7 Seborrheic Dermatitis (Dandruff)

CLINICAL APPLICATION QUESTIONS A somewhat irascible 70-year-old woman with a highly stylized bouffant hairdo com- plains of intolerable scalp pruritus. You notice white flakes on the shoulders of her black sweater. You suspect seborrheic dermatitis. 1. What history should you attempt to elicit from this patient? 2. When you examine this patient’s scalp, what primary and secondary lesions would support your diagnosis of seborrheic dermatitis? 3. Where else on this patient’s body should you look for active dermatitis? 4. How should you approach treatment in this patient? 5. What should you tell this patient is the prognosis for seborrheic dermatitis?

APPLICATION GUIDELINES Specific History Onset Seborrheic dermatitis (SD), and its diminutive scalp variant, dandruff, first appear at puberty, exhibiting a peak incidence in the third and fourth decades. A significant number of cases also occur in elderly patients, where there is an association with chronic neurologic disease, especially Parkinsonism. The disease begins insidiously and patients often delay for long intervals before seeking assistance. Major complaints are usually referable to appearance rather than physical discomfort. Infantile seborrheic dermatitis, which occurs during the first 6 months of life, is controversial and may represent a distinct entity. An extensive discussion is beyond the scope of this book. The disease occurs in otherwise healthy infants and usually remits spontaneously within 2 to 3 months after onset. Scalp lesions clear with Johnson’s Baby Shampoo® and other skin lesions respond to topical treatment with a group VII steroid or a topical macrolactam. Progressive, persistent, or widespread disease opens a large diff- ferential which includes infantile psoriasis, atopic dermatitis, Langerhan’s cell histiocyto- sis, acrodermatitis enteropathica, and several primary immunodeficiency diseases. Under these circumstances a dermatologic consult is advisable.

Evolution of Disease Process Adult SD classically affects the scalp, creases, and hair-bearing areas of the face and ears. On the scalp and other heavy hair-bearing regions, flaking or dandruff is usually the initial complaint. Elsewhere, the appearance of the dermatitis evokes the patient’s atten- tion. Sometimes there is an associated seborrheic blepharitis with complaints of matter- ing, redness, and chronic eye irritation. Infrequently, extensive lesions develop on the

From: Current Clinical Practice: Dermatology Skills for Primary Care: An Illustrated Guide D.J. Trozak, D.J. Tennenhouse, and J.J. Russell © Humana Press, Totowa, NJ

67 68 Part II / Papular, Papulosquamous, Papulo-Vesicular Lesions upper torso and in the body flexures. On rare occasions SD may progress to an extensive erythroderma. Diffuse scalp involvement can cause reversible hair shedding, and some authorities believe SD can hasten the onset and extent of genetic pattern hair loss.

Evolution of Skin Lesions Lesions of SD are usually persistent, but will vary in intensity and extent. Despite years of activity, there is no scarring. Cosmetic effects are usually the overriding concern. Scalp lesions can cause significant pruritus, however, and the blepharitis is associated with itching, crusting, and burning irritation.

Provoking Factors Infrequent shampooing, inadequate body hygiene, and climate conditions, especially long spells of wet weather, exacerbate existing cases and precipitate latent disease. Severe emotional stress, as well as focal and general neurologic conditions, also cause flares. When neurologic injury is focal, the flare of SD is sometimes confined to the distribution of the neurologic deficit. Extensive SD that can be refractory to therapy is very common in HIV disease. It occurs in the context of AIDS-related complex and full-blown AIDS. In these settings, the disease can have an acute and explosive onset.

Self-Medication Self-medication is common and can significantly alter SD. Obtain a history regarding the frequency of shampooing and the use of medicated shampoos. Both of these treat- ments can resolve areas of scalp involvement, which is helpful in establishing a firm diagnosis. If a patient shampoos frequently, ask why. Often the answer is, “My head itches and flakes if I don’t.” Also ask why the patient is using a medicated shampoo preparation. Ask the patient about the use of topical creams. Fluorinated corticosteroids prescribed for other conditions or obtained from friends will initially improve facial seborrhea. With contin- ued use, however, they exacerbate the disease and eventually cause atrophy and a sun- burned appearance, which hides the true nature of the problem.

Supplemental Review From General History SD is limited to the scalp and facial skin in the vast majority of patients. When it is associated with neurologic disease, it occurs as a secondary phenomenon and the neurologic problem is usually quite evident. When SD occurs in an explosive fashion, is refractory to therapy, or occurs in the context of opportunistic infection, an in-depth history for high-risk behavior and other signs and symptoms of HIV infection is indicated. HIV- associated SD can be an early symptom and herald overt AIDS by as much as 2 years.

Dermatologic Physical Exam Primary Lesions 1. Dull to yellow-red patches, usually sharply demarcated (see Photo 14). 2. Trunk lesions may begin as red-brown follicular papules that evolve into patches (uncommon). 3. Patches of erythema develop, may remain discrete or become confluent, but tend to be sharply demarcated. Chapter 7 / Dandruff 69

When seborrhea becomes quite inflammatory, the margins smudge, making the distinction from an eczema more difficult. In most locations, these patches rapidly develop a scale, which aids in the diagnosis.

Secondary Lesions Scale is most commonly loose, easily dislodged, yellow, or yellow-tan, and has an oil- soaked appearance (see Photo 15). Scale that is white but not silvery, always loose, and easily dislodged is common contrary to textbook descriptions (see Photo 16). Scale is particularly heavy in hair-bearing regions such as the scalp and beard. Sometimes the simple act of shaving a beard area is sufficient to promote clearing. Intertriginous seborrhea is sometimes an exception. The scale may be minimal or marginal, making the clinical distinction from monilia and erythrasma difficult. Fissuring is common in intertriginous regions.

Distribution Microdistribution: Follicular papules may be present with early truncal involvement. These usually evolve into patches but can remain present at the margin of larger lesions or as satellites on the adjacent skin (this is usually a subtle feature). Macrodistribution: 1. Hair-bearing areas: scalp, axillae, eyebrows in both men and women, beard, and presternal area in men (see Fig. 6). 2. Creases and folds: nasolabial folds, perialar creases, glabellar creases, postauric- ular creases, intertriginous creases in both men and women, and inframammary creases in women (see Fig. 6). 3. Pinna, concha, and the outer third of the external auditory canal. 4. Eyelid margins. 5. Upper back, shoulders, and chest, usually in the form of large patches, or may be confluent over the whole region in men (see Fig. 6). 6. Generalized erythrodermic form (rare). Involvement of the scalp alone, or combined scalp, ear, and facial SD, are the most common patterns. Eyelid and ear canal involvement is infrequent but not rare. Patch lesions over the upper trunk may simulate pityriasis rosea or pityriasis (tinea) versicolor. These distributions are distinctly uncommon. Confluent activity on the face or upper torso may be very difficult to distinguish from atopic dermatitis. Erythrodermic SD is fortu- nately very rare and must be separated from other causes of erythroderma.

Configuration Petaloid (shaped like petals on a plant) configuration is seen when SD occurs on the central and lateral chest (see Photo 17). Follicular lesions may be seen with early activity on the scalp, brows, and shoulders. These may also be noted at the periphery of large truncal patches.

Indicated Supporting Diagnostic Data Common presentations of SD are clinically diagnostic. No supporting data are indicated. 70 Part II / Papular, Papulosquamous, Papulo-Vesicular Lesions

Figure 6: Macrodistribution of seborrhea.

Less common presentations of SD may simulate atopic dermatitis, pityriasis rosea, psoriasis vulgaris, lichen simplex chronicus, intertrigo, intertriginous monilia, and pityriasis versicolor. 1. Woods lamp examination: SD has a negative examination. 2. KOH preparation of scales: SD has a negative examination. 3. Skin biopsy: As noted above, SD can simulate several other inflammatory der- matitides. Unfortunately, the histology of SD can also show features of each of these disorders. For this reason, biopsy of SD is not a definitive procedure and Chapter 7 / Dandruff 71

should not be undertaken routinely. If the disease is atypical, extensive, or refractory to treatment, it should be referred to a dermatologist, who can best decide whether this expense is cost-effective.

Therapy It is important to stress to SD patients that treatment of this condition is not curative and, at present, is an ongoing process.

Hygiene Proper cleansing and shampooing are sometimes sufficient to control mild SD. These simple measures are often overlooked. This is especially true with older female patients who have their hair done professionally and therefore shampoo infrequently. Determine each patient’s hair care and skin practices and get a feel for how much they are willing to modify this behavior. Once informed, some patients would rather change behavior, while others prefer to maintain their current styling practices and depend entirely on medication for control.

Medicated Shampoos Several types of medicated shampoos are available and effective. Most of these products contain zinc pyrithione, selenium sulfide, sulfur, parachlorometaxylenol, or tar deriv- atives. These are available without prescription and share common ingredients that inhibit growth of Pityrosporum ovale, a yeast inhabitant of the skin implicated in the etiology of SD. Other products that contain salicylic acid are mainly keratolytic. Ketoconazole, which specifically supresses P. ovale, is available as an OTC shampoo and in a more concentrated prescription preparation. Also available by prescription is Loprox® shampoo containing the broad-spectrum antifungal and anti-yeast ingredient ciclopirox. The choice of shampoos is dictated by both effectiveness and cosmetic acceptance. These products should be used initially on a daily or alternate-day basis. The scalp should be lathered with the preparation of choice, which should be left in place for 3 to 5 minutes, then thoroughly rinsed. Most of these shampoos leave the hair coarse and unmanageable; therefore, have patients follow rinsing with an application of conditioner. The conditioning application does not seem to decrease efficacy. Patients should be instructed to guard their eyes during the shampoo rinse-off, as most of these agents are quite irritating to the ocular mucous membranes. After long periods of control, a product will often lose its punch. At this point it is best to rotate the patient to a shampoo with a different active ingredient. Later, one may return to the original product, which will have regained its effectiveness. Disinfecting hair-care tools with a 5-minute application of the medicated shampoo is also recommended on a weekly basis.

Keratolytics Pure keratolytic lotions and ointments will remove scale of SD. This disease has such loose scale and is usually so responsive to treatment that keratolytic products are seldom needed.

Topical Steroids Steroids dramatically improve the treatment of SD. They provide safe, effective, and inexpensive therapy when prescribed appropriately. Facial and truncal seborrhea should 72 Part II / Papular, Papulosquamous, Papulo-Vesicular Lesions be treated with the weaker nonfluorinated steroids in potency groups VI and VII. Products that contain hydrocortisone, desonide, and aclometasone are very effective. These are available in acceptable vanishing cream and lighter lotion bases. The composition of the base is often as critical as the active ingredient. Over-the-counter hydrocortisone preparations often have irritating bases that can override the clinical effect of the steroid. Fluorinated steroid products should be shunned on the facial skin because they can rapidly cause atrophy and induce telangectasia. Although this is uncommon with the weaker products, vigilance is still necessary. Fluorinated steroids have been reported to exacerbate facial seborrhea after an initial period of improvement. For resistant disease, 0.5 to 1% precipitated sulfur can be added to the steroids to enhance effectiveness. Ketoconazole cream compounded with 1 to 2.5% hydrocortisone powder is also very effective and cosmetically more acceptable. Scalp lesions respond well to foam and lotion preparations that contain potency group VI and VII steroids. These products add to the expense of therapy and should be consid- ered adjunctive treatment to proper hygiene and a medicated shampoo. With older female patients who are unwilling to shampoo regularly, steroids may add needed control in between grooming. Although aerosol foams are more expensive, the ease and precision of application makes them cost-effective. Most seborrhea patients prefer products with a foam or alcohol lotion base. Products that contain betamethasone valerate, triamcinolone acetonide, fluocinonide, or clobetasol proprionate are used most often. On rare occasions where heavy scale persists, 1 to 2% salicylic acid can be added to the nonaerosol products for keratolytic effect and to enhance potency. Intertriginous seborrhea usually has an inflammatory and bacteriological component. Ketoconazole cream compounded with 1 to 2.5% hydrocortisone is particularly effective. Iodochlorhydroxoquin 3% with 1% hydrocortisone is also effective, but it stains clothing a bright yellow color.

Topical Antifungal Agents Ketoconazole cream 2% has been demonstrated effective and has been approved for treatment of SD. Loprox® and Oxistat® preparations are equally effective.

Systemic Therapy Systemic agents are indicated only in extensive or extremely refractory disease and only after other entities have been ruled out. Antifungal agents of the azole group can be used in pulse doses to temporarily reduce skin colonization by the yeast P. ovale. Either 200 mg/day fluconazole once weekly or 100 mg itraconazole BID for 1 week out of four until improved should be effective when combined with standard topical measures. Systemic ketoconazole is also effective but has a greater risk of serious side effects. Systemic steroids and retinoids have also been reported effective; however, disease of this severity should be referred to a dermatologic consultant.

Treatment of Seborrheic Blepharitis This is a special and uniquely irritating facet of SD that is often ignored. The lid margins are red and scaly and there is often an associated conjunctivitis, which is very symptomatic. This blepharitis usually responds rapidly to short courses of 10% sodium Chapter 7 / Dandruff 73 sulamyd ophthalmic solution or ointment administered BID. Chlortetracycline and tetra- cycline ophthalmic ointments are also effective. These preparations need be used only intermittently on a symptomatic basis. Products that contain steroids should be avoided, as the steroid is not essential and could mask or exacerbate other unrelated eye conditions.

Conditions That May Simulate Seborrheic Dermatitis Psoriasis Vulgaris Psoriasis vulgaris (PV) of the scalp, face, and ears may be clinically and microscopically indistinguishable from SD. Biopsy is often of no value, as at this point both diseases can show similar findings. Family history and follow-up will usually separate the two. The lesions of PV develop a deeper color, are more raised, and develop a silvery rather than yellow scale. In addition, PV lesions tend to be more fixed and circumscribed than SD lesions. In the absence of other lesions, the presence of linear nail pitting points to a diagnosis of PV.

Bacterial Intertrigo This condition is caused by flexural infection with corynebacteria. It can be difficult to distinguish from flexural SD. Wood’s lamp exam will show a distinct coral-red fluo- rescence with bacterial intertrigo, which is due to a porphyrin secreted by the bacteria.

Intertriginous Monilia Monilia of the inframammary creases, axillae, groins, and external genitalia can develop scale and can simulate intertriginous SD. Satellite lesions, moist fissures, and pus- tules favor monilia. A KOH preparation that demonstrates spores and/or pseudohyphae is definitive (see Part I, Photo 52).

Pityriasis (Tinea) Versicolor Petaloid SD and pityriasis versicolor can have a substantial resemblance to each other. The distribution of SD is usually more limited to the central truncal regions and the scale is evident. Pityriasis versicolor scale usually is evident only after gentle scraping, and the white spotting effect seen after solar exposure does not occur with SD. A KOH preparation revealing grouped spores and short hyphae in pityriasis versicolor distinguishes the two (see Part I, Photo 51).

Pityriasis Rosea Resemblance of generalized SD to pityriasis rosea is fairly superficial. SD lesions have a duskier yellow-red hue and a looser, greasier scale, which does not form a defined collarette. SD lesions also tend to become confluent, whereas PR lesions remain discrete. In addition, SD has a slow gradual onset, and lacks a herald plaque.

Nummular Eczema This common problem should be clinically separable from SD. The lesions of nummular eczema are less numerous and differ in morphology. The wet form has a beefy-red moist surface and the dry form has a fissured surface often compared to the crackle finish on oriental pottery. Both variants of nummular eczema are widely distributed rather than central truncal. Pruritus is intense. 74 Part II / Papular, Papulosquamous, Papulo-Vesicular Lesions

Atopic Dermatitis Inflammatory diffuse facial SD can be difficult to distinguish from atopic dermatitis. Both affect the scalp and face with diffuse erythema. SD tends to produce more scaling, is associated with less pruritus, and does not show the circum-oral pallor or white dermo- graphism of atopic dermatitis. Personal and family histories for other atopic problems are helpful.

Lichen Simplex Chronicus This condition, which occurs frequently in adult women, can be confused with SD when it is localized to the posterior scalp. Patients complain of unremitting itching and the lesions show thickening, lichenification, and excoriation, which are normally absent with SD.

Secondary Syphilis Although this is at present a relatively rare disease, the incidence of syphilis is again rising and it is an important differential diagnosis with any of the papulosquamous diseases. Secondary-stage lues can simulate the facial and petaloid chest lesions of SD. Normally the onset is more abrupt and victims have constitutional symptoms and generalized lymphadenopathy. Usually, other skin lesions are present on the mucous membranes, palms, or soles. Suspicion should prompt a history for high-risk behavior and a syphilis serology. Serologies in this stage are almost universally positive. If negative in the face of strong suspicion, ask the lab to dilute the serum looking for the prozone effect, which can give a false-negative test in patients with very high titers. Negative syphilis titers with active infection have also been reported on rare occasions in HIV infection.

Pediculosis Capitis This differential occurs most often in adult patients who present with severe pruritus and may have minimal scalp finding or concurrent SD. Always look at the hair for evidence of nits. The itching with pediculosis is usually much more severe than that of SD.

ANSWERS TO CLINICAL APPLICATION QUESTIONS History Review A somewhat irascible 70-year-old woman with a highly stylized bouffant hairdo com- plains of intolerable scalp pruritus. You notice white flakes on the shoulders of her black sweater. You suspect seborrheic dermatitis.

1. What history should you attempt to elicit from this patient? Answer: a. How frequently does she shampoo? b. With what does she shampoo her hair? c. Does she frequently wear wigs? Chapter 7 / Dandruff 75

2. When you examine this patient’s scalp, what primary and secondary lesions would support your diagnosis of seborrheic dermatitis? Answer: a. Dull, sharply demarcated red patches. b. Loose, easily dislodged yellow or white scale.

3. Where else on this patient’s body should you look for active dermatitis? Answer: a. Post-auricular folds. b. Concha of the ears. c. Eyebrows. d. Mid-glabella. e. Perinasal, nasolabial, and mental creases of the face. f. Mid-chest and inframammary creases. g. Upper back.

4. How should you approach treatment in this patient? Answer: Treatment approach depends on the patient’s willingness to alter hair style and hygiene practices. The best approach is daily use of an antidandruff shampoo with adjuvant use of a topical steroid when required. Patients who refuse to shampoo regularly will require a topical steroid as primary therapy with use of an antidandruff shampoo.

5. What should you tell this patient is the prognosis for seborrheic dermatitis? Answer: Seborrhea usually responds promptly to treatment. It is however, a lifelong condition subject to exacerbations, and will require lifelong maintenance treatment.