radiation of narrow-band UVB
- Topical or oral psoralens followed by long wavelength ultraviolet radiation (UVA): Must be used with great caution and administered by a health care provider experienced in their use
- Autologous skin grafts
Teenagers often spend long days at the beach or are involved in outdoor athletic activities without protecting their skin from the sun. Sunburn can be a frequent summer problem. Recommendations to adolescents include the following:
- Midday exposure: Avoid unprotected exposure from 10 a.m. to 3 p.m., when the sun's short ultraviolet rays are at their peak. Seek shade when appropriate.
- Clothing: Wear protective clothing and a hat when possible. Hatch and Osterwalder (2006) reviewed the use of protective clothing as sunscreen material.
- Sunscreens: Sunscreens may not prevent a tan, but they do lessen burning. Generous application of a sunscreen with a sun protection factor (SPF) of 15 or greater with a broad spectrum of coverage (UVA and UVB) should be used regularly (Table 20.4).
- Temperature: The cooling effect of water and wind at the beach decreases the ability to detect sunburn; therefore, the adolescent must be educated about the sun's strong effects.
- Medications: Certain medications can increase photosensitivity. These include tetracycline, NSAIDs, oral contraceptives, sulfonamide, diphenhydramine, phenothiazines, thiazides, griseofulvin, psoralen, and tranquilizers. Photoallergic reactions are uncommon immunologically mediated responses to small amounts of the offending agent. Phototoxic reactions appear as exaggerated sunburns and occur in nearly all individuals with sufficient exposure to the offending drug.
- Both tanning and sunburn cause DNA damage and may increase one's risk of developing nonmelanoma and melanoma skin cancer, as well as photoaging. Tanning beds and sunlamps should be avoided. Most tanning beds and sunlamps emit mainly UVA radiation, which may increase one's risk of skin cancer and cause premature skin aging.
Prevention of sunburn is more effective than treatment. Treatment of sunburn includes soothing moisturizers and an oral NSAID as indicated.
Urticaria, or hives, is an extremely common problem, occurring in 15% of all individuals.
Characterized by extremely pruritic, transient, discrete, erythematous, edematous wheals, which may coalesce and form large plaques with raised borders. Individual lesions generally last a few hours to <24 hours. Simple urticaria involves only the superficial layers of the skin, whereas angioedema involves edema in the deeper subcutaneous and submucosal tissues, particularly involving the palms of the hands, the soles of the feet, and the head and neck. Angioedema of the throat may cause respiratory obstruction in severe cases. Urticaria is defined as acute if it lasts <6 weeks and chronic if it lasts >6 weeks.
The triggers involved in urticaria involve many factors; however, in up to 50% of cases of both acute and chronic urticaria and angioedema, no cause is identified.
- Type I hypersensitivity
- Drug induced: Almost any medication can cause urticaria. Antibiotics, pain medications, sedatives, and tranquilizers are the most common drugs involved.
- Food: Urticaria after eating most commonly involves ingestion of nuts, fish, eggs, fresh berries, shellfish, or food additives. Some of these reactions are IgE-mediated, whereas others are caused by direct release of histamine.
- Insect and arthropod bites and stings
- Type III hypersensitivity
- Infections: Various bacterial, viral, and parasitic infections may cause urticaria.
- Autoimmune diseases: Systemic lupus, thyroid diseases, and certain malignancies
- Drugs: Penicillin and sulfonamides
- Direct mast cell degranulation
- Food chemicals such as benzoates and tartrazine
- Drugs such as aspirin, opiates, and NSAIDs
- Hyperosmolar radiocontrast media
- Physical urticarias
- Cholinergic urticaria: This reaction can be triggered by heat, exercise, or stress. Cholinergic urticaria is produced by the reaction of acetylcholine on the mast cell. It is characterized by highly pruritic, punctate wheals 1 to 3 mm in diameter. These wheals are surrounded by large areas of erythema. The palms and soles are spared. Aquagenic urticaria may be a form of cholinergic urticaria that produces a similar reaction on contact with water. The diagnosis can be confirmed by soaking a foot in hot water, exercising the adolescent, or using a methacholine (mecholyl) skin test. All these will reproduce the lesions.
- Heat urticaria
- Cold urticaria: Localized or generalized hives develop with exposure to cold air or water, rarely accompanied by syncope, hypotension, and drowning. Hereditary and acquired variants exist. The diagnosis may be confirmed in most cases with an ice cube test. Cyproheptadine (Periactin) is helpful, but desensitization may be necessary.
- Pressure urticaria: Urticaria in response to slight pressure, such as sitting or clapping
- Solar urticaria
- Vibratory urticaria
- Dermatographism: Characterized by the development of localized wheals and erythema, following stroking of the skin with a blunt instrument
- Chronic urticaria: Chronic urticaria can be a serious disabling condition sometimes associated with insomnia and fatigue. The cause of this type of urticaria is usually much more difficult to determine than acute urticaria. Autoimmune diseases such as systemic lupus erythematosus may present with urticaria and should be considered in the differential diagnosis of chronic urticaria.
Acute transient urticarias do not need a further evaluation. Chronic urticarias can be associated with a long list of conditions and further tests should be ordered only after thorough history and physical examination looking for underlying etiologies.
- The best treatment is removal and avoidance of the inciting factor.
- Antihistamines are effective for suppression of acute urticaria. Hydroxyzine (Atarax) (25 mg three times a day) is the drug of choice in cholinergic urticaria and dermatographism.
- Topical therapy: Cold baths or showers may be helpful in relieving some of the itching.
- Epinephrine is useful if the urticaria is associated with angioedema.
- Systemic steroids are beneficial in severe acute reactions, particularly with associated angioedema.
Hair loss can be extremely frightening to an adolescent. Evaluating an adolescent with a complaint of hair loss involves a thorough history and physical examination, as well as an understanding of hair physiology.
Scalp hair grows at the rate of 0.35 mm/day. The average daily loss is 25 to 100 hairs, from a total of approximately 100,000. Eighty percent to 90% of hair is in the growing, or anagen, phase. Anagen hairs have a heavy external root sheath that looks like a gelatinous capsule around the lower third of the hair. Ten percent to 15% of hair is in the resting, or telogen, phase. These hairs have a smooth shaft, ending in a short bulbous root. Approximately 5% or less of hair is in a transitional or catagen phase.
- Male pattern alopecia: This occurs in genetically susceptible individuals, resulting in a loss of hair secondary to the effects of androgenic hormones. Usually, only scalp hair is involved. Baldness usually does not occur until the late twenties or thirties, but premature alopecia can occur in the teens or early twenties.
- Telogen effluvium: Acute illness, surgery, or other severe stress can stop hair growth and cause hairs to go into the telogen phase. Several weeks (6–10) later, resting hair is shed. This condition presents as acute general hair loss 2 to 4 months after a stressful event. Illness, surgery, “crash dieting,” parturition, discontinuation of oral contraceptives, anticoagulants, and hypervitaminosis A have been known to trigger an episode of telogen effluvium. Thyroid disease may also be a cause.
- Anagen effluvium: Anagen effluvium is hair loss caused by disruption of hair during the growth phase. Causes include antimitotic drugs used for chemotherapy, immunosuppressive drugs, warfarin (Coumadin), heparin, arsenic, and gentamicin. In anagen effluvium, the hair develops a focal weakness above the bulb, so the anagen bulb is usually not shed with the hair.
- Alopecia areata: Alopecia areatais characterized by complete hair loss in small, round patches, usually involving the scalp, bearded area, eyebrows, or eyelashes. If the hair loss involves the entire scalp, the condition is referred to as alopecia totalis, and if the loss includes the whole body, alopecia universalis. Alopecia areata may be associated with pitting of the nails. The tendency is for spontaneous recovery, but the prognosis is worse with increasing involvement. In 25% of cases, the condition is permanent.
- Etiology: Autoimmunity is probably the cause in most individuals. Activated CD4 and CD8 lymphocytes have been found around the affected anagen hair bulbs. There also appears to be a strong association with certain HLA types including DQB103 and DRB11104. Two other types are associated with alopecia totalis and universalis.
- Diagnosis: Clinical presentation of sharply circumscribed patches of alopecia with exclamation point hairs at the periphery of the bald patch
- Differential diagnosis: Tinea capitis, early discoid or systemic lupus erythematosus, and trichotillomania
- Treatment: Focal alopecia areata often regrows, but the course of the disease is variable and unpredictable. Potent topical, intralesional, or oral corticosteroids have been used to promote hair regrowth, although they are not curative of the condition. Other treatments include anthralin; topical immunotherapy including dinitrochlorobenzene, squaric acid dibutyl ester, diphencyprone; or minoxidil solution. Price (1999) reviewed the therapy for hair loss and the use of these agents. Treatment may take months or years.
- Hair loss secondary to physical factors
- Traction alopecia: Hair loss at the margin of scalp, occurring primarily in African-American females and in women who wear hair tightly braided.
- Hot comb alopecia
- Trichotillomania: Irregular patches of hair loss secondary to breaking or removal of hairs on the scalp, eyebrows, or eyelashes by plucking, twirling, or rubbing. It is associated with emotional stress, or less commonly a psychiatric disorder.
- Secondary scalp disease: Hair loss can occur secondary to various scalp diseases, including psoriasis, fungal disease, seborrhea, or eczema.
- Metabolic disorders: Hair loss can be found with iron deficiency, hypothyroidism, hyperthyroidism, diabetes mellitus, or hypopituitarism.
- Systemic diseases: Hair loss can be seen with systemic lupus erythematosus.
- Scarring alopecia: This form of irreversible hair loss is the result of various inflammatory processes or trauma. Some dermatological conditions that may result in scarring include discoid lupus erythematosus, scleroderma, lichen planus, acne keloidalis, folliculitis decalvans, and dissecting cellulitis of the scalp.
- Hair-shaft structural defects: Various defects in hair structure can result in hair loss. These defects are often associated with abnormalities of the skin, teeth, breast, nails, and bones. Metabolic disorders and mental retardation can also occur. These conditions include pili torti, monilethrix, trichorrhexis, pili annulati, and Menkes kinky-hair syndrome.
- History: An extensive history is indicated, including the onset and duration of hair loss, drug use, skin or scalp disease, and recent stress, surgery, illness, or dietary changes.
- Physical examination: Check particularly for evidence of seborrhea, scalp disease, or an endocrine disorder.
- Pull test: Lightly grasp approximately 20 hairs and pull gently. Normally one or two telogen hairs will come out. In an adolescent with hair-shaft damage, telogen effluvium, alopecia areata, or anagen effluvium, hair pulls out in great quantities. If many hairs pull out,
microscopic examination of the hairs will determine whether anagen or telogen hair loss is present.
- Examine scalp closely and perform a potassium hydroxide test if indicated. A fungal culture of the hair and scalp may also be productive.
- A complete blood count, urinalysis, liver function tests, thyroid studies, serum ferritin, and a fasting blood glucose test may be ordered as indicated.
- Referral to a dermatologist may be necessary for further evaluation and scalp biopsy may be required if diagnosis is in question.
Therapy depends on the etiology.
- Male pattern alopecia: In men, androgenetic alopecia ranges from bitemporal recession of hair to thinning of the frontal area of scalp to complete baldness. Most adolescents have not begun significant hair thinning, but young adults may have significant concerns and early hair thinning. The goal of therapy for young adults with visible hair thinning or balding is to increase coverage of the scalp and retard further hair thinning. The only drugs approved for promoting hair growth in men in the United States are oral finasteride (1 mg/day) and topical solution of 5% and 2% minoxidil. Both can increase scalp coverage by enlarging existing hairs, and both retard further thinning in both the vertex and frontal regions. In general, treatment for 6 to 12 months is needed to improve scalp coverage, and continuous treatment is used to retain a clinical improvement.
- Telogen effluvium: Generally reassurance is all that is needed, because there is usually no significant hair loss. This condition will usually be self-limited.
- Alopecia areata: See previous discussion on treatment.
- Scalp disease: Treat underlying condition.
Tattoos and Body Piercing
Body piercing and tattooing have become more common among adolescents and young adults. Body piercing and tattooing have been practiced in many societies throughout history with influences impacting extent of use and style of “body art” used. Popular piercing sites in addition to ears are the nasal septum, eyebrow, tongue, cheek, nipple, navel, labia, penis, scrotum, and foreskin. Piercing and tattooing may occur in relation to gang activity or peer pressure. Body piercing and tattooing entails infectious risks including hepatitis, tetanus, bacterial infections, as well as rashes, allergies, and scars. In most states, minors cannot consent for body piercing and tattoos without parental consent, although this is not always followed.
Complications include the following:
- Hypersensitivity to the dye.
- Unsanitary methods have resulted in bacterial infections, hepatitis, tuberculosis, and syphilis. Concern about transmission of HIV infection exists.
- Scarring, including keloids can form.
- Milk ducts may be damaged when piercing a woman's nipple.
Larzo and Poe (2006) reviewed the adverse consequences of tattoos and body piercings in adolescents.
New laser systems can effectively remove many tattoos with minimal scarring or other adverse sequelae. However, not all tattoos can be completely eliminated. Limitations of treatment include the need for multiple treatment sessions, expense, incomplete response of some individuals, and the possibility of pigmentary changes.
It is important to discuss the possibility of HIV and hepatitis transmission. It is also important to promote regulatory control over tattooing and body-piercing establishments to ensure sanitary conditions.
Primary Syphilis and Herpes Simplex
For a discussion of primary syphilis and herpes simplex see Chapters 64 and 65, respectively.
Hyperhidrosis is excessive sweating in response to heat or emotional stimuli. Treatment with topical aluminum chloride preparations such as Certain Dri, Xerac AC, or Drysol is often beneficial. Systemic anticholinergic agents, glutaraldehyde, and iontophoresis have also been used with varying degrees of success. Referral for botulinum toxin type A (Botox) injection may be warranted in more severe cases. Rarely should surgical intervention be considered.
Bromhidrosis is malodorous sweating that may be apocrine or eccrine in origin and is caused by bacteria. Good hygiene includes the use of antibacterial soaps, topical antibiotics, antiperspirants, Burow solution, or potassium permanganate soaks, and absorbent powders.
Pink Pearly Penile Papules
Pink pearly penile papules are a normal occurrence in approximately 15% of postpubertal males. The lesions appear as elongated papillae, approximately 1 to 3 mm in diameter, located on the coronal margin of the penis, particularly the anterior border. They often appear in one to five rows and are usually of uniform size and shape. The color tends to be pearly white. Microscopically, they have a normal epidermal appearance except for absent pigment in the basal layer. In contrast, condylomata acuminata tend to be of less uniform size and shape, change over time, and are not neatly arranged around the corona of the penis. No treatment is necessary except reassurance.
Acanthosis nigricans appears as a gray-brown thickening of the skin. It is manifested as symmetrical, velvety, papillomatous plaques, with increased skin-fold markings. The lesions are commonly located on the base of the neck,
axilla, groin, and antecubital fossa. The lesions may also occur on the dorsum of the hand, elbow, periumbilical skin, and mucous membranes. It may be commonly found during a routine physical examination in an otherwise healthy obese adolescent. Occasionally, a parent is concerned about the “dirty” appearance.
Most acanthosis nigricans lesions in adolescents are associated with insulin resistance secondary to obesity. These individuals may have type 2 diabetes or are at increased risk for type 2 diabetes and hyperlipidemia. Acanthosis nigricans can also be associated with hyperandrogenism, and rarely with malignant conditions.
Weight loss effectively treats obesity-related acanthosis nigricans. Lactic acid or α-hydroxyacid containing emollients, and tretinoin (Retin-A) have been tried but without any controlled studies demonstrating efficacy.
For Teenagers and Parents
http://www.mckinley.uiuc.edu/health-info/discond/commdis/contderm.html. Contact dermatitis handout from the University of Illinois student health center.
http://my.webmd.com/content/asset/adam_disease_poison_ivy. WebMD on contact dermatitis.
http://www.psoriasis.org/. National Psoriasis Association.
http://www.niams.nih.gov/hi/topics/psoriasis/psoriafs.htm. Questions and answers about psoriasis from the National Institutes of Health (NIH).
http://www.aad.org/pamphlets/Urticaria.html. Handouts on, tinea versicolor, eczema, seborrheic dermatitis, vitiligo, warts, and urticaria from the American Academy of Dermatology.
http://familydoctor.org/handouts/209.html. American Academy of Family Physician handout on warts.
http://www.nlm.nih.gov/medlineplus/warts.html. Information from the NIH on warts.
http://www.alopeciaareata.com. National Alopecia Areata Foundation.
http://www.nvfi.org. National Vitiligo Foundation.
http://www.eczema.org. National Eczema Society.
http://www.dermnet.org.nz/index.html. Information from New Zealand Dermatologic Society on various conditions including atopic dermatitis.
For Health Professionals
http://tray.dermatology.uiowa.edu/DPT/PathBase.html. Dermatology slides from the University of Iowa.
http://www.emedicine.com/EMERG/topic131.htm. E-medicine section on contact dermatitis.
http://www.aafp.org/afp/980700ap/noble.html. American Academy of Family Physicians article on tinea infections.
http://www.emedicine.com/emerg/topic628.htm. E-medicine section on urticaria.
http://www.emedicine.com/derm/topic396.htm. E-medicine section on seborrheic dermatitis.
http://www.emedicine.com/derm/topic300.htm. E-medicine section on onychomycosis.
References and Additional Readings
Adams BB. Tinea corporis gladiatorum: a cross-sectional study. J Am Acad Dermatol 2000;43:1039.
Alper BS. SOAP: solutions to often asked problems–choice of antihistamines for urticaria. Arch Fam Med 2000;9:748.
Bacelieri R, Johnson SM. Cutaneous warts: an evidence-based approach to therapy. Am Fam Physician 2005;72(4):647.
Baxi S, Dinakar C. Urticaria and angioedema. Immunol Allergy Clin North Am 2005;25(2):353.
Bertolino AP. Alopecia areata: a clinical overview. Postgrad Med 2000;107:81.
Boguniewicz M, Leung DY. Atopic dermatitis. J Allergy Clin Immunol 2006;117(2 Suppl Mini-Primer):S475.
Braithwaite RL, Stephens T, Sterk C, et al. Risks associated with tattooing and body piercing. J Public Health Policy 1999;20:459.
Bravender T. Index of suspicion. Case: 3. Diagnosis: telogen effluvium. Pediatr Rev 2000;21:354.
Brown S, Reynolds NJ. Atopic and non-atopic eczema. BMJ 2006;332(7541):584.
Cobb MW. Human papillomavirus infection. J Am Acad Dermatol 1990;22:547.
Cohn MS. Superficial fungal infections: topical and oral treatment of common types. Postgrad Med 1992;91:239.
Dibbern DA Jr. Urticaria: selected highlights and recent advances. Med Clin North Am 2006;90(1):187.
Dunagin WG, Millikan LE. Drug eruptions. Med Clin North Am 1980;64:983.
Dunn JF Jr. Vitiligo. Am Fam Physician 1986;33:137.
Dunn JF Jr. Pseudofolliculitis. Am Fam Physician 1988;38:169.
Eichenfield LF, Leung DYM. The eczemas. New York: Summit Communications, 2004:9.
Elder JT, Nair RP, Sun-Wei G, et al. The genetics of psoriasis. Arch Dermatol 1994;130:216.
Farber EM, Nall L. Guttate psoriasis. Cutis 1993;51:157.
Federman DG, Froelich CW. Topical psoriasis therapy. Am Fam Physician 1999;59:957.
Feldman SR, Clark AR. Psoriasis. Med Clin North Am 1998;82:1135.
Feldman SR, Fleischer AB, McConnell C. Most common dermatologic problems identified by internists, 1990–1994. Arch Intern Med 1998;158:726.
Fenske NA, Johnson SA. Major causes of alopecia, with suggestions for history taking, work up, and therapy. Postgrad Med 1976;60:79.
Ferguson H. Body piercing. BMJ 1999;319:1627.
Fragola LA Jr, Watson PE. Common groin eruptions: diagnosis and treatment. Postgrad Med 1981;69:159.
Friedmann PS. Allergy and the skin. II—contact and atopic eczema. BMJ 1998;316:1226.
Friedmann PS. Assessment of urticaria and angio-edema. Clin Exp Allergy 1999;29:109.
Galan EB, Janniger CK. Pityriasis alba. Cutis 1998;61:11.
Gambichler T, Laperre J, Hoffmann K. The European standard for sun-protective clothing. J Eur Acad Dermatol Venereol 2006;20(2):125.
Gonzalez LM, Allen R, Janniger CK, et al. Pityriasis rosea: an important papulosquamous disorder. Int J Dermatol 2005;44(9):757.
Greaves MW. Chronic urticaria. N Engl J Med 1995;332:1767.
Greaves MW, Weinstein GD. Treatment of psoriasis. N Engl J Med 1994;332:581.
Greenberger PA. 8. Drug allergy. J Allergy Clin Immunol 2006;117(2 Suppl Mini-Primer):S464.
Grimes PE. Vitiligo: an overview of therapeutic approaches. Dermatol Clin 1993;11(20):325.
Guercio-Hauer C, Macfarlane DF, Deleo VA. Photodamage, photoaging and photoprotection of the skin. Am Fam Physician 1994;50:327.
Halder RM, Young CM. New and emerging therapies for vitiligo. Dermatol Clin 2000;18:79.
Hatch KL, Osterwalder U. Garments as solar ultraviolet radiation screening materials. Dermatol Clin 2006;24(1):85.
Headington JT. Telogen effluvium: new concepts and review. Arch Dermatol 1993;129:356.
Helm TN. Evaluation of alopecia. JAMA 1995;273:897.
Hennino A, Berard F, Guillot I, et al. Pathophysiology of urticaria. Clin Rev Allergy Immunol 2006;30(1):3.
Howard R, Frieden IJ. Tinea capitis—new perspectives on an old disease. Semin Dermatol 1995;14:2.
Huang DB, Ostrosky-Zeichner L, Wu JJ, et al. Therapy of common superficial fungal infections. Dermatol Ther 2004;17:517.
Hurwitz S. Clinical pediatric dermatology. Philadelphia: WB Saunders, 1993.
Jackson EA. Hair disorders. Prim Care (Clin Office Pract) 2000;27:319.
Jacobs PH. Ketoconazole use in tinea versicolor. West J Med 1987;147:547.
Jimbow K. Vitiligo: therapeutic advances. Dermatol Clin 1998;16:399.
Kilmer SL. Laser treatment of tattoos. Dermatol Clin 1997;15:409.
Kovacs SO. Vitiligo. J Am Acad Dermatol 1998;38:647.
Kwong KY, Maalouf N, Jones CA. Urticaria and angioedema: pathophysiology, diagnosis, and treatment. Pediatr Ann 1998;27:719.
Lange DS, Richards HM, Guarnieri J, et al. Ketoconazole 2% shampoo in the treatment of tinea verisolor: a multicenter, randomized, double-blind, placebo-controlled trial. J Am Acad Dermatol 1998;39:944.
Larzo MR, Poe SG. Adverse consequences of tattoos and body piercings. Pediatr Ann 2006;35(3):187.
Laude TA. Approach to dermatologic disorders in black children. Semin Dermatol 1995;14:15.
Lebwohl MG. Advances in psoriasis. Arch Dermatol 2005;141(12):1589.
Levy ML. Disorders of the hair and scalp in children. Pediatr Clin North Am 1991;38(4):905.
Linden KG, Weinstein GD. Psoriasis: current perspectives with an emphasis on treatment. Am J Med 1999;107:595.
Madani S, Shapiro J. Alopecia areata update. J Am Acad Dermatol 2000;42:549.
Mahmood T. Urticaria. Am Fam Physician 1995;51:811.
Malcolm B. Tinea pedis. Practitioner 1998;242:225.
Mallory SB, Watts JC. Sunburn, sun reactions, and sun protection. Pediatr Ann 1987;16:77.
Mark BJ, Slavin RG. Allergic contact dermatitis. Med Clin North Am 2006;90(1):169.
Mathelier-Fusade P. Drug-induced urticarias. Clin Rev Allergy Immunol 2006;30(1):19.
McBurnery EL. Vitiligo: clinical picture and pathogenesis. Arch Intern Med 1979;139:1295.
Mortz CG, Andersen KE. Allergic contact dermatitis in children and adolescents. Contact Dermatitis 1999;41:121.
Muldoon KA. Body piercing in adolescents. J Pediatr Health Care 1997;11:298.
Nadalo D, Montoya C, Hunter-Smith D. What is the best way to treat tinea cruris? J Fam Pract 2006;55(3):256.
Nielson TA, Reichel M. Alopecia: diagnosis and management. Am Fam Physician 1995;51:1513.
Noble SL, Forbes RC, Stamm PL. Diagnosis and management of common tinea infections. Am Fam Physician 1998;58:163.
Obrien JM. Common skin problems of infancy, childhood, and adolescence. Prim Care 1995;22:99.
Odom R. Diagnosis and treatment of common fungal infections. Mod Med 1987;55:34.
Odom R. A practical review of antifungals. Mod Med 1987;55:59.
Pardasani AG, Feldman SR, Clark AR. Treatment of psoriasis: an algorithm-based approach for primary care physicians. Am Fam Physician 2000;61:725.
Parish LC, Witkowski JA. Cutaneous bacterial infections: how to manage primary, secondary, and tertiary lesions. Postgrad Med 1992;91:119.
Plasencia JM. Cutaneous warts: diagnosis and treatment. Prim Care (Clin Office Pract) 2000;27:423.
Price VH. Treatment of hair loss. N Engl J Med 1999;341:964.
Przybilla B, Eberlein-Konig B, Rueff E. Practical management of atopic eczema. Lancet 1994;343:1342.
Rietschel RL, Fowler JF Jr. Fisher's contact dermatitis, 4th ed. Baltimore: Williams & Wilkins, 1995.
Roberts BJ, Friedlander SF. Tinea capitis: a treatment update. Pediatr Ann 2005;34:201.
Rosen CF. Photoprotection. Semin Cutan Med Surg 1999;18:307.
Ross EK, Shapiro J. Management of hair loss. Dermatol Clin 2005;23(2):227.
Rupke SJ. Fungal skin disorders. Prim Care (Clin Office Pract) 2000;27:407.
Saary J, Qureshi R, Palda V, et al. A systematic review of contact dermatitis treatment and prevention. J Am Acad Dermatol 2005;53(5):845.
Satin EE. Alopecia areata in childhood. Semin Dermatol 1995;14:9.
Schon MP, Boehncke WH. Psoriasis. N Engl J Med 2005;352(18):1899.
Schmitt-Egenolf M, Eierman TH, Boehnke WH. Familial juvenile onset psoriasis is associated with the human leukocyte antigen (HLA) class I side of the extended haplotype Cw6-B57-DRB*0701-DQA1*0201-DQB1*0303: a population and family based study. J Invest Dermatol 1996;106:711.
Seville RH. Stress and psoriasis: the importance of insight and empathy in prognosis. J Am Acad Dermatol 1989;20:97.
Sex Transm Infect. National guideline for the management of molluscum contagiosum. Clinical effectiveness group (Association of Genitourinary Medicine and the Medical Society for the Study of Venereal Diseases). 1999;75(Suppl 1):S80.
Sharma PK, Yadav TP, Gautam RK, et al. Erythromycin in pityriasis rosea: a double-blind, placebo-controlled clinical trial. J Am Acad Dermatol 2000;42:241.
Shapiro J, Madani S. Alopecia areata: diagnosis and management. Int J Dermatol 1999;38(Suppl 1):19.
Shenenberger DW. Curbing the psoriasis cascade. Therapies to minimize flares and frustration. Postgrad Med 2005;117(5):9.
Simpson EL, Hanifin JM. Atopic dermatitis. Med Clin North Am 2006;90(1):149.
Sperling LC, Mezebish DS. Hair diseases. Med Clin North Am 1998;82:1155.
Starr NB. Sun smarts: the essentials of sun protection. J Pediatr Health Care 1999;13:136.
Sterling GB. Sunscreens: a review. Cutis 1992;50:221.
Stuart CA, Driscoll MS, Lundquist KF, et al. Acanthosis nigricans. J Basic Clin Physiol Pharmacol 1998;9:407.
Sunenshine PJ, Schwartz RA, Janniger CK. Tinea versicolor. Int J Dermatol 1998;37:648.
Svejgaard A, Platz P, Ryder L, et al. HLA and disease association- a survey. Transplant Rev 1975;22:1.
Tariq A, Ross JD. Viral sexually transmitted infections: current management strategies. J Clin Pharmacol Ther 1999;24:409.
Thiers BH. Dermatology therapy update. Med Clin North Am 1998;82:1405.
Uter W, Johansen JD, Orton DI, et al. Clinical update on contact allergy. Curr Opin Allergy Clinl Immunol 2005;5(5):429.
Verbov J. How to manage warts. Arch Dis Child 1999;80:97.
Westerhof W. Vitiligo management update. Skin Ther 2000;5:1.
Weston WL, Badgett JT. Urticaria. Pediatr Rev 1998;19:240.
Wharton JR, Wilson PL, Kincannon JM. Erythrasma treated with single-dose clarithromycin. Arch Dermatol 1998;134:671.