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Common dermatoses
PRIMARY
CARE
Common dermatoses Vandana Irvine,
S. Nanda,
MD
California
Skin diseases are an essential part of primary care medicine. Most dermatologic care is delivered in an outpatient setting. The initial evaluation is usually petformed by the primary care physician. Women account for nearly 60% of all visits for dermatologic complaints. (AM J OBSTET GYNECOL 1995;173:488-95.)
Key words:
Papulosquamous
dermatoses,
inflammatory
diseases, acneiform
eruptions
Dermatology is an essential part of primary care medicine. Diseases of the skin are a common occurrence, although the true prevalence of skin disease is difficult to determine. Dermatologic care is delivered mainly in the outpatient setting. As part of the National Ambulatory Care Survey, patients with dermatologic complaints accounted for 7.3% of office-based physician visits. ‘, ’ Women accounted for 58% of all visits for dermatologic complaints. This manuscript focuses on common dermatologic diseases. The topics incIuded are papulosquamous diseases, inflammatory diseases, acne, and acneiform eruptions. Pigmented lesions and cutaneous neoplasms will be the subject of a future article.
Papulosquamous
dermatoses
Psoriasis. In the United States psoriasis affects 1% of the population.” It is a disease characterized by a chronic, relapsing nature. The clinical presentation may be mild with just a few localized plaques limited to the elbows and scalp or quite severe with generalized erythema, scaling, and pustulation. Psoriasis can be disabling in the presence of concomitant joint disease. There is a genetic predisposition to development of psoriasis. One third of patients with psoriasis report having some relative with the disease. There is a 65% concordance for psoriasis in monozygotic twins in contrast to 30% in dizygotic twins.4 There is a bimodal onset of presentation. The peak incidence is at age 22 years and the second peak of onset is around age 55 years. An earlier onset (before puberty) portends more severe disease.
From the Department of Dermatology, University of California, Irvine. Reprint requests: Vandana S. Nanda, MD, lJniversi$ of Calafornia, Irvine Medical Center, Department of Dermatology, Rt. 81, 101 City Dr. South, Orange, CA 92668. Copyright 0 1995 by Mosby-Year Book, Inc. 0002-9378/95 $3.00 + 0 6/l/66025
488
Fig. 1. Psoriasis on elbow. Common location. with
thick
white
adherent
Pink papules
scale.
Clinical features. The cutaneous lesions of psoriasis are characteristic and proper diagnosis is easy. The lesions vary from pinpoint red papules to large plaques. The plaques are red, raised, and sharply circumscribed and consist of superficial silvery scales (Fig. 1). Most common areas of involvement are the elbows, the knees, the scalp, the lumbar area, and the umbilicus. In the inverse variant skin folds such as the axilla, the inframammary folds, the genitourinary region, and the neck are involved (Fig. 2). Candidiasis must be ruled out in this clinical setting. Frequently in women the labia majora are involved. Several nail changes are frequent. They range from minor alterations in the nail plate, such as pits, to severe changes showing yellow keratinous substance or complete loss of nail plate (Fig. 3). Several trigger factors or external factors are known to start an onset of or to exacerbate preexisting psoriasis. These include infections, particularly of the upper respiratory tract.” In patients with the human immunodeficiency virus type 1, psoriasis may be the first clinical manifes-
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Fig. 3. Psoriasis plate dystrophy.
Fig.
2. Psoriasis
of labia
of nail,
with
yellow
discoloration
and
489
nail
majora.
Stress worsens psori a sis in tation of the infection.’ 30% to 40% of patients. Hormonal influences, such as during pregnancy or while a woman is using oral contraceptives, do not appear to have an effect on triggering or causing a remission in psoriasis. Certain drugs such as lithium, antimalarials, P-adrenergic receptor blockers, and discontinuation of corticosteroids have all been reported to cause or to trigger a flare of psoriasis.3 Treatment. A variety of treatment options is available. These include topical therapies, ultraviolet light, and systemic treatments. The combination of several therapies helps shorten the time to clearing. The topical treatments used for psoriasis are corticosteroids, tars, anthralin, and a newly introduced vitamin D, analog, calcipotriene. Corticosteroids are the most popular, especially for limited extent of involvement. High-potency (Halobetasol propionate, clobetasol propionate, etc.) corticosteroids are invaluable in short-term management, but most patients do well with mid- to lowpotency formulations (e.g., triamcinolone acetonide, alclometasone dipropionate). Ointments are preferable since they keep the plaques greasy. Intensive additional lubrication with greasy ointments such as hydrophilic petrolatum (Aquaphor), petrolatum, or a moisturizing cream (Eucerin) must be stressed and incorporated into the daily treatment regimen. Tar therapy is effective, especially in conjunction with ultraviolet B radiation. This form of therapy is known as the Goeckerman regimen. Anthralin preparations are effective but difficult to
Fig. 4. Lichen plaques. Linear
planus. lesions
Violaceous demonstrate
polygonal Koebner’s
papules and phenomenon.
use as topical therapy because they irritate the skin. Calcipotriene, a new vitamin D, analog, has been shown effective for moderate plaque psoriasis within 8 weeks of therapy.6 It is not to be used on the face because it produces irritation. Calcipotriene ointment avoids the local side effects of corticosteroids (i.e., atrophy and telangiectasia). An elevation of the serum calcium level is a possible and reversible side effect of calcipotriene treatment. Photochemotherapy (methoxsalen plus ultraviolet radiation) and systemic chemotherapy such as methotrexate and cyclosporine are highly effective, but because of serious side effects, their use is limited to patients with extensive disease.7 Lichen planus. Lichen planus is an intensely pruritic eruption. Less than 1% of the population is thought to be affected. There is no racial or sexual predisposition.*
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Fig. 5. Lichen planus of nails, with dystrophia unguium pigmentation.
and
Most patients affected are between the ages of 30 and 60. Clinical features. The lesions of lichen planus are present on the skin and mucous membranes. The classic lesion is a violaceous, flat-topped polygonal papule with a thin scale and delicate white lines known as Wickham’s striae (Fig. 4). Lesions are usually present bilaterally on the flexor aspects of the arms, wrists, sides of the neck, thighs, and shins. Oral and genital mucosa are also involved. The buccal mucosa is most often affected. Lesions are also found on the tongue, lips, pharynx, gastrointestinal tract, and vaginal and vulvar mucosa. The lesions appear to be lacelike. Follicular papules on the scalp can result. As in psoriasis, cutaneous trauma may induce the development of new lesions (Koebner’s phenomenon). Lesions are pruritic but vary in severity. There is a 10% incidence of nail changes, which characteristically include a brown discoloration, longitudinal grooving, splitting, and roughening9 (Fig. 5). Pterygium formation can result from involvement of adjacent paronychial tissue.” There are several drugs that cause lichen planus-like eruptions, such as antimalarials, angiotensin-converting enzyme inhibitors, gold, hypoglycemic agents, and thiazides.” Psoriasis must be considered in the differential diagnosis. Treatment. The treatment of lichen planus can be difficult. Numerous treatments including antibiotics, antimalarials, ultraviolet radiation, vitamins, and heavy metals have been used. None have been confirmed with controlled studies. Corticosteroids are useful in treating lichen planus. Potent topical corticosteroids cause regression of typical cutaneous lesions. Oral lesions should be treated with a topical corticosteroid in a preparation that is adherent to mucous membranes, Intralesional injections of corticostesuch as Orabase.” roids (e.g., triamcinolone acetonide 5 to 10 mgiml) are useful for recalcitrant lesions. More severe, generalized
Fig. 6. Pityriasis rosea. “Herald precedes eruption.
patch’-primary
1995 Gynecol
plaque that
cases may be treated with oral corticosteroids, photochemotherapy (methoxsalen and ultraviolet A radiation), and immunomodulators such as cyclosporine.‘“-‘” The course of the disease tends to be long, lasting between several months and years. There are recurrences in 12% to 20% of patients, generally in those who have had extensive cutaneous involvement. Pityriasis rosea. Pityriasis rosea is an acute exuberant skin eruption. The incidence is highest between the ages of 15 and 40 years, and the disease is most prevalent in the spring and autumn.‘” Women are more frequently affected.‘” The cause of pityriasis rosea is unknown. A viral infection is most frequently suggested but has not been proved. Several drugs can cause pityriasis rosea-like eruptions. These include captopril, arsenic compounds, gold, bismuth, clonidine, ketotifen, and barbiturates.” Clinical features. Characteristically, a “Christmas tree” pattern is seen with the lesions distributed in the lines of cleavage of the skin. The disease usually begins with a single “herald” or “mother patch” (Fig. 6), usually preceding the full-blown eruption by 1 to 2 weeks. The individual lesions are oval and salmon-colored with a collarette of scale. The “herald patch” may be confused with a lesion of tinea corporis. The fully developed eruption is generalized, affecting mainly the trunk and sparing the sun-exposed areas. The differential diagnosis includes viral exanthem, guttate psoriasis, and secondary syphilis. Pruritus is usually mild. As the lesions start to involute and become dry, the patients experience more pruritus. Course. The course of pityriasis rosea is mild and can last between 4 and 10 weeks. Occasionally the course may be more protracted. Treatment. Treatment is not necessary except in complicated cases. Ultraviolet B radiation is therapeutic in cases complicated with severe pruritus.‘” Involution of
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Fig.
7. Atopic
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dermatitis.
Typical
flexural
involvement.
lesions may also be expedited with ultraviolet radiation in protracted cases. For dryness and irritation, bland emollients are advised.
Inflammatory
dermatoses
Atopic dermatitis. Atopic dermatitis, also commonly known as eczema, is a chronically relapsing skin condition. It arises in infancy, early childhood, or adolescence. The prevalence of atopic dermatitis has been increasing over the last several decades and now affects 10% to 15% of the population at some point during their lifetime.‘” The cause is unknown. It is associated with marked pruritus, elevated serum immunoglobulin E levels, and a personal or family history of atopic dermatitis, allergic rhinitis, and/or asthma. Defective cell-mediated immunity occurs in up to 80% of affected patientsI It is manifested by increased susceptibility to severe skin infections with viruses (herpes simplex, vaccinia, coxsackie virus), and chronic dermatophyte infections.” Clinical features. The main features include the extremely pruritic nature of the rash, typical morphologic features and distribution, and its tendency toward a chronic course.” The typical lesion is papulovesicular, red, scaly, and possibly crusted (Fig. 7). Other features such as periorbital darkening, infraorbital fold (Morgan’s line or Dennie’s sign), and hyperlinearity of the palms are common but nonspecific. In teenagers and adults the flexural surfaces, face, hands, and feet are frequently involved. Extreme xerosis, lichenification, and hyperpigmentation are common. Patients may have symptom-free periods that may last for months. These patients retain a tendency toward dry skin. Seborrheic dermatitis and contact dermatitis are commonly confused with atopic dermatitis. Treatment. A variety of “trigger factors” that are known to exacerbate the condition must be avoided. These include irritants (soaps, chemicals), heat, humid-
Fig. 8. Seborrheic bial and melolabial
dermatitis. folds.
Erythema
and scaling
in nasola-
ity, wool clothing, and known allergens.” Because atopic skin is dry and pruritic, both these symptoms can be alleviated with hydration. Soaking in plain tepid water daily for 20 minutes followed by immediate lubrication (e.g., Aquaphor, petrolatum, Eucerin) is recommended. In addition, oral antihistamines are used to help control the pruritus. Topical corticosteroids are the mainstay of therapy in atopic dermatitis. Midpotency corticosteroids such as 0.1% triamcinolone ointment or cream are used for general management. Potent fluorinated corticosteroids are used to suppress acute flares. Low-potency corticosteroids such as Aclovate (alclometasone dipropionate) and Desowen (desonide) are used on the face. Use of potent corticosteroids should be limited to 2 weeks for any given lesion. Oral corticosteroids should be avoided since many patients have rebound flares after a short course. Superinfections with Staphylococcus aureus or herpes simplex need appropriate oral antibiotics and antiviral treatment. Ultraviolet light and methoxsalen photochemotherapy are helpful in some patients with recalcitrant conditions.” Cyclosporine, thymopentin, and interferon gamma are other, possibly promising agents for severe cases.23-‘5 Seborrheic dermatitis. Seborrheic dermatitis is common, affecting 2% to 5% of the population, and is easily recognizable.‘6 It affects babies and adults and is associated with increased sebum production of the scalp and hair-bearing areas of the face (i.e., the eyebrows, nasolabial folds, and ears). Seborrheic dermatitis has two age peaks,, one in early infancy and the second around the fourth to seventh decades of life. A markedly higher prevalence and severity are noted in patients with the acquired immunodeficiency syndrome.27 Seborrheic dermatitis is often associated with a variety of neurologic abnormalities and is worsened with emotional stress. The cause of seborrheic dermatitis is unknown.
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Fig. 9. Nummular
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dermatitis. Coin-shaped,
dry pink plaques.
Pityrosporum ovale, a lipophilic yeast, is more abundant in patients with seborrheic dermatitis.” Some authors believe that this microbe is important in the pathogenesis of this disease. Clinical features. Clinically the involved skin of the central face and scalp appears red and inflamed and has a greasy yellow-white scale (Fig. 8).” Prominent follicular openings can be noted. The course is chronic, usually lasting for years to decades. The differential diagnosis commonly includes psoriasis, contact dermatitis, and rosacea. Treatment. Therapy is aimed at reducing the inflammation and scaling. Crusting and scaling in the scalp are removed by nightly applications of topical corticosteroids and keratolytics. Examples of these preparations include Derma-Smoothe/FS (Hill Pharmaceuticals, Inc., Orlando) topical oil T/Gel (Neutrogena Dermatologics, Los Angeles) therapeutic shampoo, P and S (Baker Cummins Pharm., Inc., Miami) liquid, and others. Several recommended shampoos include DHS (Person and Covey, Inc.), zinc, Head and Shoulders (Procter & Gamble, Cincinnati), Ionil Plus (Galderma Laboratories, Inc., Fort Worth), T/Gel, and X Seb (Baker Cummins). Facial inflammation is controllable with low-potency glucocorticosteroids. Side effects of long-term corticosteroid application include atrophy, telangiectasia, corticosteroid rosacea, perioral dermatitis, and acne. Good control is also achieved with topical application of antifungal agents. Preparations of 2% ketoconazole in cream and shampoo formulations have been studied and found effective.‘6 Nummular dermatitis. Nummular dermatitis is defined by its clinical appearance of coin-shaped lesions. The eruption most commonly begins on the legs and can spread to the upper extremities and the trunk. There are two peaks of onset in women, one between 15 and 25 years and the second between 55 and 65 years.
Peak incidence is noted in the winter months. Lesions last from weeks to months with frequent remissions and recurrences. Although the cause is unknown, several causative factors such as bacteria, dry weather conditions, irritability to wool, soaps, and frequent bathing have all been proposed.” Clinical features. The acute eruption appears as tiny pink papules and vesicles that enlarge to form plaques that are coin-shaped (Fig. 9). In the acute lesions there is edema, exudate, and crust formation. The chronic lesion appears dry, scaly, and lichenified. Prominent excoriations may be seen, and the patient may experience moderate to severe pruritus and occasional burning. Treatment. Treatment is aimed at rehydrating the skin by soaking in plain tepid water for 15 to 20 minutes. Mid- to high-potency topical corticosteroids should be applied to involved areas immediately after a bath. Further emolliation with thick creams and petrolatumbased preparations is necessary. Lotions are discouraged because of their net drying effect of component alcohols and water. Topical use of high-potency corticosteroids should be limited to 2 weeks. Pruritus may be treated with Hl antihistamines or with ultraviolet B therapy.‘Y
Acne and acneiform eruptions Acne vulgaris. Acne vulgaris is a self-limited disease seen mostly in adolescents. Acne vulgaris involves the sebaceous hair follicles. The majority of patients are seen in the mid to late teenage years, and since it is common, it is thought to be physiologic. In women acne may persist into the third and fourth decades or later. Acne is less severe in women than in men. The basic cause of acne is not understood, but there are several factors involved in its pathogenesis. Primarily there is altered keratinization within the follicle. Patients with severe acne produce increased amounts of sebum.3” Sebum is comedogenic and inflammatory.“” The predominant organism in the follicle is Propionibacterium acnes, which also produces inflammation.30 Recent studies show that one or more tissue androgens may be increased in acne patients, particularly in older women with a recalcitrant condition3’ Clinical features. The primary sites of acne are the face, chest, and back. Acne lesions may be divided into noninflammatory and inflammatory lesions. Comedones, both open (blackheads) and closed (whiteheads), are noninflammatory. Inflammatory acne is traditionally characterized by the presence of papules, pustules, and nodules (cysts). Resolution of inflammatory lesions may cause erythematous or pigmented macules that can persist for many months. Treatment. The therapeutic modalities used in acne treatment aim to correct the follicular keratinization
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process, decrease follicular bacterial content, decrease sebum production, and produce antiinflammatory action. Topical treatment is very effective for mild acne. Vitamin A acid, tretinoin cream, is comedolytic and highly effective for treatment of comedones.s2 Retin-A (Ortho Pharmaceutical Corp., Dermatological Div., Raritan, N.J.) cream 0.025% can be tolerated by most patients without irritation. Benzoyl peroxide preparations have both antibacterial and antiinflammatory action. These are available in lotions and gels. Topical antibiotics used routinely contain erythromycin or clindamycims3 Systemic antibiotics should be added to the treatment regimen when moderate acne is treated. Tetracycline or its derivatives are most commonly used.30 Initial doses range from 500 to 1000 mg/day. To promote absorption, tetracycline must be taken on an empty stomach. Minocycline is used in patients who are unresponsive to tetracycline, but blue-black pigmentation is a potential side effect. Tetracycline should not be administered to pregnant women because it inhibits skeletal growth and causes irreversible yellow staining of developing teeth. The treatment of severe nodulocystic acne has been revolutionized with the use of isotretinoin, a synthetic oral retinoid. Isotretinoin should be reserved only for patients with severe acne.34 The recommended daily dose is in the range of 0.5 to 1 mg/kg per day. Treatment is necessary for 4 to 5 months. Serum triglyceride levels and liver function tests are obtained before treatment and then repeated monthly. Common side effects include cheilitis, dry mucous membranes, conjunctivitis, pruritus, and xerosis. The greatest concern during isotretinoin therapy is the risk of the drug being administered during pregnancy. Isotretinoin is a teratogen. It affects organogenesis very early in pregnancy. Woman of childbearing age must be fully informed of the risk of pregnancy. Effective contraception must be used, and the manufacturer recommends pretreatment pregnancy testing and continuation during treatment. Rosacea. Rosacea is quite common in fair-skinned people and occurs in the third and fourth decades. It is more common and runs a milder course in women than in men. The pathogenesis of rosacea is unknown. It is accepted that patients with rosacea are predisposed to easy blushing evoked by numerous factors: ultraviolet radiation, heat, cold, spices, alcoholic drinks, and caffeine.35 Clinical features. Rosacea is a disease of the central face. It is present on the nose, medial cheeks, glabella, upper lip, and chin. The sun-exposed areas such as the V of the neck and the back can be involved. Papules and papulopustules are present on bright red erythema (Fig. 10). Telangiectasias are common. Plaquelike edema may be present, in addition to persistent erythema. With disease progression edema becomes a
Nanda
Fig.
10.
493
Rosacea.
constant feature, telangiectasia enlarges, and facial pores become more prominent. In the worst of cases large inflammatory nodules develop, along with tissue hyperplasia and distortion of facial features. Anterior ocular inflammation (blepharitis, conjunctivitis) is commonly present.35 Treatment. Rosacea is difficult to treat. Treatment is determined by the severity of the disease. Topical erythromycin and clindamycin available in various formulations are effective.3’ Topical metronidazole 0.75% gel (Metrogel) is effective for the papules and pustules of moderate rosacea.36 Metrogel, an antiinflammatory agent and antiparasitic agent, is indicated in patients with infestation of Demodex folliculorum. The use of sunscreens with SPF (sun-protecting factor) of 15 should be encouraged. Topical corticosteroids should not be used because they worsen erythema and telangiectasias and cause rebound flares when discontinued. Systemic therapy also resembles that of acne.3’ Rosacea responds well to oral tetracyclines and erythromycin. Tetracycline should be initiated at 1.0 to 1.5 gm/day. When control is achieved, the dose may be reduced to 250 to 500 mgiday. Isotretinoin is very effective for severe cases with the nodulocystic component. Lasers can be used effectively to treat the telangiectasias and possibly keep the background erythema in some control. Perioral dermatitis. Perioral dermatitis is a disease of the central face that affects primarily young women of childbearing age. It resembles acne and is therefore thought by many authors to be a distinctive acne variant. The cause of this disorder is uncertain. An external irritant, possibly cosmetics or topical corticosteroids, has been suggested as a stimulant.3’, 38 Clinical features. The eruption consists of discrete 1 to 3 mm papules, papulovesicles, and papulopustules. Typically it begins in one nasolabial fold and spreads to become symmetric, involving the chin and upper lip
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while sparing a rim at the vermilion edge. The glabella, eyelids, and forehead may be affected. Pruritus is variable, but a burning sensation is more common. The differential diagnosis includes rosacea, seborrheic dermatitis, contact dermatitis, and acne. Treatment. The treatment is generally successful. Short-term use of systemic tetracyclines ranging in dose from 500 mgiday to 1 gm/day is highly effective.“* The use of topical corticosteroids must be avoided.39 The untreated disease can persist for several years. Its course is marked by periodic exacerbations and remissions. With appropriate therapy the prognosis is excellent with recurrence being uncommon.
Key points 1. In the United States psoriasis affects 1% to 3% of the population. 2. Sudden onset of severe psoriasis may be the first clinical manifestation of infection with the immunodeficiency virus type 1. 3. Calcipotriene ointment 0.005%, a vitamin D analog, is indicated for treatment of moderate plaque psoriasis. Hypercalcemia is a possible and reversible side effect. 4. Diffuse pityriasis rosea can mimic secondary syphilis. 5. Atopic dermatitis affects 10% to 15% of the population. 6. Nipple dermatitis is a very specific manifestation of atopic dermatitis. and lubrication of the skin are of 7. Rehydration prime importance in controlling the symptoms of atopic dermatitis. 8. A total of 8% of 25 to 34-year-olds and 3% of 35to 44-year-olds have acne. 9. A potential androgen excess and polycystic ovary disease should be considered, particularly in the older, treatment-resistant acne patient. 10. Isotretinoin is absolutely contraindicated before or during pregnancy. 11. Minocycline use may result in blue-black pigmentation within acne scars. REFERENCES 1. Stern
RS, Johnson ML, DeLozier J. Utilization of physician services for determatologic complaints. The United States, 1974. Arch Dermatol 1977;113:1062-6. 2. Stern RS, Gardocki GJ. Office-based care of dermatologic disease. J Am Acad Dermatol 1986;14:286-93. 3. Christophers E, Sterry W. Psoriasis. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, eds. Volume 1: dermatology in general medicine. New York: McGrawHill, 1993:489-514. GG, Eyre RW. Trigger factors in psoriasis. In: 4. Krueger Weinstein GW, Voorhees J, eds. Dermatology clinics. Philadelphia: WB Saunders, 1984;373-81. 5. Sadick NS, McNutt NS, Kaplan MH. Papulosquamous dermatoses of AIDS. J Am Acad Dermatol 1990; 22:1270-7.
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6. Bruce S, Epinette WW, Funicella T, et al. Comparative study of calcipotriene (MC903) ointment and fluocinonide ointment in the treatment of psoriasis. J Am Acad Dermato1 1994;31:755-9. 7. Henseler T, Wolff K, Honigsmann T, Christophers E. Oral 8methoxypsoralen photochemotherapy of psoriasis. European PUVA study: a cooperative study among 18 European centers. Lancet 1981;1:853-7. K. Lichen planus. In: Fitzpatrick TB, Eisen AZ, 8. Arndt Wolff K, Freedberg IM, Austin KF, eds. Volume 1: dermatology in general medicine. New York: McGraw-Hill, 1993:1134-44. 9. Scher RK, Fischbein R, Ackerman AB. Twenty nail dystrophy. A variant of lichen planus. Arch Dermatol 1978;114: 612-3. 10. Zaias N. The nail in health and disease. New York: SP Medical and Scientific Books, 1990:113-20. 11. Ellis CN, Voorhees JJ. Etretinate therapy. J Am Acad Dermatol 1987;16:267-91. 12. Lozada F, Silverman S. Topically applied thiocinonide in an adhesive base in the treatment of oral vesiculoerosive diseases. Arch Dermatol 1980;116:898-901. 13. Snyder RA, Schwartz RA, Schneider JS, Elias PM. Intermittent megadose corticosteroid therapy for lichen planus. J Am Acad Dermatol 1982;6:1089-91. 14. Gonzalez E, Momtax-TK, Freedman S. Bilateral comparison of generalized lichen planus treated with psoralens and ultraviolet-A. J Am Acad Dermatol 1984;10:958-61. 15. Ho VC, Gupta AK, Ellis CN, Nickoloff BJ, Voorhees JJ. Treatment of severe lichen planus with cyclosporine. J Am Acad Dermatol 1990;22:64-8. 16 Parsons JM. Pityriasis rosea update. J Am Acad Dermatol 1986;15:159-67. A. Pityriasis rosea. In: Fitzpatrick TB, Eisen AZ, 17 Bjornberg Wolff K, Freedberg IM, Austen KF, eds. Volume 1: dermatology in general medicine. New York: McGraw-Hill, 1993:1117-23. 18 Arndt KA, Paul BS, Stern RS, Parrish JA. Treatment of pityriasis rosea with ultraviolet radiation. Arch Dermatol 1983;119:381-2. dermatitis: clinical aspects. In: Rajka G, 19 Rajka G. Atopic ed. Essential aspects of atopic dermatitis. Berlin: SpringerVerlag, 1989:4-55. JM, Rajka G. Diagnostic features of atopic derma20. Hanifin titis. Acta Dermatol Venereol 1980;92(suppl):44-7. 21. Sampson HA. Atopic dermatitis. Ann Allerg 1992;69:46979. DJ, Cababott F, Glover MT, Hawk JLM. The role 22. Atherton of psoralen chemotherapy (PUVA) in the treatment of severe atopic eczema in adolescence. Br J Dermatol 1988; 178791-5. 23. Sowden JM, Berth Jones J, Ross JS, et al. Double-blind, controlled crossover study of cyclosporin in adults with severe refractory atopic dermatitis. Lancet 1991;338:13740. RL, Schneider L, et al. Thymopentin 24. Leung DYM, Hirsch therapy reduces the clinical severity of atopic dermatitis. J Allerg Clin Immunol 1990;85:927-33. 25. Hanifin JM, Schneider LC, Leung DYM, et al. Recombinant interferon gamma therapy for atopic dermatitis. J Am Acad Dermatol 1993;28:189-97. 26. Plewig G. Seborrheic dermatitis. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, eds. Volume 1: dermatology in general medicine. New York: McGrawHill, 1993:1569-74. 27. Soeprano FF, Schinella RA, Cockerell CJ, Comite SL. Seborrheic-like dermatitis of acquired immunodeficiency syndrome. J Am Acad Dermatol 1986;14:242-8. CL, Barker DC, Haberfeldge G. 28. Heng MCY, Henderson Correlation of pityrosporum ovale density with clinical severity of seborrheic dermatitis as assessed by a simplified technique. J Am Acad Dermatol 1990;23:82-6. 29 Soter NA. Nummular eczematous dermatitis. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF,
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30.
31.
32.
33. 34.
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eds. Volume 1: dermatology in general medicine. New York: McGraw-Hill, 1993:1564-6. Strauss JS. Sebaceous glands. In: Fitzpatrick TB, Eisen AZ, Wolff K. Freedberg IM. Austen KF. eds. Volume 1: dermatology in gene& medicine. New York: McGraw-Hill, 1993:709-26. Lookingbill DP, Horton R, Demers LM, Egan N, Marks JG, Santen RJ. Tissue production of androgens in women with acne. J Am Acad Dermatol 1985;12:481-7. Leyden JJ, Shalita A. Rational therapy for acne vulgaris: an update on topical treatment. J Am Acad Dermatol 1986;15:907-15. Cunliffe WJ. In: Acne. Chicago: Year Book, 1989. Farrell LN, Strauss JS, Stranieri AM. Treatment of severe
35.
36. 37. 38. 39.
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cystic acne with 13-cis-retinoic acid. Evaluation of sebum production and the clinical response in a multiple dose trial. I Am Acad Dermatol 1980:3:602-11. Plewig G. Rosacea. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, eds. Volume 1: dermatology in general medicine. New York: McGraw-Hill, 1993:72?:35. Bleicher PA, Charles IH. Sober AT. Touical metronidazole therapy for’rosacea. &ch Dermitol 1987;123:609-14. Marks R, Black MM. Perioral dermatitis: a histologic study of 26 cases. Br J Dermatol 1971;84:242-7. Wilkinson DS, Kirton V, Wilkinson JD. Perioral dermatitis. Br J Dermatol 1979;101:245-57. Cohen MJ. Perioral dermatitis. J Am Acad Dermatol 1981;4:739-40.
CARE
Common dermatoses Vandana Irvine,
S. Nanda,
MD
California
Skin diseases are an essential part of primary care medicine. Most dermatologic care is delivered in an outpatient setting. The initial evaluation is usually petformed by the primary care physician. Women account for nearly 60% of all visits for dermatologic complaints. (AM J OBSTET GYNECOL 1995;173:488-95.)
Key words:
Papulosquamous
dermatoses,
inflammatory
diseases, acneiform
eruptions
Dermatology is an essential part of primary care medicine. Diseases of the skin are a common occurrence, although the true prevalence of skin disease is difficult to determine. Dermatologic care is delivered mainly in the outpatient setting. As part of the National Ambulatory Care Survey, patients with dermatologic complaints accounted for 7.3% of office-based physician visits. ‘, ’ Women accounted for 58% of all visits for dermatologic complaints. This manuscript focuses on common dermatologic diseases. The topics incIuded are papulosquamous diseases, inflammatory diseases, acne, and acneiform eruptions. Pigmented lesions and cutaneous neoplasms will be the subject of a future article.
Papulosquamous
dermatoses
Psoriasis. In the United States psoriasis affects 1% of the population.” It is a disease characterized by a chronic, relapsing nature. The clinical presentation may be mild with just a few localized plaques limited to the elbows and scalp or quite severe with generalized erythema, scaling, and pustulation. Psoriasis can be disabling in the presence of concomitant joint disease. There is a genetic predisposition to development of psoriasis. One third of patients with psoriasis report having some relative with the disease. There is a 65% concordance for psoriasis in monozygotic twins in contrast to 30% in dizygotic twins.4 There is a bimodal onset of presentation. The peak incidence is at age 22 years and the second peak of onset is around age 55 years. An earlier onset (before puberty) portends more severe disease.
From the Department of Dermatology, University of California, Irvine. Reprint requests: Vandana S. Nanda, MD, lJniversi$ of Calafornia, Irvine Medical Center, Department of Dermatology, Rt. 81, 101 City Dr. South, Orange, CA 92668. Copyright 0 1995 by Mosby-Year Book, Inc. 0002-9378/95 $3.00 + 0 6/l/66025
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Fig. 1. Psoriasis on elbow. Common location. with
thick
white
adherent
Pink papules
scale.
Clinical features. The cutaneous lesions of psoriasis are characteristic and proper diagnosis is easy. The lesions vary from pinpoint red papules to large plaques. The plaques are red, raised, and sharply circumscribed and consist of superficial silvery scales (Fig. 1). Most common areas of involvement are the elbows, the knees, the scalp, the lumbar area, and the umbilicus. In the inverse variant skin folds such as the axilla, the inframammary folds, the genitourinary region, and the neck are involved (Fig. 2). Candidiasis must be ruled out in this clinical setting. Frequently in women the labia majora are involved. Several nail changes are frequent. They range from minor alterations in the nail plate, such as pits, to severe changes showing yellow keratinous substance or complete loss of nail plate (Fig. 3). Several trigger factors or external factors are known to start an onset of or to exacerbate preexisting psoriasis. These include infections, particularly of the upper respiratory tract.” In patients with the human immunodeficiency virus type 1, psoriasis may be the first clinical manifes-
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Fig. 3. Psoriasis plate dystrophy.
Fig.
2. Psoriasis
of labia
of nail,
with
yellow
discoloration
and
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nail
majora.
Stress worsens psori a sis in tation of the infection.’ 30% to 40% of patients. Hormonal influences, such as during pregnancy or while a woman is using oral contraceptives, do not appear to have an effect on triggering or causing a remission in psoriasis. Certain drugs such as lithium, antimalarials, P-adrenergic receptor blockers, and discontinuation of corticosteroids have all been reported to cause or to trigger a flare of psoriasis.3 Treatment. A variety of treatment options is available. These include topical therapies, ultraviolet light, and systemic treatments. The combination of several therapies helps shorten the time to clearing. The topical treatments used for psoriasis are corticosteroids, tars, anthralin, and a newly introduced vitamin D, analog, calcipotriene. Corticosteroids are the most popular, especially for limited extent of involvement. High-potency (Halobetasol propionate, clobetasol propionate, etc.) corticosteroids are invaluable in short-term management, but most patients do well with mid- to lowpotency formulations (e.g., triamcinolone acetonide, alclometasone dipropionate). Ointments are preferable since they keep the plaques greasy. Intensive additional lubrication with greasy ointments such as hydrophilic petrolatum (Aquaphor), petrolatum, or a moisturizing cream (Eucerin) must be stressed and incorporated into the daily treatment regimen. Tar therapy is effective, especially in conjunction with ultraviolet B radiation. This form of therapy is known as the Goeckerman regimen. Anthralin preparations are effective but difficult to
Fig. 4. Lichen plaques. Linear
planus. lesions
Violaceous demonstrate
polygonal Koebner’s
papules and phenomenon.
use as topical therapy because they irritate the skin. Calcipotriene, a new vitamin D, analog, has been shown effective for moderate plaque psoriasis within 8 weeks of therapy.6 It is not to be used on the face because it produces irritation. Calcipotriene ointment avoids the local side effects of corticosteroids (i.e., atrophy and telangiectasia). An elevation of the serum calcium level is a possible and reversible side effect of calcipotriene treatment. Photochemotherapy (methoxsalen plus ultraviolet radiation) and systemic chemotherapy such as methotrexate and cyclosporine are highly effective, but because of serious side effects, their use is limited to patients with extensive disease.7 Lichen planus. Lichen planus is an intensely pruritic eruption. Less than 1% of the population is thought to be affected. There is no racial or sexual predisposition.*
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Fig. 5. Lichen planus of nails, with dystrophia unguium pigmentation.
and
Most patients affected are between the ages of 30 and 60. Clinical features. The lesions of lichen planus are present on the skin and mucous membranes. The classic lesion is a violaceous, flat-topped polygonal papule with a thin scale and delicate white lines known as Wickham’s striae (Fig. 4). Lesions are usually present bilaterally on the flexor aspects of the arms, wrists, sides of the neck, thighs, and shins. Oral and genital mucosa are also involved. The buccal mucosa is most often affected. Lesions are also found on the tongue, lips, pharynx, gastrointestinal tract, and vaginal and vulvar mucosa. The lesions appear to be lacelike. Follicular papules on the scalp can result. As in psoriasis, cutaneous trauma may induce the development of new lesions (Koebner’s phenomenon). Lesions are pruritic but vary in severity. There is a 10% incidence of nail changes, which characteristically include a brown discoloration, longitudinal grooving, splitting, and roughening9 (Fig. 5). Pterygium formation can result from involvement of adjacent paronychial tissue.” There are several drugs that cause lichen planus-like eruptions, such as antimalarials, angiotensin-converting enzyme inhibitors, gold, hypoglycemic agents, and thiazides.” Psoriasis must be considered in the differential diagnosis. Treatment. The treatment of lichen planus can be difficult. Numerous treatments including antibiotics, antimalarials, ultraviolet radiation, vitamins, and heavy metals have been used. None have been confirmed with controlled studies. Corticosteroids are useful in treating lichen planus. Potent topical corticosteroids cause regression of typical cutaneous lesions. Oral lesions should be treated with a topical corticosteroid in a preparation that is adherent to mucous membranes, Intralesional injections of corticostesuch as Orabase.” roids (e.g., triamcinolone acetonide 5 to 10 mgiml) are useful for recalcitrant lesions. More severe, generalized
Fig. 6. Pityriasis rosea. “Herald precedes eruption.
patch’-primary
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cases may be treated with oral corticosteroids, photochemotherapy (methoxsalen and ultraviolet A radiation), and immunomodulators such as cyclosporine.‘“-‘” The course of the disease tends to be long, lasting between several months and years. There are recurrences in 12% to 20% of patients, generally in those who have had extensive cutaneous involvement. Pityriasis rosea. Pityriasis rosea is an acute exuberant skin eruption. The incidence is highest between the ages of 15 and 40 years, and the disease is most prevalent in the spring and autumn.‘” Women are more frequently affected.‘” The cause of pityriasis rosea is unknown. A viral infection is most frequently suggested but has not been proved. Several drugs can cause pityriasis rosea-like eruptions. These include captopril, arsenic compounds, gold, bismuth, clonidine, ketotifen, and barbiturates.” Clinical features. Characteristically, a “Christmas tree” pattern is seen with the lesions distributed in the lines of cleavage of the skin. The disease usually begins with a single “herald” or “mother patch” (Fig. 6), usually preceding the full-blown eruption by 1 to 2 weeks. The individual lesions are oval and salmon-colored with a collarette of scale. The “herald patch” may be confused with a lesion of tinea corporis. The fully developed eruption is generalized, affecting mainly the trunk and sparing the sun-exposed areas. The differential diagnosis includes viral exanthem, guttate psoriasis, and secondary syphilis. Pruritus is usually mild. As the lesions start to involute and become dry, the patients experience more pruritus. Course. The course of pityriasis rosea is mild and can last between 4 and 10 weeks. Occasionally the course may be more protracted. Treatment. Treatment is not necessary except in complicated cases. Ultraviolet B radiation is therapeutic in cases complicated with severe pruritus.‘” Involution of
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Typical
flexural
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lesions may also be expedited with ultraviolet radiation in protracted cases. For dryness and irritation, bland emollients are advised.
Inflammatory
dermatoses
Atopic dermatitis. Atopic dermatitis, also commonly known as eczema, is a chronically relapsing skin condition. It arises in infancy, early childhood, or adolescence. The prevalence of atopic dermatitis has been increasing over the last several decades and now affects 10% to 15% of the population at some point during their lifetime.‘” The cause is unknown. It is associated with marked pruritus, elevated serum immunoglobulin E levels, and a personal or family history of atopic dermatitis, allergic rhinitis, and/or asthma. Defective cell-mediated immunity occurs in up to 80% of affected patientsI It is manifested by increased susceptibility to severe skin infections with viruses (herpes simplex, vaccinia, coxsackie virus), and chronic dermatophyte infections.” Clinical features. The main features include the extremely pruritic nature of the rash, typical morphologic features and distribution, and its tendency toward a chronic course.” The typical lesion is papulovesicular, red, scaly, and possibly crusted (Fig. 7). Other features such as periorbital darkening, infraorbital fold (Morgan’s line or Dennie’s sign), and hyperlinearity of the palms are common but nonspecific. In teenagers and adults the flexural surfaces, face, hands, and feet are frequently involved. Extreme xerosis, lichenification, and hyperpigmentation are common. Patients may have symptom-free periods that may last for months. These patients retain a tendency toward dry skin. Seborrheic dermatitis and contact dermatitis are commonly confused with atopic dermatitis. Treatment. A variety of “trigger factors” that are known to exacerbate the condition must be avoided. These include irritants (soaps, chemicals), heat, humid-
Fig. 8. Seborrheic bial and melolabial
dermatitis. folds.
Erythema
and scaling
in nasola-
ity, wool clothing, and known allergens.” Because atopic skin is dry and pruritic, both these symptoms can be alleviated with hydration. Soaking in plain tepid water daily for 20 minutes followed by immediate lubrication (e.g., Aquaphor, petrolatum, Eucerin) is recommended. In addition, oral antihistamines are used to help control the pruritus. Topical corticosteroids are the mainstay of therapy in atopic dermatitis. Midpotency corticosteroids such as 0.1% triamcinolone ointment or cream are used for general management. Potent fluorinated corticosteroids are used to suppress acute flares. Low-potency corticosteroids such as Aclovate (alclometasone dipropionate) and Desowen (desonide) are used on the face. Use of potent corticosteroids should be limited to 2 weeks for any given lesion. Oral corticosteroids should be avoided since many patients have rebound flares after a short course. Superinfections with Staphylococcus aureus or herpes simplex need appropriate oral antibiotics and antiviral treatment. Ultraviolet light and methoxsalen photochemotherapy are helpful in some patients with recalcitrant conditions.” Cyclosporine, thymopentin, and interferon gamma are other, possibly promising agents for severe cases.23-‘5 Seborrheic dermatitis. Seborrheic dermatitis is common, affecting 2% to 5% of the population, and is easily recognizable.‘6 It affects babies and adults and is associated with increased sebum production of the scalp and hair-bearing areas of the face (i.e., the eyebrows, nasolabial folds, and ears). Seborrheic dermatitis has two age peaks,, one in early infancy and the second around the fourth to seventh decades of life. A markedly higher prevalence and severity are noted in patients with the acquired immunodeficiency syndrome.27 Seborrheic dermatitis is often associated with a variety of neurologic abnormalities and is worsened with emotional stress. The cause of seborrheic dermatitis is unknown.
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Fig. 9. Nummular
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dermatitis. Coin-shaped,
dry pink plaques.
Pityrosporum ovale, a lipophilic yeast, is more abundant in patients with seborrheic dermatitis.” Some authors believe that this microbe is important in the pathogenesis of this disease. Clinical features. Clinically the involved skin of the central face and scalp appears red and inflamed and has a greasy yellow-white scale (Fig. 8).” Prominent follicular openings can be noted. The course is chronic, usually lasting for years to decades. The differential diagnosis commonly includes psoriasis, contact dermatitis, and rosacea. Treatment. Therapy is aimed at reducing the inflammation and scaling. Crusting and scaling in the scalp are removed by nightly applications of topical corticosteroids and keratolytics. Examples of these preparations include Derma-Smoothe/FS (Hill Pharmaceuticals, Inc., Orlando) topical oil T/Gel (Neutrogena Dermatologics, Los Angeles) therapeutic shampoo, P and S (Baker Cummins Pharm., Inc., Miami) liquid, and others. Several recommended shampoos include DHS (Person and Covey, Inc.), zinc, Head and Shoulders (Procter & Gamble, Cincinnati), Ionil Plus (Galderma Laboratories, Inc., Fort Worth), T/Gel, and X Seb (Baker Cummins). Facial inflammation is controllable with low-potency glucocorticosteroids. Side effects of long-term corticosteroid application include atrophy, telangiectasia, corticosteroid rosacea, perioral dermatitis, and acne. Good control is also achieved with topical application of antifungal agents. Preparations of 2% ketoconazole in cream and shampoo formulations have been studied and found effective.‘6 Nummular dermatitis. Nummular dermatitis is defined by its clinical appearance of coin-shaped lesions. The eruption most commonly begins on the legs and can spread to the upper extremities and the trunk. There are two peaks of onset in women, one between 15 and 25 years and the second between 55 and 65 years.
Peak incidence is noted in the winter months. Lesions last from weeks to months with frequent remissions and recurrences. Although the cause is unknown, several causative factors such as bacteria, dry weather conditions, irritability to wool, soaps, and frequent bathing have all been proposed.” Clinical features. The acute eruption appears as tiny pink papules and vesicles that enlarge to form plaques that are coin-shaped (Fig. 9). In the acute lesions there is edema, exudate, and crust formation. The chronic lesion appears dry, scaly, and lichenified. Prominent excoriations may be seen, and the patient may experience moderate to severe pruritus and occasional burning. Treatment. Treatment is aimed at rehydrating the skin by soaking in plain tepid water for 15 to 20 minutes. Mid- to high-potency topical corticosteroids should be applied to involved areas immediately after a bath. Further emolliation with thick creams and petrolatumbased preparations is necessary. Lotions are discouraged because of their net drying effect of component alcohols and water. Topical use of high-potency corticosteroids should be limited to 2 weeks. Pruritus may be treated with Hl antihistamines or with ultraviolet B therapy.‘Y
Acne and acneiform eruptions Acne vulgaris. Acne vulgaris is a self-limited disease seen mostly in adolescents. Acne vulgaris involves the sebaceous hair follicles. The majority of patients are seen in the mid to late teenage years, and since it is common, it is thought to be physiologic. In women acne may persist into the third and fourth decades or later. Acne is less severe in women than in men. The basic cause of acne is not understood, but there are several factors involved in its pathogenesis. Primarily there is altered keratinization within the follicle. Patients with severe acne produce increased amounts of sebum.3” Sebum is comedogenic and inflammatory.“” The predominant organism in the follicle is Propionibacterium acnes, which also produces inflammation.30 Recent studies show that one or more tissue androgens may be increased in acne patients, particularly in older women with a recalcitrant condition3’ Clinical features. The primary sites of acne are the face, chest, and back. Acne lesions may be divided into noninflammatory and inflammatory lesions. Comedones, both open (blackheads) and closed (whiteheads), are noninflammatory. Inflammatory acne is traditionally characterized by the presence of papules, pustules, and nodules (cysts). Resolution of inflammatory lesions may cause erythematous or pigmented macules that can persist for many months. Treatment. The therapeutic modalities used in acne treatment aim to correct the follicular keratinization
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process, decrease follicular bacterial content, decrease sebum production, and produce antiinflammatory action. Topical treatment is very effective for mild acne. Vitamin A acid, tretinoin cream, is comedolytic and highly effective for treatment of comedones.s2 Retin-A (Ortho Pharmaceutical Corp., Dermatological Div., Raritan, N.J.) cream 0.025% can be tolerated by most patients without irritation. Benzoyl peroxide preparations have both antibacterial and antiinflammatory action. These are available in lotions and gels. Topical antibiotics used routinely contain erythromycin or clindamycims3 Systemic antibiotics should be added to the treatment regimen when moderate acne is treated. Tetracycline or its derivatives are most commonly used.30 Initial doses range from 500 to 1000 mg/day. To promote absorption, tetracycline must be taken on an empty stomach. Minocycline is used in patients who are unresponsive to tetracycline, but blue-black pigmentation is a potential side effect. Tetracycline should not be administered to pregnant women because it inhibits skeletal growth and causes irreversible yellow staining of developing teeth. The treatment of severe nodulocystic acne has been revolutionized with the use of isotretinoin, a synthetic oral retinoid. Isotretinoin should be reserved only for patients with severe acne.34 The recommended daily dose is in the range of 0.5 to 1 mg/kg per day. Treatment is necessary for 4 to 5 months. Serum triglyceride levels and liver function tests are obtained before treatment and then repeated monthly. Common side effects include cheilitis, dry mucous membranes, conjunctivitis, pruritus, and xerosis. The greatest concern during isotretinoin therapy is the risk of the drug being administered during pregnancy. Isotretinoin is a teratogen. It affects organogenesis very early in pregnancy. Woman of childbearing age must be fully informed of the risk of pregnancy. Effective contraception must be used, and the manufacturer recommends pretreatment pregnancy testing and continuation during treatment. Rosacea. Rosacea is quite common in fair-skinned people and occurs in the third and fourth decades. It is more common and runs a milder course in women than in men. The pathogenesis of rosacea is unknown. It is accepted that patients with rosacea are predisposed to easy blushing evoked by numerous factors: ultraviolet radiation, heat, cold, spices, alcoholic drinks, and caffeine.35 Clinical features. Rosacea is a disease of the central face. It is present on the nose, medial cheeks, glabella, upper lip, and chin. The sun-exposed areas such as the V of the neck and the back can be involved. Papules and papulopustules are present on bright red erythema (Fig. 10). Telangiectasias are common. Plaquelike edema may be present, in addition to persistent erythema. With disease progression edema becomes a
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Rosacea.
constant feature, telangiectasia enlarges, and facial pores become more prominent. In the worst of cases large inflammatory nodules develop, along with tissue hyperplasia and distortion of facial features. Anterior ocular inflammation (blepharitis, conjunctivitis) is commonly present.35 Treatment. Rosacea is difficult to treat. Treatment is determined by the severity of the disease. Topical erythromycin and clindamycin available in various formulations are effective.3’ Topical metronidazole 0.75% gel (Metrogel) is effective for the papules and pustules of moderate rosacea.36 Metrogel, an antiinflammatory agent and antiparasitic agent, is indicated in patients with infestation of Demodex folliculorum. The use of sunscreens with SPF (sun-protecting factor) of 15 should be encouraged. Topical corticosteroids should not be used because they worsen erythema and telangiectasias and cause rebound flares when discontinued. Systemic therapy also resembles that of acne.3’ Rosacea responds well to oral tetracyclines and erythromycin. Tetracycline should be initiated at 1.0 to 1.5 gm/day. When control is achieved, the dose may be reduced to 250 to 500 mgiday. Isotretinoin is very effective for severe cases with the nodulocystic component. Lasers can be used effectively to treat the telangiectasias and possibly keep the background erythema in some control. Perioral dermatitis. Perioral dermatitis is a disease of the central face that affects primarily young women of childbearing age. It resembles acne and is therefore thought by many authors to be a distinctive acne variant. The cause of this disorder is uncertain. An external irritant, possibly cosmetics or topical corticosteroids, has been suggested as a stimulant.3’, 38 Clinical features. The eruption consists of discrete 1 to 3 mm papules, papulovesicles, and papulopustules. Typically it begins in one nasolabial fold and spreads to become symmetric, involving the chin and upper lip
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while sparing a rim at the vermilion edge. The glabella, eyelids, and forehead may be affected. Pruritus is variable, but a burning sensation is more common. The differential diagnosis includes rosacea, seborrheic dermatitis, contact dermatitis, and acne. Treatment. The treatment is generally successful. Short-term use of systemic tetracyclines ranging in dose from 500 mgiday to 1 gm/day is highly effective.“* The use of topical corticosteroids must be avoided.39 The untreated disease can persist for several years. Its course is marked by periodic exacerbations and remissions. With appropriate therapy the prognosis is excellent with recurrence being uncommon.
Key points 1. In the United States psoriasis affects 1% to 3% of the population. 2. Sudden onset of severe psoriasis may be the first clinical manifestation of infection with the immunodeficiency virus type 1. 3. Calcipotriene ointment 0.005%, a vitamin D analog, is indicated for treatment of moderate plaque psoriasis. Hypercalcemia is a possible and reversible side effect. 4. Diffuse pityriasis rosea can mimic secondary syphilis. 5. Atopic dermatitis affects 10% to 15% of the population. 6. Nipple dermatitis is a very specific manifestation of atopic dermatitis. and lubrication of the skin are of 7. Rehydration prime importance in controlling the symptoms of atopic dermatitis. 8. A total of 8% of 25 to 34-year-olds and 3% of 35to 44-year-olds have acne. 9. A potential androgen excess and polycystic ovary disease should be considered, particularly in the older, treatment-resistant acne patient. 10. Isotretinoin is absolutely contraindicated before or during pregnancy. 11. Minocycline use may result in blue-black pigmentation within acne scars. REFERENCES 1. Stern
RS, Johnson ML, DeLozier J. Utilization of physician services for determatologic complaints. The United States, 1974. Arch Dermatol 1977;113:1062-6. 2. Stern RS, Gardocki GJ. Office-based care of dermatologic disease. J Am Acad Dermatol 1986;14:286-93. 3. Christophers E, Sterry W. Psoriasis. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, eds. Volume 1: dermatology in general medicine. New York: McGrawHill, 1993:489-514. GG, Eyre RW. Trigger factors in psoriasis. In: 4. Krueger Weinstein GW, Voorhees J, eds. Dermatology clinics. Philadelphia: WB Saunders, 1984;373-81. 5. Sadick NS, McNutt NS, Kaplan MH. Papulosquamous dermatoses of AIDS. J Am Acad Dermatol 1990; 22:1270-7.
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6. Bruce S, Epinette WW, Funicella T, et al. Comparative study of calcipotriene (MC903) ointment and fluocinonide ointment in the treatment of psoriasis. J Am Acad Dermato1 1994;31:755-9. 7. Henseler T, Wolff K, Honigsmann T, Christophers E. Oral 8methoxypsoralen photochemotherapy of psoriasis. European PUVA study: a cooperative study among 18 European centers. Lancet 1981;1:853-7. K. Lichen planus. In: Fitzpatrick TB, Eisen AZ, 8. Arndt Wolff K, Freedberg IM, Austin KF, eds. Volume 1: dermatology in general medicine. New York: McGraw-Hill, 1993:1134-44. 9. Scher RK, Fischbein R, Ackerman AB. Twenty nail dystrophy. A variant of lichen planus. Arch Dermatol 1978;114: 612-3. 10. Zaias N. The nail in health and disease. New York: SP Medical and Scientific Books, 1990:113-20. 11. Ellis CN, Voorhees JJ. Etretinate therapy. J Am Acad Dermatol 1987;16:267-91. 12. Lozada F, Silverman S. Topically applied thiocinonide in an adhesive base in the treatment of oral vesiculoerosive diseases. Arch Dermatol 1980;116:898-901. 13. Snyder RA, Schwartz RA, Schneider JS, Elias PM. Intermittent megadose corticosteroid therapy for lichen planus. J Am Acad Dermatol 1982;6:1089-91. 14. Gonzalez E, Momtax-TK, Freedman S. Bilateral comparison of generalized lichen planus treated with psoralens and ultraviolet-A. J Am Acad Dermatol 1984;10:958-61. 15. Ho VC, Gupta AK, Ellis CN, Nickoloff BJ, Voorhees JJ. Treatment of severe lichen planus with cyclosporine. J Am Acad Dermatol 1990;22:64-8. 16 Parsons JM. Pityriasis rosea update. J Am Acad Dermatol 1986;15:159-67. A. Pityriasis rosea. In: Fitzpatrick TB, Eisen AZ, 17 Bjornberg Wolff K, Freedberg IM, Austen KF, eds. Volume 1: dermatology in general medicine. New York: McGraw-Hill, 1993:1117-23. 18 Arndt KA, Paul BS, Stern RS, Parrish JA. Treatment of pityriasis rosea with ultraviolet radiation. Arch Dermatol 1983;119:381-2. dermatitis: clinical aspects. In: Rajka G, 19 Rajka G. Atopic ed. Essential aspects of atopic dermatitis. Berlin: SpringerVerlag, 1989:4-55. JM, Rajka G. Diagnostic features of atopic derma20. Hanifin titis. Acta Dermatol Venereol 1980;92(suppl):44-7. 21. Sampson HA. Atopic dermatitis. Ann Allerg 1992;69:46979. DJ, Cababott F, Glover MT, Hawk JLM. The role 22. Atherton of psoralen chemotherapy (PUVA) in the treatment of severe atopic eczema in adolescence. Br J Dermatol 1988; 178791-5. 23. Sowden JM, Berth Jones J, Ross JS, et al. Double-blind, controlled crossover study of cyclosporin in adults with severe refractory atopic dermatitis. Lancet 1991;338:13740. RL, Schneider L, et al. Thymopentin 24. Leung DYM, Hirsch therapy reduces the clinical severity of atopic dermatitis. J Allerg Clin Immunol 1990;85:927-33. 25. Hanifin JM, Schneider LC, Leung DYM, et al. Recombinant interferon gamma therapy for atopic dermatitis. J Am Acad Dermatol 1993;28:189-97. 26. Plewig G. Seborrheic dermatitis. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, eds. Volume 1: dermatology in general medicine. New York: McGrawHill, 1993:1569-74. 27. Soeprano FF, Schinella RA, Cockerell CJ, Comite SL. Seborrheic-like dermatitis of acquired immunodeficiency syndrome. J Am Acad Dermatol 1986;14:242-8. CL, Barker DC, Haberfeldge G. 28. Heng MCY, Henderson Correlation of pityrosporum ovale density with clinical severity of seborrheic dermatitis as assessed by a simplified technique. J Am Acad Dermatol 1990;23:82-6. 29 Soter NA. Nummular eczematous dermatitis. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF,
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eds. Volume 1: dermatology in general medicine. New York: McGraw-Hill, 1993:1564-6. Strauss JS. Sebaceous glands. In: Fitzpatrick TB, Eisen AZ, Wolff K. Freedberg IM. Austen KF. eds. Volume 1: dermatology in gene& medicine. New York: McGraw-Hill, 1993:709-26. Lookingbill DP, Horton R, Demers LM, Egan N, Marks JG, Santen RJ. Tissue production of androgens in women with acne. J Am Acad Dermatol 1985;12:481-7. Leyden JJ, Shalita A. Rational therapy for acne vulgaris: an update on topical treatment. J Am Acad Dermatol 1986;15:907-15. Cunliffe WJ. In: Acne. Chicago: Year Book, 1989. Farrell LN, Strauss JS, Stranieri AM. Treatment of severe
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cystic acne with 13-cis-retinoic acid. Evaluation of sebum production and the clinical response in a multiple dose trial. I Am Acad Dermatol 1980:3:602-11. Plewig G. Rosacea. In: Fitzpatrick TB, Eisen AZ, Wolff K, Freedberg IM, Austen KF, eds. Volume 1: dermatology in general medicine. New York: McGraw-Hill, 1993:72?:35. Bleicher PA, Charles IH. Sober AT. Touical metronidazole therapy for’rosacea. &ch Dermitol 1987;123:609-14. Marks R, Black MM. Perioral dermatitis: a histologic study of 26 cases. Br J Dermatol 1971;84:242-7. Wilkinson DS, Kirton V, Wilkinson JD. Perioral dermatitis. Br J Dermatol 1979;101:245-57. Cohen MJ. Perioral dermatitis. J Am Acad Dermatol 1981;4:739-40.