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Eczema, Psoriasis, Cutaneous Infections, Acne, and Other Common Skin Disorders

Eczema, Psoriasis, Cutaneous Infections, Acne, and Other Common Skin Disorders

Calvin O. McCall

Thomas J. Lawley

ECZEMA AND DERMATITIS

Eczema, or dermatitis, is a reaction pattern that presents with variable clinical and histologic findings and is the final common expression for a number of disorders, including atopic dermatitis, allergic contact and irritant contact dermatitis, dyshidrotic eczema, nummular eczema, lichen simplex chronicus, asteatotic eczema, and seborrheic dermatitis. Primary lesions may include papules, erythematous macules, and vesicles, which can coalesce to form patches and plaques. In severe eczema, secondary lesions from infection or excoriation, marked by weeping and crusting, may predominate. Long-standing dermatitis is often dry and is characterized by thickened, scaling skin (lichenification).

ATOPIC DERMATITIS

Atopic dermatitis (AD) is the cutaneous expression of the atopic state, characterized by a family history of asthma, hay fever, or dermatitis in up to 70% of patients. Some of the features of atopic eczema are shown in Table -1. The prevalence of atopic dermatitis is increasing worldwide, with a point prevalence in Norwegian school children as high as 23%.

The etiology of AD is only partially defined, but there is a clear genetic predisposition. When both parents are affected by AD, over 80% of their children manifest the disease. When only one parent is affected, the prevalence drops to slightly over 50%. Patients with AD may display a variety of immunoregulatory abnormalities including increased IgE synthesis; increased serum IgE; increased specific IgE to foods, aeroallergens, bacteria, and bacterial products; increased expression of CD23 (low-affinity IgE receptor) on monocytes and B cells; and impaired delayed type hypersensitivity reactions.

The clinical presentation often varies with age. Half of patients with AD present within the first year of life, and 80% present by 5 years of age. About 80% ultimately coexpress allergic rhinitis or asthma. The infantile pattern is characterized by weeping inflammatory patches and crusted plaques that occur on the face, neck, and extensor surfaces. The childhood and adolescent pattern is marked by dermatitis of flexural skin, particularly in the antecubital and popliteal fossae. AD may resolve spontaneously, but over half of all individuals affected as children will have dermatitis in adult life. The distribution of lesions may be similar to those seen in childhood. However, adults frequently have localized disease, manifesting as hand eczema or lichen simplex chronicus (see below). In patients with localized disease, AD may be suspected because of a typical personal history, family history, or the presence of cutaneous stigmata of AD such as perioral pallor, an extra fold of skin beneath the lower eyelid (Dennie's line), increased palmar skin markings, and an increased incidence of cutaneous infections, particularly with Staphylococcus aureus. Regardless of other manifestations, pruritus is a prominent characteristic of AD and is exacerbated by dry skin. Many of the cutaneous findings in affected patients, such as lichenification, are secondary to rubbing and scratching.

Histologic examination of the skin affected by AD may demonstrate features of acute or chronic dermatitis. Immunopathology shows activated, memory T helper cells. AD skin lesions may also demonstrate IgE-bearing CD1a+ Langerhans cells, and these cells have been implicated in AD disease pathophysiology through mediation of hypersensitivity responses to environmental antigens.

TREATMENT

Therapy of AD should include avoidance of cutaneous irritants, adequate moisturizing, judicious use of topical anti-inflammatory agents, and prompt treatment of secondary infection. Patients should be instructed to bathe using warm, but not hot, water and to limit their use of soap. Immediately after bathing while the skin is still moist, a topical anti-inflammatory agent in a cream or ointment base should be applied to areas of dermatitis, and all other skin areas should be lubricated with a moisturizer. Approximately 30 g of a topical agent is required to cover the entire body surface of an average adult.

Until recently, low- to midpotency topical glucocorticoids were employed in most treatment regimens for AD. Skin atrophy and the potential for systemic absorption, especially with more potent agents, were constant concerns. Two non-glucocorticoid anti-inflammatory agents are now available, tacrolimus ointment and pimecrolimus cream. These agents are macrolide immunosuppressants derived from soil fungi and are approved for use in AD. Reports of broader effectiveness appear in the literature. These agents do not cause skin atrophy and do not suppress the hypothalamic-pituitary-adrenal axis. They may replace topical glucocorticoids in some patients, but they are more costly than generic topical glucocorticoids. The non-steroid agents or low-potency topical glucocorticoids should be selected for use on the face or intertriginous areas to minimize the risk of skin atrophy.

Crusted and weeping skin lesions should be treated with systemic antibiotics with activity against S. aureus since secondary infection often exacerbates eczema. The frequency of macrolide-resistant organisms makes the use of penicillinase-resistant penicillins or cephalosporins preferable. Dicloxacillin or cephalexin (250 mg four times daily for 7 to 10 days) is generally adequate to decrease heavy colonization. As an adjunct, the use of triclosan-containing antibacterial washes and intermittent nasal mupirocin may be useful as prophylactic measures. The role of dietary allergens in atopic dermatitis is controversial, and there is little evidence that they play any role outside of infancy.

Control of pruritus is essential for treatment, since AD often represents “an itch that rashes.” Antihistamines are most often used to control pruritus, and mild sedation may be responsible for their antipruritic action. Sedation may also limit their usefulness. Unlike their effects in urticaria, nonsedating antihistamines and selective H₂ blockers are of little use in controlling the pruritus of AD.

Treatment with systemic glucocorticoids should be limited to severe exacerbations unresponsive to conservative topical therapy. In the patient with chronic AD, therapy with systemic glucocorticoids will generally clear the skin only briefly, but cessation of the systemic therapy will invariably be accompanied by return, if not worsening, of the dermatitis. Patients who do not respond to conventional therapies should be considered for patch testing to rule out allergic contact dermatitis. Immunotherapy with aeroallergens has not proven useful in AD, unlike its effect in allergic rhinitis and extrinsic asthma.

CONTACT DERMATITIS

Contact dermatitis is an inflammatory process in skin caused by an exogenous agent or agents that directly or indirectly injure the skin. This injury may be caused by an inherent characteristic of a compound—irritant contact dermatitis (ICD). An example of ICD would be dermatitis induced by a concentrated acid or base. Agents that cause allergic contact dermatitis (ACD) induce an antigen-specific immune response. The clinical lesions of contact dermatitis may be acute (wet and edematous) or chronic (dry, thickened, and scaly), depending on the persistence of the insult. The most common presentation of contact dermatitis is hand eczema, and it is frequently related to occupational exposures. Occupation-related contact dermatitis represents a significant proportion of occupation-induced injury, affecting over 60,000 persons annually.

ICD is generally strictly demarcated and often localized to areas of thin skin (eyelids, intertriginous areas) or to areas where the irritant was occluded. Lesions may range from minimal skin erythema to areas of marked edema, vesicles, and ulcers. Chronic low-grade irritant dermatitis is the most common type of ICD, and the most common area of involvement is the hands (see below). The most common irritants encountered are chronic wet work, soaps, and detergents. Treatment should be directed to avoidance of irritants and use of protective gloves or clothing.

ACD is a manifestation of delayed-type hypersensitivity mediated by memory T lymphocytes in the skin. The most common cause of ACD is exposure to plants, especially to members of the family Anacardiaceae, including the genus Toxicodendrun. Poison ivy, poison oak, and poison sumac are members of this genus and cause an allergic reaction marked by erythema, vesiculation, and severe pruritus. The eruption is often linear, corresponding to areas where plants have touched the skin. The sensitizing antigen common to these plants is urushiol, an oleoresin containing the active ingredient pentadecylcatechol. The oleoresin may adhere to skin, clothing, tools, and pets, and contaminated articles may cause dermatitis even after prolonged storage. Blister fluid does not contain urushiol and is not capable of inducing skin eruption in exposed subjects. Other allergens may be more difficult to identify, especially if the exposure is chronic and the skin becomes thickened and scaly.

TREATMENT

If ACD is suspected and an offending agent is identified and removed, the eruption will resolve. Usually, treatment with high-potency fluorinated topical glucocorticoids is enough to relieve symptoms while the ACD runs its course. For those patients who require systemic therapy, daily oral prednisone beginning at 1 mg/kg, but usually not exceeding 60 mg/d, is sufficient. It should be tapered over 2 to 3 weeks, and each daily dose given in the morning with food.

Identification of a contact allergen can be a difficult and time-consuming task. Patients with dermatitis unresponsive to conventional therapy or with an unusual and patterned distribution should be suspected of having ACD. They should be questioned carefully regarding occupational exposures, topical medicaments, and oral medications. Common sensitizers include preservatives in topical preparations, nickel sulfate, potassium dichromate, thimerosal, neomycin sulfate, fragrances, formaldehyde, and rubber-curing agents. Patch testing is helpful in identifying these agents, but should not be attempted on patients with widespread active dermatitis or on those taking systemic glucocorticoids.

HAND ECZEMA

Hand eczema is a very common, chronic skin disorder. It represents a large proportion of occupation-associated skin disease. It may be associated with other cutaneous disorders such as AD or may occur by itself. Similar to other forms of dermatitis, both exogenous and endogenous factors play important roles in the expression of hand dermatitis. Chronic, excessive exposure to water and detergents may initiate or aggravate this disorder. It may present with dryness and cracking of the skin of the hands as well as with variable amounts of erythema and edema. Often, the dermatitis will begin under rings where water and irritants are trapped. A variant of hand dermatitis, dyshidrotic eczema, presents with multiple, intensely pruritic, small papules and vesicles occurring on the thenar and hypothenar eminences and the sides of the fingers. Lesions tend to occur in crops that slowly form crusts and heal.

The evaluation of a patient with hand eczema should include an assessment of potential occupation-associated exposures. Predominant involvement of the dorsal surface of the hands with sparing of the palmar surface suggests a possible contact dermatitis. The history should be directed to identifying possible irritant or allergen exposures. The use of rubber gloves to protect dermatitic skin is sometimes associated with the development of delayed-type hypersensitivity reactions to agents used for cross-linking rubber. Such reactions can be detected by patch testing. Less commonly, patients may manifest hand dermatitis as a consequence of developing immediate-type hypersensitivity reactions to latex. These are of particular concern since these patients are at risk for anaphylactic reactions. The most sensitive method of detection is the use of scratch testing with latex extract. However, this should be done with extreme caution only in a setting where an anaphylactic reaction can be treated. A latex radioallergosorbent test is available but is only about 60% sensitive.

TREATMENT

Therapy of hand dermatitis is directed toward avoidance of irritants, identification of possible contact allergens, treatment of coexistent infection, and application of topical glucocorticoids. Whenever possible, the hands should be protected by gloves, preferably vinyl. Most patients can be treated with cool moist compresses (dressings) to dry and debride acute inflammatory lesions and to decrease swelling, followed by application of a mid- to high-potency topical glucocorticoid in a cream or ointment base. As with atopic dermatitis, treatment of secondary infection by staphylococci or streptococci is essential for good control. Additionally, patients with hand dermatitis should be examined for dermatophyte infection by KOH preparation and culture (see below).

NUMMULAR ECZEMA

Nummular eczema is characterized by circular or oval “coinlike” lesions. Initially, this eruption consists of small edematous papules that become crusted and scaly. The most common locations are on the trunk or the extensor surfaces of the extremities, particularly on the pretibial areas or dorsum of the hands. It occurs more frequently in men and is most commonly seen in middle age. The etiology of nummular eczema is unknown. The treatment of nummular eczema is similar to that for other forms of dermatitis.

LICHEN SIMPLEX CHRONICUS

Lichen simplex chronicus may represent the end stage of a variety of pruritic and eczematous disorders. It consists of a well-circumscribed plaque or plaques with lichenified or thickened skin due to chronic scratching or rubbing. Common areas involved include the posterior nuchal region, dorsum of the feet, or ankles. Treatment of lichen simplex chronicus centers around breaking the cycle of chronic itching and scratching, which often occur during sleep. High-potency topical glucocorticoids are helpful in alleviating pruritus in most cases, but in recalcitrant cases, application of topical glucocorticoids under occlusion or intralesional injection of glucocorticoids may be required. Oral antihistamines such as hydroxyzine (10 to 25 mg every 6 h) or tricyclic antidepressants with antihistaminic activity such as doxepin (10 to 25 mg at bedtime) are useful as antipruritics primarily due to their sedating action. Higher doses of these agents may be required, but sedation can become bothersome. Patients need to be counseled regarding driving or operating heavy equipment after taking these medications due to their potentially potent sedative activity.

ASTEATOTIC ECZEMA

Asteatotic eczema, also known as xerotic eczema or “winter itch,” is a mildly inflammatory dermatitis that develops in areas of extremely dry skin, especially during the dry winter months. This form of eczema accounts for a large number of physician visits because of the associated pruritus. Fine cracks and scale, with or without erythema, characteristically develop in areas of dry skin, especially on the anterior surfaces of the lower extremities in elderly patients. Asteatotic eczema responds well to topical moisturizers and the avoidance of cutaneous irritants. Overbathing and the use of harsh soaps exacerbate asteatotic eczema. Moisturizers should be applied to dry skin areas twice daily and always applied to damp skin after bathing. Prescription emollients containing ammonium lactate or urea are useful in patients with extremely dry skin, but they may be associated with skin irritation. Emollients should be applied after leaving the bath or shower to avoid increasing the risk of falling.

STASIS DERMATITIS AND STASIS ULCERATION

Stasis dermatitis develops on the lower extremities secondary to venous incompetence and chronic edema. Early findings in stasis dermatitis consist of mild erythema and scaling associated with pruritus. The typical initial site of involvement is the medial aspect of the ankle, often over a distended vein. As the disorder progresses, the dermatitis becomes progressively pigmented, due to chronic erythrocyte extravasation leading to cutaneous hemosiderin deposition. As with other forms of dermatitis, stasis dermatitis may become acutely inflamed, with crusting and exudate. Chronic stasis dermatitis is often associated with dermal fibrosis that is recognized clinically as brawny edema of the skin. Stasis dermatitis is often complicated by secondary infection and contact dermatitis. Severe stasis dermatitis may precede the development of stasis ulcers.

TREATMENT

Patients with stasis dermatitis and stasis ulceration benefit greatly from leg elevation and the routine use of compression stockings with a gradient of at least 30 to 40 mmHg. Stockings providing less compression, such as antiembolism hose, are poor substitutes. Use of emollients and/or midpotency topical glucocorticoids and avoidance of irritants are also helpful in treating stasis dermatitis. Protecting the legs from injury, including scratching, and control of chronic edema are essential to prevent ulcers.

Stasis ulcers are difficult to treat, and resolution of these lesions is slow. It is extremely important to elevate the affected limb as much as possible. The ulcer should be kept clear of necrotic material by gentle debridement and covered with a semipermeable dressing under pressure. Glucocorticoids should not be applied to ulcers, since they may retard healing. Secondarily infected lesions should be treated with appropriate oral antibiotics, but it should be noted that all ulcers will become colonized with bacteria, and the purpose of antibiotic therapy should not be to clear all bacterial growth. Care must be taken to exclude treatable causes of leg ulcers (hypercoagulation, vasculitis) before beginning the chronic management outlined above.

SEBORRHEIC DERMATITIS

Seborrheic dermatitis is a common, chronic disorder, characterized by greasy scales overlying erythematous patches or plaques. The most common location is in the scalp where it may be recognized as severe dandruff. On the face, seborrheic dermatitis affects the eyebrows, eyelids, glabella, and nasolabial folds. Scaling of the external auditory canal is common in seborrheic dermatitis and may be mistaken for a fungal infection (otomycosis). The postauricular areas often become macerated and tender. Additionally, seborrheic dermatitis may develop in the central chest, axilla, groin, submammary folds, and gluteal cleft. Rarely, it may cause a widespread generalized dermatitis.

Seborrheic dermatitis may be evident within the first few weeks of life, and within this context it occurs in the scalp (“cradle cap”), face, or groin. It is rarely seen in children beyond infancy but becomes evident again during adult life. Although it is frequently seen in patients with Parkinson's disease, in those who have had cerebrovascular accidents, and in those with HIV infection, the overwhelming majority of individuals with seborrheic dermatitis have no underlying disorder.

TREATMENT

Treatment with low-potency topical glucocorticoids in conjunction with a topical antifungal agent, such as ketoconazole cream or ciclopirox cream, is often effective. The scalp and beard areas may benefit from shampoos containing coal tar and/or salicylic acid. Shampoos should be left in place 3 to 5 min before rinsing. High-potency topical glucocorticoid solutions (betamethasone or fluocinonide) are effective for control of severe scalp involvement. Fluorinated topical glucocorticoids should not be used on the face since this is often associated with the development of rebound worsening and steroid-induced rosacea or atrophy.

PAPULOSQUAMOUS DISORDERS

PSORIASIS

Psoriasis is one of the most common dermatologic diseases, affecting up to 2.5% of the world's population. It is a chronic inflammatory skin disorder clinically characterized by erythematous, sharply demarcated papules and rounded plaques, covered by silvery micaceous scale. The skin lesions of psoriasis are variably pruritic. Traumatized areas often develop lesions of psoriasis (Koebner or isomorphic phenomenon). Additionally, other external factors may exacerbate psoriasis including infections, stress, and medications (lithium, beta blockers, and antimalarials).

The most common variety of psoriasis is called plaque type. Patients with plaque-type psoriasis will have stable, slowly enlarging plaques, which remain basically unchanged for long periods of time. The most common areas for plaque psoriasis to occur are the elbows, knees, gluteal cleft, and the scalp. Involvement tends to be symmetric. Inverse psoriasis affects the intertriginous regions including the axilla, groin, submammary region, and navel; it also tends to affect the scalp, palms, and soles. The individual lesions are sharply demarcated plaques but may be moist due to their location. Plaque psoriasis generally develops slowly and runs an indolent course. It rarely remits spontaneously.

Eruptive psoriasis (guttate psoriasis) is most common in children and young adults. It develops acutely in individuals without psoriasis or in those with chronic plaque psoriasis. Patients present with many small erythematous, scaling papules, frequently after upper respiratory tract infection with β-hemolytic streptococci. The differential diagnosis should include pityriasis rosea and secondary syphilis. Pustular psoriasis is another variant. Patients may have disease localized to the palms and soles or generalized and associated with fever, malaise, diarrhea, and arthralgias.

About half of all patients with psoriasis have fingernail involvement, appearing as punctate pitting, nail thickening, or subungual hyperkeratosis. About 5 to 10% of patients with psoriasis have associated joint complaints, and these are most often found in patients with fingernail involvement. Although some have the coincident occurrence of classic rheumatoid arthritis, many have joint disease that falls into one of three types associated with psoriasis: (1) asymmetric inflammatory arthritis most commonly involving the distal and proximal interphalangeal joints and less commonly the knees, hips, ankles, and wrists; (2) a seronegative rheumatoid arthritis–like disease; a significant portion of these patients go on to develop a severe destructive arthritis; or (3) disease limited to the spine (psoriatic spondylitis).

The etiology of psoriasis is still poorly understood, but there is clearly a genetic component to the disease. Over 50% of patients with psoriasis report a positive family history. Psoriasis has been linked to HLA-Cw6 and, to a lesser extent, to HLA-DR7. Psoriatic lesions are characterized by infiltration of skin with activated T cells, which appear to have a role in the pathophysiology of psoriasis. Presumably, cytokines from activated T cells elaborate growth factors that stimulate keratinocyte hyperproliferation. Agents that inhibit T cell activation, clonal expansion, or release of proinflammatory cytokines are often effective for the treatment of severe psoriasis.

TREATMENT

Treatment of psoriasis depends on the type, location, and extent of disease. All patients should be instructed to avoid excess drying or irritation of their skin and to maintain adequate cutaneous hydration. Most patients with localized, plaque-type psoriasis can be managed with midpotency topical glucocorticoids, although their long-term use is often accompanied by loss of effectiveness (tachyphylaxis) and atrophy of the skin. A topical vitamin D analogue (calcipotriene) and a retinoid (tazarotene) are also efficacious in the treatment of psoriasis and have largely replaced other topical agents such as coal tar, salicylic acid, and anthralin.

Ultraviolet light, natural or artificial, is an effective therapy for patients with widespread psoriasis. Ultraviolet B (UV-B) light is effective alone, or may be combined with coal tar or anthralin. The combination of the ultraviolet A (UV-A) spectrum with either oral or topical psoralens (PUVA) is also extremely effective for the treatment of psoriasis, but long-term use may be associated with an increased incidence of squamous cell cancer and melanoma of the skin.

Various other agents can be used for severe, widespread psoriatic disease. Oral glucocorticoids should not be used for the treatment of psoriasis due to the potential for developing life-threatening pustular psoriasis when therapy is discontinued. Methotrexate is an effective agent, especially in patients with psoriatic arthritis; however, liver toxicity and bone marrow suppression limit its use. The synthetic retinoid, acitretin, is effective in some patients with severe psoriasis. It is a potent teratogen and should not be used in women of childbearing potential. The evidence implicating psoriasis as a T cell–mediated disorder has directed therapeutic efforts to immunoregulation. Cyclosporine is highly effective in selected patients with severe disease, but nephrotoxicity and hypertension complicate its use. Much attention is currently directed toward the development of biologic agents with more selective immunosuppressive properties and better safety profiles. Etanercept, a tumor necrosis factor α (TNF-α) inhibitor, is now approved for psoriatic arthritis and is in clinical trials for psoriasis. Other agents in clinical trials target TNF-α and other proinflammatory cytokines, T cell activation, and lymphocyte trafficking in an attempt to suppress the inflammation characteristic of psoriasis.

LICHEN PLANUS

Lichen planus (LP) is a papulosquamous disorder in which the primary lesions are pruritic, polygonal, flat-topped, violaceous papules. Close examination of the surface of these papules often reveals a network of gray lines (Wickham's striae). The skin lesions may occur anywhere but have a predilection for the wrists, shins, lower back, and genitalia. Involvement of the scalp may lead to hair loss. LP commonly involves mucous membranes, particularly the buccal mucosa, where it can present as a white netlike eruption. Its etiology is unknown, but cutaneous eruptions clinically resembling LP have been observed after administration of numerous drugs, including thiazide diuretics, gold, antimalarials, penicillamine, and phenothiazines, and in patients with skin lesions of chronic graft-versus-host disease. Additionally, LP may be associated with hepatitis C infection. The course of LP is variable, but most patients have spontaneous remissions 6 months to 2 years after the onset of disease. Topical glucocorticoids are the mainstay of therapy.

PITYRIASIS ROSEA

Pityriasis rosea (PR) is a papulosquamous eruption of unknown etiology that occurs more commonly in the spring and fall. Its first manifestation is the development of a 2- to 6-cm annular lesion (the herald patch). This is followed in a few days to a few weeks by the appearance of many smaller annular or papular lesions with a predilection to occur on the trunk. The lesions are generally oval, with their long axis parallel to the skin-fold lines. Individual lesions may range in color from red to brown and have a trailing scale. PR shares many clinical features with the eruption of secondary syphilis, but palm and sole lesions are extremely rare in PR and common in secondary syphilis. The eruption tends to be moderately pruritic and lasts 3 to 8 weeks. Treatment is generally directed at alleviating pruritus and consists of oral antihistamines, midpotency topical glucocorticoids, and, in some cases, the use of UV-B phototherapy.

CUTANEOUS INFECTIONS

IMPETIGO AND ECTHYMA

Impetigo is a common superficial bacterial infection of skin caused by group A β-hemolytic streptococci or S. aureus. The primary lesion is a superficial pustule that ruptures and forms a characteristic yellow-brown honey-colored crust. Lesions caused by staphylococci may be tense, clear bullae, and this less common form of the disease is called bullous impetigo. Lesions may occur on normal skin or in areas already affected by another skin disease. Ecthyma is a variant of impetigo that generally occurs on the lower extremities and causes punched-out ulcerative lesions. Treatment of both ecthyma and impetigo involves gentle debridement of adherent crusts, which is facilitated by the use of soaks and topical antibiotics, in conjunction with appropriate oral antibiotics.

ERYSIPELAS AND CELLULITIS

DERMATOPHYTOSIS

Dermatophytes are fungi that infect skin, hair, and nails and include members of the genera Trichophyton, Microsporum, and Epidermophyton. Tinea corporis, or infection of the relatively hairless skin of the body (glabrous skin), may have a variable appearance depending on the extent of the associated inflammatory reaction. It may have the typical annular appearance of “ringworm” or appear as deep inflammatory nodules or granulomas. Involvement of the groin (tinea cruris) is more common in males than females. It presents as a scaling, erythematous eruption that spares the scrotum. Infection of the foot (tinea pedis) is the most common dermatophyte infection and is often chronic; it is characterized by variable erythema, edema, scaling, pruritus, and occasionally vesiculation. Involvement may be widespread or localized, but almost invariably involves the web space between the fourth and fifth toes. Infection of the nails (tinea unguium or onychomycosis) occurs in many patients with tinea pedis and is characterized by opacified, thickened nails and subungual debris. Dermatophyte infection of the scalp (tinea capitis) has returned in epidemic proportions, particularly affecting inner-city children, but it also affects adults. The predominant organism is T. tonsurans, which can produce a relatively noninflammatory infection with mild scale and hair loss that is diffuse or localized. Localized disease may be well defined or irregular. T. tonsurans can also cause a markedly inflammatory dermatosis with edema and nodules. This latter presentation is a kerion.

The diagnosis of tinea can be made from skin scrapings, nail scrapings, or hair by culture or direct microscopic examination with potassium hydroxide (KOH). Hair, nail scrapings, and scrapings from markedly inflamed skin may fail to show hyphae on direct examination.

TREATMENT

Both topical and systemic therapies may be used to treat dermatophyte infections. Treatment depends on the site involved and the type of infection. Topical therapy is generally effective for uncomplicated tinea corporis, tinea cruris, and limited tinea pedis. It is not effective as a monotherapy for tinea capitis or onychomycosis. Topical imidazoles, triazoles, and allylamines may all be effective topical therapies for dermatophyte infections. Haloprogin, undecylenic acid, ciclopirox olamine, and tolnaftate are also effective, but nystatin is not active against dermatophytes. Topicals are generally applied twice daily, and treatment should continue 1 week beyond clinical resolution of the infection. Tinea pedis often requires longer treatment courses and frequently relapses. Oral antifungal agents may be required for recalcitrant tinea pedis or tinea corporis with a nodular (granulomatous) component.

Oral antifungal agents are required for dermatophyte infections involving the hair and nails and for other infections unresponsive to topical therapy. A fungal etiology should be confirmed by direct microscopic examination or by culture prior to prescribing oral antifungal agents. All of the oral agents may cause hepatotoxicity and should not be used in women who are pregnant or breast-feeding.

Griseofulvin is the only oral agent approved in the United States for dermatophyte infections involving the skin, hair, or nails. Itraconazole and terbinafine are approved for onychomycosis; however, the literature cites multiple examples of their effective use in other dermatophyte infections. When griseofulvin is used, a daily dose of 500 mg of microsized or 350 mg of ultramicrosized griseofulvin administered with a fatty meal is an adequate dose for most dermatophyte infections. Higher doses are required for tinea pedis and onychomycosis. The duration of therapy may be 2 weeks for uncomplicated tinea corporis or as long as 6 to 18 months for nail infections. Due to high relapse rates, griseofulvin is seldom used for nail infections. The usual adult dose of griseofulvin for tinea capitis is 1 g of microsized or 0.5 g of ultramicrosized given daily for 6 to 8 weeks or until cultures are negative. The adjunctive use of topical antifungal agents may be useful, but topical therapy alone is not adequate for tinea capitis. Markedly inflammatory tinea capitis may result in scarring and hair loss, and systemic or topical glucocorticoids may be helpful in preventing these sequelae. Common side effects of griseofulvin include gastrointestinal distress, headache, and urticaria.

Oral itraconazole and terbinafine are approved for onychomycosis. Itraconazole is given as either continuous daily therapy (200 mg/d) or pulses (200 mg twice daily for 1 week per month) administered with food. Fingernails require 2 months of continuous therapy or two pulses. Toenails require 3 months of continuous therapy or three pulses. Itraconazole has the potential for serious interactions with other drugs requiring the P450 enzyme system for metabolism. Terbinafine (250 mg/d) is also effective for onychomycosis. Therapy with terbinafine is continued for 6 weeks for fingernail infections and 12 weeks for toenail infections. Terbinafine has fewer drug-drug interactions, but caution should be used when patients are on multiple medications.

TINEA VERSICOLOR

Tinea versicolor is caused by a non-dermatophyte, dimorphic fungus, Malassezia furfur, a normal inhabitant of the skin. As the yeast form, it generally does not cause disease (except for folliculitis in certain individuals). However, in some individuals, it converts to the hyphal form and causes characteristic lesions. The expression of infection is promoted by heat and humidity. The typical lesions consist of oval scaly macules, papules, and patches concentrated on the chest, shoulders, and back but only rarely on the face or distal extremities. On dark skin, they often appear as hypopigmented areas, while on light skin, they are slightly erythematous or hyperpigmented. In some darkly pigmented individuals, they may only appear as scaling patches. A KOH preparation from scaling lesions will demonstrate a confluence of short hyphae and round spores (so-called spaghetti and meatballs). Solutions containing sulfur, salicylic acid, or selenium sulfide will clear the infection if used daily for a week and then intermittently thereafter. Treatment with a single 400-mg oral dose of ketoconazole is also effective.

CANDIDIASIS

Candidiasis is a fungal infection caused by a related group of yeasts, whose manifestations may be localized to the skin, or rarely, may be systemic and life-threatening. The causative organism is usually Candida albicans, but may also be C. tropicalis, C. parapsilosis, or C. krusei. These organisms are normal saprophytic inhabitants of the gastrointestinal tract but may overgrow (usually due to broad-spectrum antibiotic therapy) and cause disease at a number of cutaneous sites. Other predisposing factors include diabetes mellitus, chronic intertrigo, oral contraceptive use, and cellular immune deficiency. Candidiasis is a very common infection in HIV-infected individuals. The oral cavity is commonly involved. Lesions may occur on the tongue or buccal mucosa (thrush) and appear as white plaques. Microscopic examination of scrapings demonstrate both pseudohyphae and yeast forms. Fissured, macerated lesions at the corners of the mouth (perlèche) are often seen in individuals with poorly fitting dentures and may also be associated with candidal infection. Additionally, candidal infections have an affinity for sites that are chronically wet and macerated and may occur around nails (onycholysis and paronychia) and in intertriginous areas. Intertriginous lesions are characteristically edematous, erythematous, and scaly, with scattered “satellite pustules.” In males, there is often involvement of the penis and scrotum as well as the inner aspect of the thighs. In contrast to dermatophyte infections, candidal infections are frequently painful and accompanied by a marked inflammatory response. Diagnosis of candidal infection is based upon the clinical pattern and demonstration of yeast on KOH preparation or culture.

TREATMENT

Treatment routinely involves removing any predisposing factors such as antibiotic therapy or chronic wetness and the use of appropriate topical or systemic antifungal therapy. Effective topical agents include nystatin or topical azoles (miconazole, clotrimazole, econazole, or ketoconazole). These agents are generally effective in clearing mucous membrane or glabrous skin involvement in nonimmunosuppressed patients. The associated inflammatory response that often accompanies candidal infection on glabrous skin can be treated with a mild glucocorticoid lotion or cream (2.5% hydrocortisone). Systemic therapy is generally reserved for immunosuppressed patients or individuals with chronic or recurrent disease who fail to respond to or tolerate appropriate topical therapy.

WARTS

Warts are cutaneous neoplasms that are caused by papilloma viruses. Approximately 80 different human papilloma viruses (HPV) have been described, and this number will likely increase. Typical verruca vulgaris lesions are sessile, dome-shaped, usually about a centimeter in diameter, and their surface is hyperkeratotic consisting of many small filamentous projections. The HPV that cause typical verruca vulgaris also cause typical plantar warts, flat warts (or verruca plana), and filiform warts in intertriginous areas. Plantar warts are endophytic and are covered by thick keratin. Paring of the wart will generally demonstrate a central core of keratinized debris and punctate bleeding points. Filiform warts are most commonly seen on the face, neck, and skin folds and present as papillomatous lesions on a narrow base. Flat warts are only slightly elevated and have a velvety, nonverrucous surface. They have a propensity for the face, arms, and legs and are often spread by shaving.

Genital warts generally begin as small papillomas that may grow to form large fungating lesions. In women, they may involve either the labia, perineum, or perianal skin. Additionally, the mucosa of the vagina, urethra, and anus can be involved, as well as the cervical epithelium. In men, the lesions often occur initially in the coronal sulcus, but may be seen on the shaft of the penis, the scrotum, perianal skin, or in the urethra.

Within the past decade, appreciable evidence has accumulated that suggests HPV plays a role in the development of neoplasia of the uterine cervix and external genitalia. HPV types 16 and 18 have been most intensely studied, while recent evidence also implicates other types. Lesions may initially appear as small, flat, velvety, hyperpigmented papules occurring on the genitalia or perianal skin. Histologic examination of biopsies from affected sites may reveal changes associated with typical warts and/or features typical of intraepidermal carcinoma (Bowen's disease). Squamous cell carcinomas associated with HPV infections have also been observed in extragenital skin. This is most commonly seen in patients immunosuppressed after organ transplantation.

TREATMENT

There are many modalities available to treat warts, but no single therapy is universally effective. Factors that influence the choice of therapy include the location of the wart, extent of disease, the age and immunologic status of the patient, and the patient's desire for therapy. Perhaps the most useful and convenient method for treating warts in almost any location is cryotherapy with liquid nitrogen. Equally effective, but requiring much more patient compliance, is the use of keratolytic agents such as salicylic acid plasters or solutions. For genital warts, in-office application of a podophyllin solution is moderately effective but may be associated with marked local reactions. Prescription preparations of dilute, purified podophyllin are available for home use. Topical imiquimod, a potent inducer of local cytokine release, has also been approved for use in genital warts. Conventional and laser surgical procedures may be required for recalcitrant warts. Recurrence of warts appears to be common to all these modalities.

Treatment of warts, other than anogenital warts, should be tempered by the observation that a majority of warts in normal individuals resolve spontaneously within 1 to 2 years. Also, very few warts are associated with malignancy, and those are usually located in the anogenital region.

ACNE

ACNE VULGARIS

Acne vulgaris is a self-limited disorder primarily of teenagers and young adults, although perhaps 10 to 20% of adults may continue to experience some form of the disorder. The permissive factor for the expression of the disease in adolescence is the increase in sebum production by sebaceous glands after puberty. Small cysts, called comedones, form in hair follicles due to blockage of the follicular orifice by retention of sebum and keratinous material. The activity of bacteria (Proprionobacterium acnes) within the comedones releases free fatty acids from sebum, causes inflammation within the cyst, and results in rupture of the cyst wall. An inflammatory foreign-body reaction develops as a result of extrusion of oily and keratinous debris from the cyst.

The clinical hallmark of acne vulgaris is the comedone, which may be closed (whitehead) or open (blackhead). Closed comedones appear as 1- to 2-mm pebbly white papules, which are accentuated when the skin is stretched. They are the precursors of inflammatory lesions of acne vulgaris. The contents of closed comedones are not easily expressed. Open comedones, which rarely result in inflammatory acne lesions, have a large dilated follicular orifice and are filled with easily expressible oxidized, darkened, oily debris. Comedones are usually accompanied by inflammatory lesions: papules, pustules, or nodules.

The earliest lesions seen in early adolescence are generally mildly inflamed or noninflammatory comedones on the forehead. Subsequently, more typical inflammatory lesions develop on the cheeks, nose, and chin. The most common location for acne is the face, but involvement of the chest and back is not uncommon. Most disease remains mild and does not lead to scarring. However, a small number of patients develop large inflammatory cysts and nodules, which may drain and result in significant scarring.

Exogenous and endogenous factors can alter the expression of acne vulgaris. Friction and trauma may rupture preexisting microcomedones and elicit inflammatory acne lesions. This is commonly seen with headbands or chin straps of athletic helmets. Application of comedogenic topical agents in cosmetics or hair preparations or chronic topical exposure to certain industrial compounds that are comedogenic may elicit or aggravate acne. Glucocorticoids, applied topically or administered systemically in high doses, may also elicit acne. Other systemic medications such as lithium, isoniazid, halogens, phenytoin, and phenobarbital may produce acneiform eruptions, or aggravate preexisting acne.

TREATMENT

Treatment of acne vulgaris is directed toward elimination of comedones by normalization of follicular keratinization, decreasing sebaceous gland activity, decreasing the population of P. acnes, and decreasing inflammation. Acne vulgaris may be treated with either local or systemic medications. Minimal to moderate, pauci-inflammatory disease may respond adequately to local therapy alone. Although areas affected with acne should be kept clean, there is little evidence to suggest that removal of surface oils plays an important role in therapy. Overly vigorous scrubbing may aggravate acne due to mechanical rupture of comedones. Topical agents such as retinoic acid, benzoyl peroxide, or salicylic acid may alter the pattern of epidermal desquamation, preventing the formation of comedones and aiding in the resolution of preexisting cysts. Topical antibacterial agents such as benzoyl peroxide, azelaic acid, topical erythromycin (with or without zinc), or clindamycin are also useful adjuncts to therapy.

Patients with moderate to severe acne with a prominent inflammatory component will benefit from the addition of systemic therapy, such as tetracycline or erythromycin, in doses of 250 to 1000 mg/d. Such antibiotics appear to have an anti-inflammatory effect independent of their antibacterial effect. Female patients who do not respond to oral antibiotics may benefit from hormonal therapy. Women placed on oral contraceptives containing ethinyl estradiol and norgestimate have demonstrated improvement in their acne when compared to a placebo control.

Patients with severe nodulocystic acne unresponsive to the therapies discussed above may benefit from treatment with the synthetic retinoid, isotretinoin. Its use is highly regulated due to its potential for severe adverse events, primarily teratogenicity. Recently there have also been concerns that it is associated with severe depression in some patients. The latter has not been proved. At present, prescribers must receive from the manufacturer training, certification, and stickers to affix to each prescription. These measures are imposed to ensure that all prescribers are familiar with the risks of isotretinoin; that all female patients have two negative pregnancy tests prior to initiating therapy and a negative pregnancy test prior to each refill; and that all patients have been warned about the risks associated with isotretinoin, including depression. Additionally, patients receiving this medication develop extremely dry skin and cheilitis and must be followed for development of hypertriglyceridemia.

ACNE ROSACEA

Acne rosacea is an inflammatory disorder predominantly affecting the central face. It is seen almost exclusively in adults, only rarely affecting patients under 30 years of age. Rosacea is seen more often in women, but those most severely affected are men. It is characterized by the presence of erythema, telangiectases, and superficial pustules, but is not associated with the presence of comedones. Rosacea only rarely involves the chest or back.

There is a relationship between the tendency for pronounced facial flushing and the subsequent development of acne rosacea. Often, individuals with rosacea initially demonstrate a pronounced flushing reaction. This may be in response to heat, emotional stimuli, alcohol, hot drinks, or spicy foods. As the disease progresses, the flush persists longer and longer and may eventually become permanent. Papules, pustules, and telangiectases can become superimposed on the persistent flush. Rosacea of very long standing may lead to connective tissue overgrowth, particularly of the nose (rhinophyma). Rosacea may also be complicated by various inflammatory disorders of the eye, including keratitis, blepharitis, iritis, and recurrent chalazion. These ocular problems are potentially sight-threatening and warrant ophthalmologic evaluation.

TREATMENT

Acne rosacea can be treated topically or systemically. Mild disease often responds to topical metronidazole or sodium sulfacetamide. More severe disease requires oral tetracycline in doses ranging from 250 to 1000 mg/d. Residual telangiectasia may respond to laser therapy. Topical glucocorticoids, especially potent agents, should be avoided since chronic use of these preparations may elicit rosacea. Topical therapy of the skin is not effective treatment for ocular disease.

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