Seborrheic dermatitis – includes patient information sheets
Camila K. Janniger
Seborrheic dermatitis is one of the most common disorders, affecting persons of all ages.(1)(2)(3)(4)(5)(6) It occurs more frequently in infants within the first three months of life and in adults 30 to 60 years of age. In the latter group, it tends to affect men more often than women. In adolescents and adults, seborrheic dermatitis commonly is manifested as “dandruff” or as an erythema of the nasolabial fold, ranging in intensity from barely perceptible to marked. Interest has increased in seborrheic dermatitis in its generalized form in infants with immune deficits(7)(8)(9)(10) and in a more recent association with acquired immunodeficiency syndrome.(11)(12)(13)
In adolescents and adults, seborrheic dermatitis typically presents as mild, greasy scaling of the scalp (Figure 1), with erythema and scaling of the nasolabial folds and retroauricular skin. Seborrheic dermatitis appears in areas of increased sebaceous gland activity, often in association with an oily complexion. It may involve the auricles, beard area, eyebrows, flexures and trunk. Associated blepharitis may be present, sometimes with meibomian gland occlusion and abscess formation. Otitis externa may also occur.[ILLUSTRATION OMITTED]
Two forms of seborrheic dermatitis may be seen on the chest: a common “petaloid” type and a rare “pityriasiform” type.(2) The first form begins as small, reddish-brown follicular and perifollicular papules with a greasy scale. The papules may enlarge to form patches resembling the shape of petals on a flower or similar to a medallion in shape (“medallion” seborrheic dermatitis). The pityriasiform type presents as generalized macules and patches resembling extensive pityriasis rosea but rarely produces an erythroderma.
In infants, a greasy, thick scaling of the vertex of the scalp is common. It is popularly known by the descriptive term “cradle cap”(1)(2)(3)(4)(5)(6) (Figure 2). Cradle cap presents as a dry patch of scaling, overlying, mildly erythematous skin that has become so thickened it forms a cap.[ILLUSTRATION OMITTED]
Patients with seborrheic dermatitis typically show no evidence of acute dermatitis, such as oozing or weeping. Instead, diffuse fine scaling may be white, off-white or yellowish in color. (Drier, larger scales are sometimes termed “psoriasiform” seborrheic dermatitis.(5)) Scaling is often the only manifestation of seborrheic dermatitis in infants, and usually appears in the third or fourth week after birth. The central part of the face, forehead and ears may also be involved. On occasion, the process becomes generalized in otherwise normal, healthy infants. A widespread erythema, often with a cheesy exudate, may also be evident, principally in the flexural folds. Flexural involvement is manifested as diaper dermatitis in infants and as intertriginous and genital eruption in adults. It may also become generalized.
The generalized form of seborrheic dermatitis usually occurs in healthy, normal children; rarely, it may be associated with a variety of immune deficiencies in children, and these children usually also have diarrhea and failure to thrive.(6)(7)(8)(9) Some physicians consider generalized infantile seborrheic dermatitis in children who have immune deficiencies to be the same condition as one that occurred in an epidemic infantile eruption reported under the name “erythroderma desquamativum” in 1908 (Leiner’s disease).
Infants with generalized seborrheic dermatitis, diarrhea and failure to thrive should be evaluated for possible immune deficits, particularly a functional defect in the fifth component of complement.(6) This familial disorder is associated with recurrent infections caused by gram-negative organisms. However, other defects have also been described.(6)(7)(8)(9)(10) In both children and adults, persistent generalized seborrheic dermatitis may be associated with human immunodeficiency virus (HIV) infection.(11)(12)(13) Severe seborrheic dermatitis is quite common in infants who develop HIV-related immune suppression in the first year of life.(14)
An unusually recalcitrant eruption resembling seborrheic dermatitis has been reported in a high percentage of patients with AIDS,(11)(12) with an incidence of up to 83 percent reported in one study(13) (Figure 3).[ILLUSTRATION OMITTED] Seborrheic dermatitis in AIDS patients usually shows a predominance of inflammatory and hyperkeratotic lesions, with involvement of the trunk, groin and extremities. It occasionally progresses to erythroderma, a cradle cap of scales sometimes associated with nonscarring alopecia, and postinflammatory skin changes of either hyperpigmentation or hypopigmentation.
The diagnosis of seborrheic dermatitis is often obvious. However, if the patient fails to respond to therapy, the diagnosis should be reconsidered, unless the patient has AIDS. At times the diagnosis is complicated by the coexistence of other disorders, especially in patients with AIDS, who may also have psoriasis or deep fungal infections such as histoplasmosis.(15)
Psoriasis vulgaris of the scalp, which is common in adults, may be difficult to distinguish from seborrheic dermatitis. The term “sebopsoriasis” is sometimes used to describe sharply demarcated scalp plaques that are difficult to distinguish from pure seborrheic dermatitis or psoriasis. Other evidence of psoriasis, such as psoriasiform lesions elsewhere on the body or pitting of the nails, may also facilitate this distinction.
Seborrheic dermatitis must also be distinguished from atopic dermatitis, tinea capitis and, rarely, histiocytosis X. Atopic dermatitis in adults tends to affect the antecubital and popliteal fossae. Tinea can be diagnosed by the presence of hyphae on cytologic examination with potassium hydroxide, and candidiasis can be demonstrated by pseudohyphae.(16) In tinea versicolor, shorter hyphae are seen, together with spores (the so-called “spaghetti and meatball” pattern).(17)
Seborrheic dermatitis of the groin may resemble dermatophytosis, psoriasis and candidiasis. Seborrheic dermatitis tends to be bilaterally symmetric, with reddishbrown, fine scaling patches that respond promptly to therapy.
At times, rosacea may also require distinction.(18) Patients with rosacea usually display central facial erythema, but at times they may show involvement of the forehead only. Another condition that might be mistaken for seborrheic dermatitis of the face is systemic lupus erythematosus.
In infants, atopic dermatitis has the same sites of predilection as seborrheic dermatitis: the scalp, face, diaper areas and extensor limb surfaces. Axillary involvement favors the diagnosis of seborrheic dermatitis, as do lack of scratching and absence of oozing and weeping. The distinction is made on clinical grounds, since an elevated IgE level is a nonspecific finding in patients with atopic dermatitis.(3) In infants, a form of atopic dermatitis and seborrheic dermatitis with cradle cap may be combined. Infants with this condition may exhibit an increased incidence of atopy that falls between that of normal control subjects and that of typical atopic patients.(4)(5)
Similarly, infants with psoriasiform infantile seborrheic dermatitis have the same incidence of psoriasis vulgaris as those with classic infantile seborrheic dermatitis.(5) However, infants with psoriasiform infantile seborrheic dermatitis have a much lower incidence of atopic dermatitis.
Finally, a rare condition to consider in the differential diagnosis of seborrhea in infants is histiocytosis X. Affected infants have a scaling, seborrheic, dermatitis-like eruption on the scalp that occurs in association with fever and other systemic signs of Letterer-Siwe disease (acute disseminated histiocytosis X).(19) The differential diagnosis of seborrheic dermatitis is summarized in Table 1.
TABLE 1 Differential Diagnosis of Seborrheic Dermatitis
Atopic dermatitis Systemic lupus
Dermatophytosis Tinea capitis
Histiocytosis X Tinea versicolor
Psoriasis vulgaris Vitamin deficiency
Possible Underlying Disorders
Deficiencies of riboflavin, biotin or pyridoxine are said to be associated with seborrheic dermatitis–like eruptions.(20)(21)(22)(23) As noted, seborrheic dermatitis may also be a sign of AIDS. Seborrheic dermatitis may have an increased association with a variety of neurologic disorders, including parkinsonism, postcerebrovascular accidents, epilepsy, central nervous system trauma, facial nerve palsy and syringomyelia.(11)
The etiology of seborrheic dermatitis remains an enigma. It may be hormonally dependent, which would explain why it appears in infancy and often disappears spontaneously before puberty. It may not even be the same disorder in infants as it is in adults. The seborrheic dermatitis of AIDS may also be a different disease than adult and infantile seborrheic dermatitis.(11)(12)(13) Seborrheic dermatitis of AIDS probably represents proliferation of the resident fungus Pityrosporum ovale, caused by a wide variety of factors.(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(34) Culture results from patients with seborrheic dermatitis, as well as therapeutic responses, imply this conclusion.(29)(34) The same conclusion was drawn from culture results in patients with AIDS-associated seborrheic dermatitis.(28)
Studies in which culture of seborrheic dermatitis was performed in infants four to 16 weeks of age showed that P. ovale was a dominant organism.(23)(24)(25)(26)(27)(28) P. ovale was found with significantly more frequency in infants with seborrheic dermatitis than in infants with atopic dermatitis or other infantile dermatoses, or in healthy infants.(23)
A neurogenic theory has been proposed for the development of seborrheic dermatitis that would account for its association with parkinsonism and other neurologic disorders, and its induction by neuroleptic drugs that produce parkinsonian symptoms.(35) The extent of involvement may be impressive when confined to the area affected by syringomyelia or to the paralyzed side in a hemiplegic patient. However, no neurotransmitter chemicals have been identified that account for this phenomenon. It has been postulated that increased pooled sebum in affected areas may be the cause.(36)
It has also been postulated that seborrheic dermatitis may reflect a nutritional deficiency. A deficiency of certain vitamins may result in seborrheic dermatitis–like eruptions.(19)(20)(21)(22) However, no clear linkage has been identified. A recent study(24) of the serum essential fatty-acid patterns from 30 subjects with infantile seborrheic dermatitis suggested a transient impaired function of the enzyme delta 6-desaturase.
Treatment options for seborrheic dermatitis are listed in Table 2. Conventional therapy for adult seborrheic dermatitis of the scalp is a shampoo containing one of the four following compounds: salicylic acid (X-Seb T, Sebulex), selenium sulfide (Selsun, Exsel), coal tar (DHS Tar, Neutrogena T-Gel, Polytar) or pyrithione zinc (DHS Zinc, Danex, Sebulon).(2)(25)(37) Each of these shampoos can be used two to three times a week. After application, shampoos should be left on the hair and scalp for at least five minutes, to ensure that the medication reaches the scalp skin. Adults who have more severe cases may use topical steroid lotions once or twice daily, often in addition to a medicated shampoo.
TABLE 2 Treatment Options for Seborrheic Dermatitis
Preparations Container cost(*) Usage
Coal tar Use two to three
times in first
DHS Tar (0.5%) $ 7.00 (8 oz) then once weekly
as needed; leave
Neutrogena T/Gel 6.00 (8 oz)[dagger] for 5 minutes
(2%) before rinsing
Polytar (2.5%) 7.00 (6 oz)
Denorex (9%) 43.00 (4 oz gel)
42.00 (4 oz liquid)
Extra Strength 45.00 (4 oz)
Chloroxine Use twice weekly;
leave on for 3
Capitrol (2%) 16.00 (4 oz) minutes before
[double dagger] rinsing away
Ketoconazole Use two times
Nizoral (2%) 15.00 (4 oz)
Selenium sulfide Use two to three
Selsun Blue (1%) 3.00 (4 oz) for 2 to 3 minutes
Exsel (2.5%) 13.00 (4 oz)
Selsun (2.5%) 12.00 (4 oz)
Pyrithione zinc Use twice weekly
DHS Zinc (2%) 6.00 (6 oz)
Danex (1%) 6.00 (4 oz)
Sebulon (2%) 6.00 (4 oz)
Shampoo combinations Use twice weekly
X-Seb T (10% coal 6.00 (4 oz)
tar, 4% salicylic
Sebulex (2% sulfur, 6.00 (4 oz)
2% salicylic acid)
Combination products Use twice weekly
Sal-Oil-T (10% coal 6.00 (2 oz hair
tar, 6% salicylic
Sulfacetamide sodium Apply once or twice
Sebizon (10%) 17.00 (2.5 oz lotion) application to
[double dagger] remain on
Corticosteroids Apply once or twice
Hytone (2.5% 15.00 (30 g cream)
Lidex (0.05% 17.00 (15 g cream)
Synalar (0.01% 9.00 (15 g cream)
Valisone (0.1% 15.00 (15 g cream)
Ketoconazole Apply twice daily
Nizoral (2%) 12.00 (15 g cream)
(*)–Estimated cost to the pharmacist based on average wholesale prices, rounded to nearest dollar amount, in Red book. Montvale, N.J.: Medical Economics Data, 1995. Cost to the patient will be higher, depending on prescription filling fee.
([dagger])–Estimated price based on pharmacy cost in Kansas City, Mo., 1995.
([double dagger])–Available by prescription only.
The usual approach to infantile seborrheic dermatitis of the scalp is conservative.(1) A mild, nonmedicated shampoo should be used at the start. If the mild shampoo is not helpful, a shampoo containing coal tar or a shampoo containing 2 percent ketoconazole (Nizoral) or fluconazole can be used to attack the presumed etiologic fungus P. ovale.(22)(23)(24)(25)(26)(27)(28)(29)(30)(31)(32)(33)(38)
In one series,(11) a medicated shampoo was found to be helpful in 25 percent of patients with the often difficult-to-treat HIV–related seborrheic dermatitis. An infant’s scalp can be painted with the common dye eosin to achieve results as good as those achieved with use of topical steroids, but without the potential side effects.(39)
Topical steroids are usually not necessary in infants and should be used with care, since they may be associated with significant percutaneous absorption, local adverse effects and, rarely, suppressed adrenocortical function.(40) However, low-potency topical steroids are more likely to be required for infantile or adult seborrheic dermatitis of the flexural areas or for persistent recalcitrant adult seborrheic dermatitis. In older children and adults, higher potency steroids may be used in lotion form onthe scalp.
A new therapy is borage oil, a topical form of gamma-linoleic acid, which has been described as effective in infantile seborrheic dermatitis.(41) In adolescents, the potential of emotional distress brought on by severe seborrheic dermatitis, as well as the danger of home remedies, must be kept in mind. In one case,(42) a teenager apparently used an organic solvent as self-medication, resulting in a fatal intoxication.
A patient information handout on seborrheic dermatitis is provided on page 159.
Figure 2 (lower photograph) reprinted with permission from Cutis 1993; 51:233-5.
(1.)Janniger CK. Infantile seborrheic dermatitis: an approach to cradle cap. Cutis 1993; 51:233-5.
(2.)Gardner SS, McKay M. Seborrhea, psoriasis and the papulosquamous dermatoses. Prim Care 1989; 16:739-63.
(3.)Williams ML. Differential diagnosis of seborrheic dermatitis. Pediatr Rev 1986; &:204-11.
(4.)Podmore P, Burrows D, Eedy DJ, Stanford CF. Seborrhoeic eczema–a disease entity or a clinical variant of atopic eczema? Br J dermatol 1986; 115:341-50.
(5.)Menni S, Piccinno R, Baietta S, Ciuffreda A, Scotti L. Infantile seborrheic dermatitis: seven-year follow-up and some prognostic criteria. Pediatr Dermatol 1989; 6:13-5.
(6.)Glover MT, Atherton DJ, Levinsky RJ. Syndrome of erythroderma, failure to thrive, and diarrhea in infancy: a manifestation of immunodeficiency. Pediatrics 1988; 81:66-72.
(7.)Sonea MJ, Moroz BE, Reece ER. Leiner’s disease associated with diminished third component of complement. Pediatr Dermatol 1987; 4:105-7.
(8.)Jacobs JC, Miller ME. Fatal familial Leiner’s disease: a deficiency of opsonic activity of serum complement. Pediatrics 1972; 49:225-32.
(9.)Miller ME, Seals J, Kay R, et al. A familial plasma-associated defect of phagocytosis: a new cause of recurrent bacterial infections. Lancet 1968; 2:60-3.
(10.)Goodyear HM, Harper JI. Leiner’s disease associated with metabolic acidosis. Clin Exp Dermatol 1989; 14:364-6.
(11.)Sadick NS, McNutt NS, Kaplan MH. Papul-squamous dermatoses of AIDS. J Am Acad Dermatol 1990; 22(6 Pt 2):1270-7.
(12.)Cockerell CJ. Cutaneous manifestations of HIV infection other than Kaposi’s sarcoma: clinical and histologic aspects. J Am Acad Dermatol 1990; 22(6 Pt 2):1260-9.
(13.)Mathes BM, Douglass MC. Seborrheic dermatitis in patients with acquired immunodeficiency syndrome. J Am Acad Dermatol 1985; 13:947-51.
(14.)Prose NS. Cutaneous manifestations of pediatic HIV infection. Pediatr Dermatol 1992; 9:326-8.
(15.)Chaker MB, Cockerell CJ. Concomitant psoriasis, seborrheic dermatitis, and disseminated cutaneous histoplasmosis in a patient infected with human immunodeficiency virus. J Am Acad Dermatol 1993; 29(2 Pt 2): 311-3.
(16.)Soyer HP, Cerroni L. The significance of histopathology in the diagnosis of dermatomycoses. Acta Dermatovenerologica Alpina Panonica et Adriatica 1992; 1:84-7.
(17.)Michalowski R, Rodziewicz H. Pityriasis versicolor in children. Br J Dermatol 1963; 75:397-400.
(18.)Nowicki R, Siedlewicz A, Wilkowska A, Sadowska E, Jasiel E, Czubek M, et al. Demodicosis (acne rosacea demodes). Przegl Dermatol 1993; 80:568-70.
(19.)Zackheim H. Cutaneus lymphoma, leukemia, and related disorders. In: Schwartz RA, ed. Skin cancer: recognition and management. New York: Springer-Verlag, 1988:162-84.
(20.)Prendiville JS, Manfredi LN. Skin signs of nutritional disorders. Semin Dermatol 1992; 11:88-97.
(21.)Brenner S, Horwitz C. Possible nutrient mediators in psoriasis and seborrheic dermatitis. II. Nutrient mediators: essential fatty acids; vitamins A, E and D; vitamins B1, B2, B6, niacin and biotin; vitamin C selenium; zinc; iron. World Rev Nutr Diet 1988; 55:165-82.
(22.)Nisenson A. Seborrheic dermatitis of infants and Leiner’s disease. J Pediatr 1957; 51:537-48.
(23.)Ruiz-Maldonado R, Lopez-Matinez R, Perez Chavarria EL, Rocio Castanon L, Tamayo L. Pityrosporum ovale in infantile seborrheic dermatitis. Pediatr Dermatol 1989; 6:16-20.
(24.)Tollesson A, Frithz A, Berg A, Karlman G. Essential fatty acids in infantile seborrheic dermatitis. J Am Acad Dermatol 1993; 28:957-61.
(25.)Rebora A, Rongioletti F. The red face: seborrheic dermatitis. Clin Dermatol 1993; 11:243-51.
(26.)Bergbrant IM, Faergemann J. The role of Pityrosporum ovale in seborrheic dermatitis. Semin Dermatol 1990; 9:262-8.
(27.)Broberg A, Faergemann J. Infantile seborrhoeic dermatitis and Pityrosporum ovale. Br J Dermatol 1989; 120:359-62.
(28.)Ashbee HR, Ingham E, Holland KT, Cunliffe WJ, Gowland G. The role of Malassezia furfur serovars A, B, and C in pityriasis versicolor and seborrhoeic dermatitis [Abstract]. Br J Dermatol 1991; 125:495.
(29.)Faergemann J. Seborrhoeic dermatitis and Pityrosporum orbiculare: treatment of seborrhoeic dermatitis of the scalp with miconazole-hydrocortisone (Daktacort), miconazole and hydrocortisone. Br J Dermatol 1986; 114:695-700.
(30.)Groisser D, Bottone EJ, Lebwohl M. Association of Pityrosporum orbiculare (Malassezia furfur) with seborrheic dermatitis in patients with acquired immunodeficiency syndrome (AIDS). J Am Acad Dermatol 1989; 20(5 Pt 1):770-3.
(31.)Taieb A, Legrain V, Palmier C, Lejean S, Six M, Maleville J. Topical ketoconazole for infantile seborrhoeic dermatitis. Dermatologica 1990; 181:26-32.
(32.)Urbanowski S, Gwiezdzinski Z, Nierebinska E. Contemporary views on the etiopathogenesis and treatment of seborrheic dermatitis and dandruff. Przegl Dermatol 1992; 79:402-8.
(33.)Wasik F, Baran E, Blizanowska A, Barancewicz-Losek M, Kidler-Nockowska M, Kaniowska E, et al. Clinical efficacy of 1% metronidazole cream and gel. Przegl Dermatol 1993; 80:172-9.
(34.)Heng MC, Henderson CL, Barker DC, Haberfelde G. 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.
(35.)Binder RL, Jonelis FJ. Seborrheic dermatitis in neuroleptic-induced parkinsonism. Arch Dermatol 1983; 119:473-5.
(36.)Cowley NC, Farr PM, Shuster S. The permissive effect of sebum in seborrhoeic dermatitis: an explanation of the rash in neurological disorders. Br J Dermatol 1990; 122:71-6.
(37.)Marks R, Pearse AD, Walker AP. The effects of a shampoo containing zinc pyrithione on the control of dandruff. Br J Dermatol 1985; 112:415-22.
(38.)Rigopoulos D, Katsambas A, Antoniou C, Theocharis S, Stratigos J. Facial seborrheic dermatitis treated with fluconazole 2% shampoo. Int J Dermatol 1994; 33:136-7.
(39.)Shohat M, Mimouni M, Varsano I. Efficacy of topical application of glucocorticosteroids compared with eosin in infants with seborrheic dermatitis. Cutis 1987; 40:67-8.
(40.)Turpeinen M, Salo OP, Leisti S. Effect of percutaneous absorption of hydrocortisone on adrenocortical responsiveness in infants with severe skin disease. Br J Dermatol 1986; 115:475-84.
(41.)Tollesson A, Frithz A. Borage oil, an effective new treatment for infantile seborrhoeic dermatitis [Letter]. Br J Dermatol 1993; 129:95.
(42.)Burnett HW, Levine B, Smyth D. An unfortunate complication of self-therapy for seborrheic dermatitis. Cutis 1988; 41:284.
RELATED ARTICLE: Seborrheic Dermatitis: What It is and How to Treat It
What is seborrheic dermatitis?
Seborrheic dermatitis is a disease that causes flaking of the skin. It usually affects the scalp. In adolescents and adults, it is commonly called “dandruff.” In babies, it is known as “cradle cap.” Seborrheic dermatitis can also affect the skin on other parts of the body, such as the face and chest, and creases of the arms, legs and groin. Seborrheic dermatitis usually causes the skin to look a little greasy, and scaly or flaky.
Seborrheic dermatitis most often occurs in babies younger than three months of age and in adults from 30 to 60 years of age. In adults, it’s more common in men than in women.
What causes seborrheic dermatitis?
The exact cause of seborrheic dermatitis isn’t known. The cause may be different in infants and adults. Seborrheic dermatitis may be related to hormones, because the disorder often appears in infancy and disappears before puberty. Or the cause might be a fungus, called Pityrosporum ovale. This organism is normally present in the skin in small numbers, but sometimes its numbers increase, resulting in the skin disease.
Seborrheic dermatitis has also been linked to neurologic disorders such as Parkinson’s disease and epilepsy. The reason for this relationship isn’t known.
How is seborrheic dermatitis treated?
The treatment of seborrheic dermatitis depends on its location on the body. Treatment also depends on the age of the person affected.
SEBORRHEIC DERMATITIS OF THE SCALP (DANDRUFF) IN ADULTS AND ADOLESCENTS
Dandruff is usually treated with a shampoo that contains salicylic acid (X-Seb T, Sebulex), selenium sulfide (Selsun, Exsel) or pyrithione zinc (DHS Zinc, Danex, Sebulon). These shampoos can be used twice a week. Shampoos with coal tar (DHS Tar, Neutrogena T-Gel, Polytar) can be used three times a week. If you have dandruff, you might start by using one of these shampoos daily until your dandruff is controlled, and then use it two or three times a week.
When you use a dandruff shampoo, rub the shampoo into your hair thoroughly and let it stay on your hair and scalp for at least five minutes before rinsing, to make sure it has time to work.
If the shampoo alone doesn’t help, your doctor might want you to use steroid lotions (Hytone, Synalar, Valisone) once or twice daily, in addition to the shampoo.
SEBORRHEIC DERMATITIS OF THE FOLDS OF THE SKIN IN ADOLESCENTS AND ADULTS
Steroid lotions may be used in adolescents and adults.
SEBORRHEIC DERMATITIS OF THE SCALP (CRADLE CAP) IN BABIES
Seborrheic dermatitis of the scalp in babies is treated with products that are not as strong as those used in adults. You might start with a mild, nonmedicated baby shampoo. If that doesn’t work, you can switch to a shampoo that contains tar. Or you can try a shampoo that contains 2% ketoconazole (Nizoral).
SEBORRHEIC DERMATITIS OF THE SKIN CREASES IN BABIES
Gentle steroid lotions or creams may be used to treat seborrheic dermatitis in the skin creases of babies.
This information provides a general overview on seborrheic dermatitis and may not apply to everyone. Talk to your family doctor to find out if this information applies to you and to get more information on this subject.
This handout is provided to you by your family doctor and the American Academy of Family Physicians.
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