Version May 2024
INTRODUCTION — Seborrheic dermatitis is a chronic, relapsing, and usually mild form of dermatitis that occurs in infants and adults. The severity may vary from minimal, asymptomatic scaliness of the scalp (dandruff) to more widespread involvement. Affected individuals are usually healthy, although seborrheic dermatitis has been associated with human immunodeficiency virus (HIV) infection, Parkinson disease and other neurologic disorders, and use of neuroleptic medications.
This topic will discuss the pathogenesis, clinical manifestations, and management of seborrheic dermatitis in adolescents and adults. The infantile form of seborrheic dermatitis is discussed separately. (See "Cradle cap and seborrheic dermatitis in infants".)
EPIDEMIOLOGY — Seborrheic dermatitis has a biphasic incidence, occurring in infants between the ages of 2 weeks and 12 months and later during adolescence and adulthood. The prevalence of clinically significant seborrheic dermatitis is approximately 3 percent, with peak prevalence in the third and fourth decades [1]. The actual prevalence is probably much higher when mild cases are included. Males are affected more frequently than females.
The prevalence of seborrheic dermatitis is increased among individuals with HIV infection, in whom it may be a presenting sign. The prevalence has been estimated to be around 35 percent among patients with early HIV infection and up to 85 percent among patients with acquired immunodeficiency syndrome (AIDS) [2,3].
Patients with parkinsonism frequently present with seborrhea (oily skin) and seborrheic dermatitis, both of which may improve with L-DOPA therapy [4,5]. (See "Clinical manifestations of Parkinson disease", section on 'Nonmotor symptoms'.)
PATHOGENESIS — The cause of seborrheic dermatitis is not known. Seborrheic dermatitis is not a disease of the sebaceous glands nor is the rate of sebum excretion increased in patients with seborrheic dermatitis [6]. Nonetheless, sebaceous glands appear to be involved in the development of seborrheic dermatitis as indicated by the predilection for body sites with increased numbers of sebaceous glands and larger sebaceous glands (face, scalp, upper trunk, external auditory meatus, and anogenital area). In addition, the infantile form is common early in the first year of life, when androgen-producing, enlarged, neonatal adrenal glands and transplacental transfer of maternal androgens stimulate the growth of the infant's sebaceous glands.
●Malassezia colonization – Sebaceous glands may play a permissive role in the pathogenesis of seborrheic dermatitis, possibly by creating a favorable milieu for the growth of fungi of the genus Malassezia. The lipid-dependent Malassezia (formerly known as Pityrosporum ovale) is a saprophyte of normal skin that thrives at the sites of predilection for seborrheic dermatitis [7,8]. The use of molecular markers, such as 26S rDNA, ITS, and 5.8S, has allowed for better species identification and revealed intraspecies differences that could be related to pathogenicity [9,10]. However, there is limited direct evidence that Malassezia is implicated in the etiology of seborrheic dermatitis. Studies have failed to demonstrate a higher density of Malassezia on the skin of affected individuals or a relationship between the intensity of skin colonization and the severity of seborrheic dermatitis, although some specific Malassezia species have been detected more frequently on affected skin than on nonaffected skin [11-13]. A higher density of Malassezia has been demonstrated in patients with Parkinson disease and seborrheic dermatitis compared with controls, with a predominance of Malassezia globosa displaying high production of lipases and phosphatases [14].
Indirect evidence for a role of Malassezia in seborrheic dermatitis derives from the observation that most of the effective therapeutic agents have antifungal activity. However, the nonspecific, anti-inflammatory effect of the azole antifungal agents commonly used for seborrheic dermatitis may also explain their efficacy, given that some studies have been unable to demonstrate in vivo a decrease in Malassezia colonization after treatment with topical ketoconazole [15].
Observational studies suggest that, in some patients, seborrheic dermatitis may result from the host's immune response to Malassezia or to its byproducts [16,17]. Other studies, however, were unable to find humoral or cellular immunologic abnormalities in patients with seborrheic dermatitis [18]. The inflammation of seborrheic dermatitis may be mediated by the innate immune system response to irritants produced by Malassezia, including free fatty acids, lipase, and reactive oxygen species [16]. The lipases and phospholipases produced by Malassezia cleave free fatty acids from triglycerides present in sebum, which are known irritants and can induce inflammation. In addition, lipases and phosphatases damage surrounding cells with the release of oleic and arachidonic acid from their walls. Arachidonic acid is further metabolized by cyclooxygenase in proinflammatory eicosanoids [14]. Additional factors that may be playing a role in the inflammation of seborrheic dermatitis include oxidative stress and the overproduction of cell-damaging oxygen radicals [19]. The cascade of inflammation leads to the increased production of numerous cytokines ascribed to activation of T lymphocytes of T helper type 2 (Th2) lineage, such as interleukin (IL) 1, 2, 4, 8, and possibly 17; interferon (IFN)-gamma; and tumor necrosis factor (TNF)-alpha [20].
●HIV infection – The reason for the increased susceptibility of patients with HIV infection to seborrheic dermatitis is not known. A transgenic mouse deficient in CD4+ and CD8+ cells has been shown to develop a seborrheic dermatitis-like skin disease, an overgrowth of yeast cells in hair follicles, and an improvement with fluconazole [19]. This suggests that dysregulation of the immune system may play a role in the increased prevalence of seborrheic dermatitis in the immunocompromised host.
●Neurologic disorders – The relationship between seborrheic dermatitis and neurologic disorders is also poorly understood. Patients with Parkinson disease often have increased sebum production; in these patients, seborrhea and seborrheic dermatitis improve with L-DOPA therapy [4,5].
CLINICAL MANIFESTATIONS — Seborrheic dermatitis may first appear soon after puberty or later in life. It is usually characterized by well-demarcated, erythematous plaques with greasy-looking, yellowish scales distributed on areas rich in sebaceous glands, such as the scalp, the external ear, the center of the face, the upper part of the trunk, and the intertriginous areas (picture 1A-C).
Scalp — The mildest and most common form of scalp seborrheic dermatitis is dandruff, also known as pityriasis sicca, in which the scalp shows fine, white, diffuse scaliness without underlying erythema (picture 2). Dandruff may be asymptomatic or accompanied by mild pruritus. More severe forms of scalp seborrheic dermatitis present with visible inflammation, consisting of patchy, orange to salmon-colored or grayish plaques covered with yellowish, greasy scales (pityriasis steatoides), mostly over the temporoparietal areas (picture 3A-B) or with concretions of scale around hair shafts (pityriasis amiantacea) (picture 3C). Lesions may extend to the postauricular areas (picture 1B), where they often develop fissures, oozing, and crusting, and to the outer canal and concha of the ear, sometimes with marked pruritus and superinfection (otitis externa). (See "External otitis: Pathogenesis, clinical features, and diagnosis", section on 'Pathogenesis and risk factors'.)
Face — Facial lesions favor the forehead below the hairline, the eyebrows and glabella (picture 3B), and the nasolabial folds. They may extend to the cheeks and malar areas in a butterfly distribution; depending on a person's skin color, lesions may look pink or red, ashy gray, or darker than normal skin (picture 1C-E). The mustache and beard area are frequently involved in patients with facial hair. Shaving helps with treatment and control of the disease.
Periocular — Blepharitis with redness of the free margin of the eyelids and yellow crusting between the eyelashes may be the sole manifestation of seborrheic dermatitis or may accompany its more classic distribution. (See "Blepharitis", section on 'Clinical findings'.)
Trunk — Five patterns of truncal involvement have been described:
●Moist, erythematous intertrigo of the axillae, inframammary folds, umbilicus, and genitocrural area (picture 3D)
●The "petaloid pattern," consisting of polycyclic, finely scaly, thin plaques over the sternum or interscapular area
●Annular or arcuate, round to oval, slightly scaly plaques on the trunk, sometimes with hypopigmented central clearing, known as "seborrheic eczematids"
●The pityriasiform pattern mimicking pityriasis rosea, comprised of 5 to 15 mm, oval-shaped, scaly lesions distributed along the skin tension lines
●The psoriasiform pattern with larger red, rounded plaques, covered with thicker scales
In patients with HIV — Seborrheic dermatitis tends to be more extensive and severe in patients with HIV/AIDS. It sometimes involves unusual sites, such as the extremities, and may be difficult to control [3,21]. Seborrheic dermatitis is frequently observed in patients with CD4 counts <400 cells/microL and is more diffuse and severe in patients with CD4 counts <200 cells/microL [22,23]. It may regress with antiretroviral therapy (ART). However, seborrheic dermatitis may also be a cutaneous manifestation of the immune reconstitution inflammatory syndrome in patients on ART [24]. (See "Immune reconstitution inflammatory syndrome", section on 'Miscellaneous syndromes possibly associated with IRIS'.)
CLINICAL COURSE — Seborrheic dermatitis is a chronic, relapsing condition that may go on for decades. It tends to worsen with stress and during the cold and dry winter months. It tends to improve during the summer months, probably from sun exposure, although it may be precipitated by psoralen plus ultraviolet A (PUVA) therapy [25]. The available treatments do not cure seborrheic dermatitis and must be continued or repeated intermittently to prevent recurrence. (See 'Management' below.)
DIAGNOSIS — The diagnosis of seborrheic dermatitis is usually made clinically based on the appearance and location of the lesions. (See 'Clinical manifestations' above.)
Biopsy is not routinely necessary but may be indicated when the diagnosis is uncertain. (See 'Differential diagnosis' below.)
Histopathology — There are no uniquely characteristic or pathognomonic histologic features in seborrheic dermatitis. In patients who are HIV negative, histology shows focal parakeratosis in the horny layer of the epidermis; mounds of scale-crusts with pyknotic neutrophils on the lips of dilated, sometimes plugged, follicular ostia; psoriasiform acanthosis; and mild to moderate spongiosis. The dermis harbors a sparse, perivascular, lymphohistiocytic, inflammatory infiltrate. In chronic cases, the histologic picture may be difficult to distinguish from psoriasis, but the presence of even a minimal degree of spongiosis should favor a diagnosis of seborrheic dermatitis.
In patients with HIV/AIDS, the histopathologic changes parallel the severity of the disease. Parakeratosis is more widespread, and the epidermis shows necrotic keratinocytes. Spongiosis is less prominent; the inflammatory infiltrate is denser and, in some areas, obliterates the dermoepidermal junction. It contains numerous plasma cells and foci of leukocytoclasis [3].
DIFFERENTIAL DIAGNOSIS — The differential diagnosis of seborrheic dermatitis includes psoriasis, rosacea, tinea versicolor, pityriasis rosea, tinea corporis, secondary syphilis, systemic lupus erythematosus (SLE), and pemphigus foliaceous. Most of these conditions can be distinguished clinically. Syphilis, SLE, and pemphigus foliaceous require laboratory confirmation. Allergic contact dermatitis may also be considered, particularly when the presentation is atypical or pruritus is significant.
●Psoriasis – Psoriasis is the main condition in the differential diagnosis of seborrheic dermatitis in adolescents and adults. Sometimes the two diseases may coexist, and the term "sebopsoriasis" has been given to those cases where the distinction cannot be made. Usually, however, psoriatic lesions are sharply demarcated and erythematous, and the scales are more abundant and silvery white (picture 4). In most cases, the extensor areas (eg, the elbows and knees) are involved, although the lesions can occur in the body folds (inverse psoriasis) (picture 5). Characteristic nail changes (picture 6A-B) as well as the presence of arthritis or a positive family history may help establish the diagnosis of psoriasis. (See "Psoriasis: Epidemiology, clinical manifestations, and diagnosis", section on 'Clinical manifestations'.)
●Rosacea – Rosacea is another condition that commonly targets the face and sometimes coexists with seborrheic dermatitis. In contrast with seborrheic dermatitis, rosacea shows a predominance of telangiectasias and papulopustules, with frequent involvement of the nose, malar, and perioral areas and minimal or no scaliness (picture 7A-E). (See "Rosacea: Pathogenesis, clinical features, and diagnosis", section on 'Clinical features'.)
●Allergic contact dermatitis – Allergic contact dermatitis may be suspected in patients with seborrheic dermatitis that does not respond to standard therapy, especially if pruritus is the predominant symptom. Allergic contact dermatitis may occur concurrently or be a complication of seborrheic dermatitis in patients allergic to components of topical medications for seborrheic dermatitis or regular skin and hair care products. Patch testing may be necessary to confirm the diagnosis [26,27]. (See "Clinical features and diagnosis of allergic contact dermatitis".)
●Tinea versicolor – On the trunk, petaloid lesions of seborrheic dermatitis may be mistaken for tinea versicolor, which usually lacks erythema (picture 8). (See "Tinea versicolor (pityriasis versicolor)", section on 'Clinical features'.)
●Pityriasis rosea – Pityriasis rosea is distinguished from seborrheic dermatitis by its abrupt onset, presence of a herald patch, and resolution within a few weeks (picture 9A-B). The pityriasiform variant of seborrheic dermatitis should be suspected when lesions appear more progressively, persist for more than three months, and are accompanied by lesions on areas usually spared by pityriasis rosea (the face and intertriginous areas). (See "Pityriasis rosea", section on 'Clinical features'.)
●Tinea corporis – Annular or arciform seborrheic dermatitis lesions on the trunk can be confused with tinea corporis (picture 10). Tinea corporis can be ruled out by negative potassium hydroxide (KOH) microscopic examination and negative fungal culture. (See "Dermatophyte (tinea) infections", section on 'Tinea corporis'.)
●Secondary syphilis – Secondary syphilis, the great imitator, can trigger widespread, pityriasiform or psoriasiform eruptions that can be mistaken for seborrheic dermatitis. Additional signs (eg, palmoplantar and mucosal lesions or peripheral adenopathy) should be looked for, and appropriate serologic testing should be ordered when indicated.
●Lupus erythematosus – Seborrheic dermatitis of the face may be mistaken for the butterfly eruption of acute SLE or the discoid plaques of cutaneous lupus erythematosus (picture 11A-B). The acute eruption of SLE rarely involves the nasolabial sulcus or crosses the bridge of the nose. Discoid lesions exhibit atrophy and sometimes scarring, along with adherent scales that may have "carpet tacking" on their undersurface (spiny projections that plug dilated, follicular openings). Histologic examination and serologic testing for antinuclear autoantibodies should be performed to confirm the diagnosis. (See "Overview of cutaneous lupus erythematosus".)
●Pemphigus foliaceous – Pemphigus foliaceous is characterized by erythema, scaling, painful erosions, and crusting that first appear on the face and scalp (picture 12A) and later involve the chest and back. Histology, direct immunofluorescence, and the measurement of circulating autoantibodies against desmoglein establish the diagnosis. Pemphigus erythematosus of Senear and Usher is a superficial variant of pemphigus foliaceous that is most likely to mimic seborrheic dermatitis. (See "Pathogenesis, clinical manifestations, and diagnosis of pemphigus", section on 'Pemphigus foliaceus'.)
MANAGEMENT — Topical antifungal agents (eg, ketoconazole, other azoles, ciclopirox olamine) are well established in the treatment of seborrheic dermatitis of the scalp and face because of their ability to decrease the population of Malassezia furfur on the affected skin and their anti-inflammatory property [28,29]. Topical anti-inflammatory agents (eg, topical corticosteroids, topical calcineurin inhibitors) are also frequently used for seborrheic dermatitis alone or in combination with topical antifungals.
Goal of treatment — Seborrheic dermatitis is a chronic condition. The main goal of therapy is to clear the visible signs of the disease and reduce associated symptoms, such as erythema and pruritus. Repeated treatment or long-term maintenance treatment is often necessary. (See 'Prevention of relapse' below.)
Seborrheic dermatitis of the scalp — Seborrheic dermatitis of the scalp is managed with antifungal shampoos, with or without topical corticosteroids, depending on dermatitis severity (algorithm 1). The addition of a shampoo containing a keratolytic agent (eg, salicylic acid) may be helpful for patients with thick scale.
●Mild dermatitis (dandruff) – For patients with mild seborrheic dermatitis of the scalp who have diffuse, fine desquamation without inflammation (dandruff), we suggest treatment with an antifungal shampoo. Antifungal shampoos include ketoconazole 2% and ciclopirox 1% (available by prescription) and zinc pyrithione 1% and selenium sulfide 2.5% shampoo (available over the counter).
●Moderate to severe dermatitis – For patients with moderate to severe seborrheic dermatitis of the scalp who have scale, inflammation, and pruritus, we suggest treatment with an antifungal shampoo (eg, ketoconazole 2% shampoo) in combination with a high-potency topical corticosteroid (table 1) in a formulation (lotion, spray aerosol, foam, or shampoo) of the patient's choice. Topical corticosteroids can be used daily for two weeks and then intermittently (eg, twice weekly).
●Use and frequency of medicated shampoos – Five to 10 mL of shampoo should be left on for three to five minutes before rinsing off. Ketoconazole shampoo or other antifungal shampoos should be used two to three times per week for two to four weeks in the initial treatment phase. Subsequently, the use of the medicated shampoo can be reduced to once a week to prevent relapse [30]. Minor adverse effects, such as irritation and/or burning sensation, are common with antifungal shampoo [31,32].
Patients sometimes complain that their shampoo is no longer effective. Given that some strains of Malassezia eventually become resistant to azole antifungals [19], it may be wise to effectuate, every few weeks to months, a rotation among shampoos based on different nonazole agents.
Shampoos containing salicylic acid and coal tar have keratolytic properties and may be helpful in softening thick scales [33,34]. Tar shampoos, however, are infrequently used as patients may find the odor of tar objectionable or be concerned about its potential carcinogenicity [35].
Nonscalp seborrheic dermatitis — Our approach to the management of nonscalp seborrheic dermatitis is illustrated in the algorithm (algorithm 2).
Seborrheic dermatitis of the face — For patients with seborrheic dermatitis of the face, we suggest treatment with a low-potency topical corticosteroid cream (groups 6 or 7 (table 1)), a topical antifungal agent (eg, ketoconazole 2% cream, other azole creams, ciclopirox 1% cream (table 2)), or a combination of the two as first-line treatment (algorithm 2). In patients with mild seborrheic dermatitis with minimal erythema and pruritus, we prefer to use topical antifungals alone. In patients with marked erythema and pruritus, we typically start treatment with a low-potency topical corticosteroid until symptoms subside or up to two weeks and then switch to topical antifungals as maintenance treatment. Topical corticosteroids can be used intermittently in case of flare-up.
Prolonged daily use (over two weeks) of topical corticosteroids on the face should be avoided due to the risk of local adverse effects (eg, skin atrophy, telangiectasias). (See "Topical corticosteroids: Use and adverse effects".)
In patients requiring frequent use of topical corticosteroids, topical calcineurin inhibitors (tacrolimus 0.1% ointment and pimecrolimus 1% cream), crisaborole 2% cream, or roflumilast 0.3% foam may be used as alternative treatments, as they lack adverse effects associated with topical corticosteroids (eg, skin atrophy, telangiectasias) [36-42]. The high cost of topical crisaborole and roflumilast may limit their use.
For patients with seborrheic dermatitis of the face who have mustaches and beards, we suggest ketoconazole 2% shampooing of the facial hair daily until remission and then once per week. A low-potency corticosteroid (group 7 (table 1)) can be added to the initial treatment to control inflammation and itching.
Seborrheic blepharitis — The management of blepharitis, including seborrheic blepharitis, is discussed separately. (See "Blepharitis", section on 'Management'.)
Seborrheic dermatitis of the trunk and intertriginous areas — For patients with seborrheic dermatitis of the trunk and intertriginous areas, we suggest treatment with topical antifungal agents, topical corticosteroids, or a combination of the two (algorithm 2). Topical antifungal agents are applied to affected areas once or twice daily until symptoms subside and then continued intermittently to prevent relapses. (See 'Prevention of relapse' below.)
Topical corticosteroids are applied to the affected areas once or twice daily only until symptoms subside to avoid potential adverse effects. A low-potency topical corticosteroid should be used in the intertriginous areas. Medium-potency topical corticosteroids (table 1) can be used for seborrheic dermatitis involving the chest or the upper back. For intertriginous areas, topical calcineurin inhibitors can be used as an alternative to topical corticosteroids.
Seborrheic dermatitis in patients with HIV infection — Seborrheic dermatitis is more diffuse and severe in patients who are HIV positive and may require a prolonged course of treatment. There are no studies evaluating the treatment of seborrheic dermatitis in patients who are HIV positive. Initial management is the same as for patients who are not HIV positive [43,44]. In severe cases or in cases that are refractory to topical treatment, a course of oral itraconazole (200 mg/day orally for one week) may be warranted.
Severe or refractory seborrheic dermatitis — Oral antifungal agents, including itraconazole, ketoconazole, fluconazole, and terbinafine, are a treatment option for seborrheic dermatitis involving multiple body areas and for recalcitrant dermatitis that is not adequately controlled with topical therapies. Among these, we suggest oral itraconazole. Oral itraconazole is given at the dose of 200 mg per day for seven days.
Whenever apparent seborrheic dermatitis does not respond to appropriate therapy, the diagnosis should be reconsidered. (See 'Differential diagnosis' above.)
Supporting evidence
Topical antifungal agents — A 2015 systematic review and meta-analysis that included 51 randomized trials with over 9000 participants found that in patients with seborrheic dermatitis of the face and scalp, topical ketoconazole 2% and ciclopirox 1% were more effective than placebo in improving erythema, pruritus, and scaling at four weeks [28]. When compared with each other, topical ketoconazole and ciclopirox showed similar efficacy. In studies comparing topical ketoconazole with topical corticosteroids, both agents had similar efficacy, although topical corticosteroids showed a twofold greater risk of side effects compared with ketoconazole [28].
However, the included studies used heterogeneous regimens and outcome measurement and were generally of poor methodologic quality.
Topical anti-inflammatory agents — Topical corticosteroids and topical calcineurin inhibitors are widely used for the treatment of seborrheic dermatitis because they reduce inflammation, erythema, and pruritus. Topical lithium sulfate and lithium gluconate (available in Europe but not in the United States) have been shown to be effective in treating seborrheic dermatitis in areas other than the scalp (probably because of their anti-inflammatory properties) [45-47].
●Topical corticosteroids – A 2014 systematic review including 36 randomized trials (2706 participants) found that short-term treatment (≤4 weeks) with topical corticosteroids (eg, hydrocortisone, betamethasone), topical calcineurin inhibitors (ie, tacrolimus, pimecrolimus), and topical preparations of lithium salts all reduced the symptoms of seborrheic dermatitis when compared with placebo [48]. The median rate of total clearance with anti-inflammatory treatments was 53 percent across studies. The frequency of adverse effects, including erythema, burning, dryness, and itching, was similar across all treatment groups. The quality of the included studies was generally low.
●Topical PDE4 inhibitors
•Topical roflumilast – Roflumilast is a selective, highly potent phosphodiesterase 4 (PDE4) inhibitor with anti-inflammatory properties. Topical roflumilast 0.3% foam was approved in 2024 by the US Food and Drug Administration (FDA) for the treatment of seborrheic dermatitis in adults and children ≥9 years [49].
In a randomized trial that included 226 adults with seborrheic dermatitis affecting ≤20 percent of the body surface area (BSA) treated with topical roflumilast 0.3% foam or vehicle, more patients in the roflumilast group than in the vehicle group achieved an Investigator Global Assessment (IGA) score of clear/almost clear at eight weeks (74 versus 41 percent, respectively [50]. Treatment was generally well tolerated. Only three adverse events (1.9 percent) in the roflumilast group (ie, application site pain, diarrhea, and insomnia) were deemed to be treatment related. Of note, application site pain is less than with crisaborole and calcineurin inhibitors.
•Crisaborole – Crisaborole is a boron-based, small molecule, topical PDE4 inhibitor approved for the treatment of mild to moderate atopic dermatitis in adults and children. In a small series of 30 adult patients with mild to moderate facial seborrheic dermatitis, crisaborole 2% cream applied twice daily for four weeks improved all signs of seborrheic dermatitis (erythema, scale, dryness, and pruritus), with 83 percent of patients achieving a "clear or almost clear" IGA score [51].
Oral antifungal agents — Evidence supporting the use of oral antifungals is limited. A 2014 systematic review including nine uncontrolled, poor-quality studies evaluating oral itraconazole for seborrheic dermatitis found that itraconazole was effective in inducing clinical improvement and mycologic cure in 59 to 93 percent and 40 to 86 percent of patients, respectively [52]. The regimen most frequently used involved the oral administration of itraconazole 200 mg per day for seven days followed by varying intermittent therapy for 2 to 11 months.
Coexistent seborrheic dermatitis and rosacea — In patients with coexistent facial seborrheic dermatitis and rosacea, adequate treatment of both conditions may be difficult. Prolonged use of even mild topical corticosteroids prescribed for seborrheic dermatitis may exacerbate rosacea and should ideally be avoided or used very sparingly and intermittently. By contrast, topical metronidazole 1% gel or cream (used for rosacea) may also help mild seborrheic dermatitis.
In patients who have papulopustular rosacea and facial seborrheic dermatitis, topical azelaic acid, which has antibacterial and antifungal properties, has been suggested as a treatment option for both conditions [53]. (See "Management of rosacea", section on 'Topical azelaic acid'.)
A case report describes the successful use of topical ruxolitinib in the treatment of recalcitrant seborrheic dermatitis combined with papular rosacea [54]. Ruxolitinib is a Janus kinase (JAK) inhibitor that blocks the inflammatory cascade and decreases the production of T helper type 2 (Th2)-driven cytokines. It is approved for the treatment of mild to moderate atopic dermatitis in nonimmunocompromised patients 12 years of age and older but has been used off-label to treat other inflammatory skin diseases, such as vitiligo and lichen planus.
PREVENTION OF RELAPSE — For most patients with seborrheic dermatitis, we suggest intermittent use of topical therapies to prevent relapse (algorithm 1 and algorithm 2).
●Seborrheic dermatitis of the scalp – Ketoconazole 2% shampoo and ciclopirox 1% shampoo used intermittently (once or twice weekly) have been shown to be effective in preventing relapses of scalp seborrheic dermatitis [30,55].
•In a six-month trial in which 312 patients who responded to initial treatment of scalp seborrheic dermatitis were randomly assigned to ketoconazole 2% shampoo once weekly, every two weeks, or placebo, relapses were observed in 19, 31, and 47 percent of the patients, respectively [55].
•In a similar study in which 428 patients were randomly assigned to four months of treatment with ciclopirox shampoo once weekly, every two weeks, or placebo, the relapse rates were 15, 22, and 35 percent, respectively [30].
●Seborrheic dermatitis of the face, trunk, and intertriginous areas – The prevention of relapse of seborrheic dermatitis of the face, trunk, and intertriginous areas has not been well studied. However, it is common practice to use antifungal cream or ketoconazole 2% shampoo (as facial or body wash) intermittently (once or twice weekly) to prevent relapse. The risk of side effects with this approach is minimal.
Intermittent use of topical tacrolimus (eg, twice weekly) may be an alternative to topical antifungal agents as a long-term maintenance treatment for severe facial seborrheic dermatitis.
In a small, randomized trial, 114 adult patients with severe seborrheic dermatitis of the face initially treated with a topical corticosteroid for seven days received twice-weekly treatment with tacrolimus 0.1% ointment or ciclopiroxolamine 1% cream until relapse and up to 24 weeks [38]. The median time to first relapse was 92 days (range 15 to 195 days) in the tacrolimus group versus 27 days (range 13 to 201 days) in the ciclopiroxolamine group. However, more treatment-related adverse effects, defined as burning, pruritus, and erythema, occurred in patients in the tacrolimus group than in those in the ciclopirox group.
SOCIETY GUIDELINE LINKS — Links to society and government-sponsored guidelines from selected countries and regions around the world are provided separately. (See "Society guideline links: Seborrheic dermatitis".)
INFORMATION FOR PATIENTS — UpToDate offers two types of patient education materials, "The Basics" and "Beyond the Basics." The Basics patient education pieces are written in plain language, at the 5th to 6th grade reading level, and they answer the four or five key questions a patient might have about a given condition. These articles are best for patients who want a general overview and who prefer short, easy-to-read materials. Beyond the Basics patient education pieces are longer, more sophisticated, and more detailed. These articles are written at the 10th to 12th grade reading level and are best for patients who want in-depth information and are comfortable with some medical jargon.
Here are the patient education articles that are relevant to this topic. We encourage you to print or e-mail these topics to your patients. (You can also locate patient education articles on a variety of subjects by searching on "patient info" and the keyword(s) of interest.)
●Basics topic (see "Patient education: Seborrheic dermatitis (The Basics)")
●Beyond the Basics topics (see "Patient education: Seborrheic dermatitis (including dandruff and cradle cap) (Beyond the Basics)")
SUMMARY AND RECOMMENDATIONS
●Definition and clinical presentation – Seborrheic dermatitis is a chronic, relapsing form of dermatitis occurring in areas rich in sebaceous glands (scalp, face, upper trunk, intertriginous areas). The mildest and most common form of scalp seborrheic dermatitis is dandruff, presenting with diffuse scaliness of the scalp (picture 2). Severe forms present with inflamed, erythematous plaques covered with yellowish, greasy scales (picture 1C, 1E, 3A-D). (See 'Clinical manifestations' above.)
●Diagnosis and differential diagnosis – The diagnosis of seborrheic dermatitis is usually made clinically based on the appearance and location of the lesions. The differential diagnosis includes psoriasis (picture 4), rosacea (picture 7A-E), tinea versicolor (picture 8), pityriasis rosea (picture 9A-B), tinea corporis (picture 10), secondary syphilis, lupus erythematosus (picture 11A-B), and pemphigus foliaceous (picture 12A-B). These conditions can be differentiated clinically and/or through laboratory tests and histology. (See 'Diagnosis' above and 'Differential diagnosis' above.)
●Management – Seborrheic dermatitis is a chronic condition. The main goal of therapy is to clear the visible signs of the disease and reduce associated symptoms. Repeated treatment or long-term maintenance treatment is often necessary (algorithm 1 and algorithm 2).
•Scalp dermatitis – For patients with mild, noninflammatory seborrheic dermatitis of the scalp (dandruff), we suggest antifungal shampoos (ketoconazole 2%, ciclopirox 1%) (Grade 2C). Alternative antifungal shampoos available over the counter include zinc pyrithione 1% and selenium sulfide 2.5%. Shampoo should be used daily or at least two or three times per week until remission is achieved. (See 'Seborrheic dermatitis of the scalp' above.)
For patients with moderate to severe, inflammatory seborrheic dermatitis of the scalp, we suggest antifungal shampoos (eg, ketoconazole 2% shampoo) in combination with a high-potency topical corticosteroid (table 1) in a formulation (lotion, spray, foam) of the patient's choice (Grade 2C). The topical corticosteroid can be used once daily for two weeks. (See 'Seborrheic dermatitis of the scalp' above.)
•Facial dermatitis – For patients with seborrheic dermatitis of the face, we suggest low-potency topical corticosteroids (groups 6 or 7 (table 1)), topical antifungal agents (table 2), or a combination of the two (Grade 2C). In patients with mild dermatitis with minimal erythema and pruritus, we prefer treatment with topical antifungals alone. In patients with marked erythema and pruritus, we typically start treatment with a low-potency topical corticosteroid once or twice daily until symptoms subside or up to two weeks and then switch to topical antifungals as maintenance treatment. Topical corticosteroids can be used intermittently in case of flare-up. Topical calcineurin inhibitors (tacrolimus 0.1% ointment and pimecrolimus 1% cream), crisaborole 2% cream, and roflumilast 0.3% foam may be alternatives to topical corticosteroids for facial seborrheic dermatitis, as they lack the local adverse effects of topical corticosteroids (eg, skin atrophy, telangiectasias). (See 'Seborrheic dermatitis of the face' above.)
For patients with seborrheic dermatitis of the face who have mustaches and beards, we suggest ketoconazole 2% shampooing of the facial hair (Grade 2C). The shampoo is used daily until remission and then once per week. A low-potency corticosteroid (group 7 (table 1)) can be added to the initial treatment to control inflammation and itching.
•Trunk/intertriginous areas – For patients with seborrheic dermatitis of the trunk and intertriginous areas, we suggest treatment with low-potency topical corticosteroid cream (groups 6 or 7 (table 1)), topical antifungal agents, or a combination of the two (Grade 2C). Medium-potency topical corticosteroids (groups 4 or 5) can be used for seborrheic dermatitis involving the chest or the upper back. We typically start treatment with topical corticosteroids once or twice daily until symptoms subside and then switch to topical antifungals. (See 'Seborrheic dermatitis of the trunk and intertriginous areas' above.)
●Prevention of relapse – For most patients with seborrheic dermatitis, intermittent use of topical therapies may be helpful to prevent relapse. (See 'Prevention of relapse' above.)
•We suggest ketoconazole 2% shampoo or ciclopirox 1% shampoo once per week for seborrheic dermatitis of the scalp (Grade 2C).
•We suggest ketoconazole 2% shampoo (as facial or body wash) or ketoconazole 2% cream once per week for seborrheic dermatitis of the face, trunk, and intertriginous areas (Grade 2C). Other topical azoles or ciclopirox can be used as alternatives to topical ketoconazole (table 2).
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