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Seborrheic dermatitis


Seborrheic dermatitis is a chronic relapsing erythematous scaly skin disease, the prevalence of which is around 1 to 3% of the general population in the United States. It has two incidence peaks, the first in the first three months of life and the second beginning at puberty and reaching its apex at 40 to 60 years of age. The prevalence of seborrheic dermatitis is higher in HIV-positive individuals and the condition tends to be more intense and refractory to treatment in these patients. Neurological disorders and other chronic diseases are also associated with the onset of seborrheic dermatitis. The currently accepted theory on the pathogenesis of this disease advocates that yeast of Malassezia spp., present on the skin surface of susceptible individuals, leads to a non-immunogenic irritation due to the production of unsaturated fatty acids deposited on the skin surface. This article provides a review of the literature on seborrheic dermatitis, focusing on immunogenetics, the clinical forms of the disease and its treatment.

Dermatitis; Dermatitis, seborrheic; Eczema

A dermatite seborreica é uma doença eritêmato-escamativa de caráter crônico-recidivante que acomete entre 1 e 3% da população geral dos Estados Unidos. Possui dois picos de incidência - o primeiro, durante os três primeiros meses de vida, e o segundo, a partir da puberdade, atingindo seu ápice entre os 40 e 60 anos de idade. Os indivíduos HIV positivos têm maior prevalência da doença, que apresenta maior intensidade e tendência à refratariedade ao tratamento. Doenças neurológicas e outras doenças crônicas também estão associadas ao desenvolvimento da dermatite seborreica. Como mecanismo fisiopatogênico, reconhece-se que o fungo Malassezia sp., presente na pele de indivíduos suscetíveis, leve a uma irritação não-imunogênica a partir da produção de metabólitos à base de ácidos graxos insaturados deixados na superfície cutânea. Este artigo faz uma revisão da literatura sobre dermatite seborreica, com ênfase nos aspectos imunogenéticos, formas clínicas e tratamento.

Dermatite; Dermatite seborreica; Eczema


Seborrheic dermatitis*

Ana Luisa Sobral Bittencourt SampaioI; Ângela Cristina Akel MameriII; Thiago Jeunon de Sousa VargasIII; Marcia Ramos-e-SilvaIV; Amanda Pedreira NunesV; Sueli Coelho da Silva CarneiroVI

IMD. Master's student in Internal Medicine, Medical School, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil

IIMaster's degree in Dermatology awarded by the Federal University of Rio de Janeiro. Head of the Dermatology Unit, Clinic of Medical Specialties, Vitória, ES, Brazil

IIIResearch Fellowship, Ackerman Academy of Dermatopathology. Physician, Preceptor and Head, Dermatopathology Department, Dermatology Unit, Hospital Federal de Bonsucesso, Rio de Janeiro, RJ, Brazil

IVPhD in Dermatology awarded by the Federal University of Rio de Janeiro. Associate Professor and Head, Dermatology Department, Clementino Fraga Filho Teaching Hospital, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil

VMedical student, School of Medicine, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil

VIPhD in Dermatology awarded by the Federal University of Rio de Janeiro. Adjunct Professor of Dermatology, School of Medical Sciences, State University of Rio de Janeiro. Collaborating Professor and Dermatologist, Clementino Fraga Filho Teaching Hospital, Federal University of Rio de Janeiro, Rio de Janeiro, RJ, Brazil

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Seborrheic dermatitis is a chronic relapsing erythematous scaly skin disease, the prevalence of which is around 1 to 3% of the general population in the United States. It has two incidence peaks, the first in the first three months of life and the second beginning at puberty and reaching its apex at 40 to 60 years of age. The prevalence of seborrheic dermatitis is higher in HIV-positive individuals and the condition tends to be more intense and refractory to treatment in these patients. Neurological disorders and other chronic diseases are also associated with the onset of seborrheic dermatitis. The currently accepted theory on the pathogenesis of this disease advocates that yeast of Malassezia spp., present on the skin surface of susceptible individuals, leads to a non-immunogenic irritation due to the production of unsaturated fatty acids deposited on the skin surface. This article provides a review of the literature on seborrheic dermatitis, focusing on immunogenetics, the clinical forms of the disease and its treatment.

Keywords: Dermatitis; Dermatitis, seborrheic; Eczema


Seborrheic dermatitis (SD) is a common, chronic inflammatory disease that affects around 1-3% of the general population in the United States, 3-5% of patients consisting of young adults. The prevalence of SD in HIV-positive individuals ranges from 20-83%. 1 The incidence of the disease has two peaks: one in newborn infants up to three months of age, and the other in adults of around 30-60 years of age. 2 The bimodal presentation of the disease (at birth and postpuberty) suggests that it may be associated with the sex hormones. Men are affected more often than women in all age groups and there is no preference for any specific ethnic group.

Malassez was the first to describe yeast-like fungal elements detected in flakes from the scalp, probably representative of the disease that would come to be known as SD following its original description by Unna in 1887. 3-5 In 1952, Leone linked Pityrosporum ovale (later baptized Malassezia spp.) with pityriasis of the scalp, seborrheic eczema and various other squamous dermatoses. 6,7

In the 1950s, the focus of research on SD was the investigation of its association with vitamin B2, B6, B12 and biotin deficiency. 8-16 Nevertheless, up to the present date the association between SD and nutritional deficiencies has yet to be confirmed. 17 Sudan defended the theory that nicotine acts as a hapten in the physiopathogenesis of SD. 18.22 Today, recent studies have shown the importance of the role played by Malassezia spp., present in the normal human flora, in the genesis of SD lesions in susceptible patients. 17, 23-25 Its participation was suggested by the fact that the disease responds to treatment with antifungal medication. 17

In addition to human immunodeficiency virus (HIV) infection, some neurological diseases such as Parkinson's disease also result in a higher incidence of SD, and Parkinson's patients in treatment with levodopa experience an improvement in SD. 26-31 The higher incidence of SD in patients with Parkinson's disease appears to be related to an increase in male sex hormone secretion and the effects of these hormones on the sebaceous glands rather than on autonomic dysfunction (dysautonomia), as was previously believed. 32 A higher prevalence of SD has also been found in cases of neuroleptic-induced Parkinsonism, in craniosynostosis, in familial amyloidotic polyneuropathy, in traumatic brain injury, traumatic spinal cord injury, cerebrovascular accidents (CVA), epilepsy and in facial nerve paralysis. 25, 33-38 SD has also been described as occurring exclusively on the side affected by paralysis in patients with CVA, following decompression for Chiari type-I malformation or in an area affected by syringomyelia. 38-40

In 1996, Ercis et al. reported that 30.9% of individuals with Down syndrome had SD; however, Daneshpazhooh et al. reported a prevalence of only 3%.41,42

Other systemic diseases in which the incidence of SD is higher include acute myocardial infarction, alcoholic pancreatitis and alcoholism. 43.47


Malassezia spp.

Malassezia spp. is a lipophilic fungus that is part of the flora normally found on the human skin. It was first described in the mid-1840s by Eichsted and Sluyter, who associated it with pityriasis versicolor. In 1853, Robin denominated it Microsporum furfur and in 1874 Malassez described this fungus in flakes taken from the scalp. 3,48

The genus Malassezia was first described by Baillon in 1889 and has taxomonic priority over the genus Pityrosporum used by Sabouraud in 1904 to refer to the same group of microorganisms. The current classification includes the genus Malassezia, which belongs to the family Cryptococcaceae of the class Basidiomycetes. 49

Malassezia is a dimorphic fungus that is highly pleomorphic. Since its initial classification was based on morphological criteria, it was denominated Pityrosporum ovale (oval yeast cells with a broad budding base) and Pityrosporum orbiculare (round yeast cells with a narrow budding base). Later it was concluded that both forms were morphological variants of the same species. Currently, following evaluation using serological and genetic methods, the genus Malassezia has been divided into seven species: M. furfur, M. pachydermatis, M. sympodialis, M. globosa, M. obtusa, M. restricta and M. slooffiae (Table 1). 49,50

Although Unna described seborrheic dermatitis as a disease in 1887, it was Malassez who first observed the fungus in flakes taken from the scalp in 1874. 3-5 Later, Moore and Kile linked Malassezia spp. directly to the disease. 48

Malassezia spp. is associated both with infectious diseases in which the microorganism is the direct etiological agent and in inflammatory diseases of multifactorial etiology in which the exaggerated growth of Malassezia spp. functions as a triggering or aggravating factor in susceptible patients. The former group includes pityriasis versicolor, Malassezia (pityrosporum) folliculitis, pneumonia due to Malassezia spp., sepsis associated with deep venous catheterization in patients on total parenteral nutrition and peritonitis in individuals submitted to outpatient peritoneal dialysis. In the latter group, SD is the prime example, together with confluent and reticulated papillomatosis (Gougerot-Carteaud syndrome), psoriasis and atopic dermatitis. 51-53

Each one of these diseases has various clinical and histological manifestations that cannot be explained by the mere presence of a certain species of Malassezia on the skin, with contributing factors including the individual's immunological and genetic profile. 54

The exact physiopathology of seborrheic dermatitis is yet to be completely established; however, today the rule is the association of the disease with the presence of Malassezia spp. yeast on the skin of affected individuals. This is known to be present on all human skin but may be present to a greater extent in individuals with SD.55,57 Nevertheless, in 1989, Bergbrant and Faergman failed to find any difference in the amount of Malassezia spp. between individuals with SD and healthy controls or between skin with SD lesions and healthy skin. 58 These findings suggest that there are other pathophysiologic mechanisms associated with an abnormal reaction to Malassezia spp. and that they are not necessarily related to its amount.

In 1984, Bourlond et al. showed that P. ovale (i.e. Malassezia spp.) could be found on any flaky surface (SD, actinic keratosis, nevi and viral warts) and that the multiplication of this fungus at these sites makes its demonstration simpler. 59

Various studies were conducted to define the most prevalent species of Malassezia in SD. Nakabayashi et al. reported having found 35% of M. furfur and 22% of M. globosa in individuals with SD.60,61 Rendic et al. found M. globosa in 67%, followed by M. furfur and sympodialis. 62 Gupta and Gaitanis reported a greater amount of M. globosa.63,64 Tajima was the only author to report M. restricta as being the most common. 65

Nakabayashi and Sei found that children with SD had a greater amount of Malassezia (M. furfur and M. globosa) compared to children without the disease. 66 Bergbrant considers that the quantity of P. ovale (i.e. Malassezia spp.) in the skin is not the determining factor for an inflammatory reaction, but rather the quantity of lipids on the skin surface and the individual's immune response to the presence of the fungus. This investigator also observed the relationship between the disease and hereditariness, seasonality and mental stress and with reduced T-cell function. 58, 67, 68 To corroborate the evidence that Malassezia spp. contributes to skin inflammation in SD, Plotkin in 1996 and De Angelis in 2007 described the production of a lipase by this fungus that is essential for its growth in vitro and in vivo. 69,70 The hypothesis would be that the fungus uses lipids from the skin surface to produce unsaturated and saturated fatty acids that, when left in the individual's skin milieu induce an inflammatory response. 71,72

The sebum in the skin permits the growth of P. ovale (i.e. Malassezia) and hence the development of SD. Therefore, maintaining reservoirs of residual sebum (when hygiene is poor, for example) may predispose to the appearance of the disease, as occurs in neuropathic patients. 73

The fact that SD responds to treatment with antifungal medication represents concrete evidence of the association between Malassezia and SD. 72, 74, 75

In 2007, Dawson argued that the development of SD depends on three factors: sebum production, the metabolism of Malassezia and the individual's susceptibility. 76


The histopathology of SD depends on the clinical stage of the disease. In the acute and sub-acute phases, an inflammatory infiltrate composed principally of lymphocytes and histiocytes is found in association with mild to moderate spongiosis and psoriasiform hyperplasia associated with parakeratosis around follicular ostia ("shoulder parakeratosis") (Figures 1 and 2). On the other hand, during the chronic phase, in addition to the above-mentioned findings, there is marked psoriasiform hyperplasia with dilatation of the capillaries and venules of the superficial plexus, which makes it very similar to psoriasis. 77 In psoriasis vulgaris, the histopathology findings are similar except for the spongiosis. 78


Faergemann described an increase in the number of natural killer (NK) T cells, as well as low titers of IgG class antibodies in patients with SD compared to controls. Lymphocyte activity decreases in individuals with SD when in contact with Malassezia spp. and there is a reduction in IL-2 and IFN-γ and an increase in IL-10 production. 79 In a subsequent study, the same author reported a greater number of NK1+ and CD16+ cells associated with complement activation in SD lesions compared to healthy skin in the same patients or to the skin of individuals without SD, suggesting the presence of an intense, irritative, nonallergic immune response. 80

In 1988, Parry and Shape failed to find either circulating antibodies against the fungus or systemic sensitivity, leading to the conclusion that there is no change in humoral response to Malassezia spp. but rather an alteration in cellular immune response. 81,82 Neuber et al. also reported an alteration in cellular immunity in SD. 83

Watanabe et al. showed that M. furfur does not lead to cytokine production by the keratinocytes, whereas this occurs with the other species of Malassezia. Furthermore, these investigators reported that, depending on the species of Malassezia, production of a certain profile of inflammatory interleukins is stimulated, thus characterizing a different disease. For example, when IL-8 is produced, neutrophils are attracted, manifested clinically in the form of Malassezia folliculitis; likewise, lack of production of monocyte chemotactic protein-1 (MCP-1) clinically determines SD. 84

No increase was found in the production of anti-Malassezia antibodies (IgM and IgG) in patients with SD. This observation was significant in patients with atopic dermatitis and suggests that there is no anti-Malassezia spp. humoral immune response in SD. 79, 82, 85

Passi et al. found decreased serum levels of vitamin E, polyunsaturated fatty acids and erythrocyte glutathione peroxidase activity in patients with SD (both in HIV-positive and HIV-negative individuals) and suggested an association between these findings and the pathogenesis of the disease. 86

In 2007, Ianosi described the inflammatory infiltrate in SD: poor in CD20+ and rich in CD45Ro. 87

Human leukocyte antigen (HLA) system

Although there is evidence that hereditariness is the predisposing factor for SD, the only description of HLA typing in patients with seborrheic dermatitis was published by Tsuji in 1976. This investigator typified HLA in patients with psoriasis vulgaris, palmoplantar pustulosis, seborrheic dermatitis and in healthy individuals. He found an increase in the frequency of HLA-A1 and HLA-BW37 in patients with psoriasis vulgaris and an increase in the frequency of HLA-AW30 and/or AW31 and HLA-B12 in seborrheic dermatitis. 88 The research group represented by these authors is conducting studies to clarify the role of immunogenetics in SD.


SD has distinct characteristics depending on the age group affected: the pediatric form is self-limiting, whereas in adults the disease is chronic. 89 The lesions consist of erythematous, flaking plaques of varying extents and degrees of intensity.

In infancy, SD is more prevalent in the first three months of life (10% in boys and 9.5% in girls), with flaking on the scalp being the most common clinical manifestation (42%). 90 It is characterized by the appearance of yellowish adherent scales of varying extent that appear shortly after birth. They may also develop on the face and in the body folds such as in the retroauricular region, neck, axillae and inguinal region. The child with SD may present with a rare, generalized form that is often associated with immunodeficiency. 17

In adults, SD is a chronic, relapsing dermatosis that may range from a mild to moderate erythema to papular, exudative and/or squamous lesions with periods of exacerbation related to stress or sleep deprivation. 17,91

The areas affected and the prevalence of each one of these areas are as follows: face (87.7%), scalp (70.3%), chest (26.8%), lower limbs (2.3%), upper limbs (1.3%) and other sites (5.4%) such as body folds (Figure 3). 92 The lesions consist of macules or thin plaques with well-defined borders that may be pink, light yellow or erythematous, with fine, dry white or even moist or oily, yellowish scales. They may be limited to small areas of the body; however, there have been reports of generalized forms and even of erythroderma.93-96 The presence of pruritus is variable. The principal complicating factor in the lesions is secondary bacterial infection, which increases the erythema and exudate, local discomfort and lymphadenomegaly close to affected areas.

The lesions develop principally on areas in which sebum production is high such as the scalp, face, external ear, retroauricular region and presternal area, eyelids and body folds (Figures 4-10).

The lesions on the scalp range from a mild desquamation (pityriasis simplex capillitii) to honey-colored crusts completely affixed to the scalp and hair, which may or may not provoke areas of alopecia (pseudo tinea amiantacea). On the face, involvement of the glabella and malar regions, the nasolabial folds and the eyebrows is characteristic. Involvement of the eyelids leads to blepharitis. In men, the beard area may also be affected with SD lesions. In the body folds (axillae, umbilicus, inguinal, inframammary and anogenital regions), lesions may acquire a moist, macerated appearance with erythema at the base and around the lesions. They may progress with fissures and secondary infection. In the presternal area, lesions may be more erythematous and scaly with arciform patterns (psoriasiform) on the borders of the lesion or in the shape of flower petals (scales over the lesion).


Differential diagnoses in cases of SD include psoriasis, atopic dermatitis (principally in the pediatric form of SD), tinea capitis, cutaneous lymphoma and cutaneous Langerhans cell histiocytosis. 17 There is also a type of dermatitis that is similar to SD and is induced by drugs (gold, buspirone, chlorpromazine, ethionamide, griseofulvin, haloperidol, IL-2, interferon-α, lithium, methoxsalen, methyldopa, phenothiazines, psoralens and stanozolol, among others) or by nutritional deficiency (riboflavin, pyridoxine, niacin and zinc). 97, 98

Infantile SD is similar to atopic dermatitis (AD); however, the sites affected (body folds in the case of SD and extensor surfaces in AD) and the absence of pruritus in SD are factors that differentiate the two conditions. Diaper dermatitis does not affect the body folds, whereas SD affects these areas predominantly. Infantile psoriasis is very similar to SD in this age group and it is almost impossible to differentiate between the two conditions.

There is a debate on the difference between SD of the scalp and a disorder referred to as pityriasis simplex capillitii, a mild, dry, desquamation of the scalp that may merely represent a physiological shedding of the stratum corneum or may be a consequence of the excess use of cosmetics such as hair creams or gels. It is also difficult to distinguish between SD and psoriasis of the scalp. The psoriasis lesions are better-defined, thick plaques with dry white flakes. 89

On the face, SD lesions are similar to those of acute cutaneous lupus erythematosus (bilateral malar eruption) and of rosacea. In the body folds, they should be differentiated from primary irritant contact dermatitis, from inverse psoriasis, dermatophytosis and erythrasma. Langerhans cell histiocytosis may affect the body folds and the scalp, leading to a clinical appearance that is very similar to that of SD; however, the presence of a purpuric component in the lesions renders the former diagnosis more likely. 89


Eisenstat first described the association of SD and acquired immunodeficiency syndrome (AIDS) in 1984. The prevalence of SD in HIV-positive individuals differs according to various authors. For Soeprono et al., 85% of individuals with AIDS have SD, whereas Berger reported this figure as 36%, Goodman as 32% and Blanes et al. as 31% of patients. 92-102

Malassezia spp. is also involved in the development of the disease. No increase was found in the amount of P. ovale (i.e. Malassezia spp.) on the skin surface when individuals with and without AIDS were compared; however, it would appear that the specific subtype of Malassezia spp. present is more important than the extent of the fungus on the skin surface. 103, 104 Rincón et al. reported a predominance of Malassezia globosa in individuals with pityriasis versicolor (67%) and in HIV-positive patients with SD (85%), whereas in HIV-negative SD patients the predominant Malassezia species were M. furfur and M. restricta, found in 72% and 26% of cases, respectively. 105

Vidal et al. described the lipid profile of the skin of individuals with AIDS as being different from that of individuals without AIDS; however, these investigators did not determine its relationship with the development of SD. 106 Passi et al. (1991) reported that the total lipid concentration on the skin surface of HIVpositive and HIV-negative patients with seborrheic dermatitis was similar; however, they reported significant alterations in the lipid fractions of HIV-positive patients including a reduction in squalene and an increase in cholesterol and in cholesterol esters. 107

SD usually occurs in HIV-positive individuals with a CD4+ T-lymphocyte count of 200-500 and is considered an early skin manifestation of AIDS. 108 Response to antiretroviral treatment is variable and there have been conflicting reports in the literature: some investigators reported an improvement in SD with the initiation of antiretroviral treatment, while others reported aggravation. 109, 110 Furthermore, there have been reports of aggravation during immune reconstitution inflammatory syndrome and reports that antiretroviral treatment does not alter the prevalence or the course of SD. 111, 112

With respect to histopathology, the findings of SD in HIV-positive patients are similar to those found in HIV-negative patients; however, there appears to be greater follicular involvement in the lesions and more plasmocytes in the inflammatory infiltrate in the HIVpositive patients. 17, 78, 101

The clinical appearance of SD is typical, affecting areas rich in sebaceous glands and accompanied or not by pruritus. Children with AIDS also have SD. 113 Nevertheless, if the disease appears for the first time or if there is an exacerbation in an HIV-positive individual who, prior to that, had a mild form of the disease, this may indicate seroconversion from the latent phase to the symptomatic phase. 104 SD may also be more extensive, more intense and refractory to conventional treatment. These cases tend to benefit from the use of oral antifungal agents or the association of drugs with antifungal agents and topical, lowpotency corticosteroids. 114 There have also been reports of a clinical improvement with the use of antiretroviral drugs. 109, 115


Since this is a chronic inflammatory disease that probably occurs in response to the presence of a fungus (Malassezia spp.) on the skin and to its metabolism through the use of lipids from the skin, the objective of treatment consists in controlling the inflammation, proliferation of the microorganism and the oiliness. Various classes of medication are used; therefore, the therapeutic arsenal for the control of SD is extensive. The first rule is to inform the patients with respect to the chronic, relapsing nature of the disease. The individual who is aware of the course of the disease gains greater confidence and complies better with treatment. 116

According to a survey conducted by Peyri et al., the most commonly used drugs are the corticosteroids (59.9%) and imidazole-based antifungals (35.1%). Moisturizing creams were also reported in 30.7% of cases, topical calcineurin inhibitors in 27.2% and other pharmacological treatments such as systemic antihistamines and a variety of natural therapies in 5.1%. 92

The following paragraph lists the drugs used for the treatment of SD, grouped according to the therapeutic modalities:

Soaps: the types of soaps available include those containing ketoconazole 2% and sulfur with or without salicylic acid. Tea tree (Melaleuca alternifolia) oil-based soaps have proven effective against SD due to their antifungal potential. 117 They are also available in the form of shampoos.

Shampoos: the shampoos used for the control of SD are classified in accordance with their effect. Antiproliferative: Based on coal tar and its derivatives, they are antimitotic and cytostatic, causing a reduction in cell division in the epidermis, which is the cause of scale formation. Other examples are selenium sulfate (1 and 2.5%) and zinc pyrithione (1 and 2%). Antifungals based on ketoconazole 2%, ciclopirox 1% and also selenium sulfide and zinc pyrithione. Keratolytics: based on salicylic acid (2-6%) with or without sulfur (2 - 5%) promote removal of the adherent flakes. Anti-inflammatories: containing corticosteroids (clobetasol propionate), they exert effects similar to those used in the form of hair tonics. 118 The combination of various classes of drugs in one single product or the use of rotational therapy are the most effective options and the ones that result in fewer recurrences.

Topical Medication:

Topical antifungal preparations: ketoconazole, as well as other imidazole derivatives, and antifungal agents of other pharmacological classes such as ciclopirox, all of which can be used in the form of lotions, creams or ointments, are always used whenever there is a recurrence of SD. Although the anti-androgenic effect of these drugs remains a subject of debate, the dose required for this effect to occur is very high (equivalent to 600-800 mg/day of oral ketoconazole) and it is improbable that this dose would be reached with topical treatment. 119 On the other hand, there are indications that some antifungals have anti-inflammatory effects comparable to the effect of hydrocortisone. 120 For example, ciclopirox olamine has been shown to inhibit the effect of 5-lipoxygenase and cyclooxygenase in vitro. 121

Topical corticosteroids: they may be used in the form of lotions, hair tonics, foams and shampoos. They result in a rapid improvement in symptoms (erythema, desquamation and pruritus); however, relapses are frequent. They should be used for the shortest time possible because of the side effects that occur with prolonged use.

Anti-inflammatory calcineurin inhibitors - tacrolimus 0.03 and 0.1% and pimecrolimus 1%. An alternative to topical corticosteroids, both tacrolimus and pimecrolimus exert an anti-inflammatory effect on SD that is equal to or superior to that of low-potency topical corticosteroids without the side effects of the latter. They can be used once or twice a day. 122-124 They are well tolerated and may be used for resistant forms of SD of the face. 125-6 They also induce a more prolonged remission than that achieved with topical corticosteroids. 127

Other therapeutic options reported in the literature include: metronidazole 1% gel commonly used for the treatment of rosacea; twice daily use of tacalcitol (1,24-(R)- dihydroxyvitamin D3) cream, a medication used for the treatment of psoriasis; topical lithium succinate, which has an anti-inflammatory effect; benzoyl peroxide, a bactericide used for the treatment of inflammatory acne. 128-131

Orally administered drugs may also be used, principally in cases of extensive SD and cases refractory to topical medication. The antifungal agents used and their respective doses are: 132

. Ketoconazole 200 mg/day for 14 days

. Itraconazole 100 mg/day for 21 days

. Terbinafine 250 mg/day for 4 weeks.

Some years ago, the use of oral isotretinoin was defended as a regulator of seborrhea and for this reason its use was suggested for the control of SD. The study carried out used very low doses of the drug (2.5 mg, three times weekly and up to 5 mg/day) with good efficacy. 133 Recently, a case of sebaceous hyperplasia was reported in which response to isotretinoin was good. 134 Scientific studies on the use of isotretinoin for seborrheic dermatitis are becoming steadily rarer, with the last having been published in 2003. 133 Furthermore, there has been a report on the appearance of an eruption on the face similar to SD in individuals in use of this medication for the treatment of acne. 135


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  • Endereço para correspondência:
    Ana Luisa Sobral Bittencourt Sampaio
    Rua Almirante João Cândido Brasil, 72/102 -Tijuca
    20511-020 Rio de Janeiro, RJ
  • *
    Trabalho realizado no Serviço de Dermatologia da Universidade Federal do Rio de Janeiro (UFRJ) - Rio de Janeiro (RJ), Brasil.
  • Publication Dates

    • Publication in this collection
      23 Jan 2012
    • Date of issue
      Dec 2011


    • Received
      18 Nov 2010
    • Accepted
      24 Mar 2011
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