Seborrheic dermatitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jesus Rosario Hernandez, M.D. [2]; Aysha Anwar, M.B.B.S[3]

Synonyms and keywords: Seborrheic eczema

Overview

Seborrheic eczema (also known as Seborrheic dermatitis AmE, seborrhea) is a skin disorder affecting the scalp, face, and trunk. Seborrheic dermatitis causes flaky, itchy, red skin and temporary hair loss. It particularly affects the sebum-gland rich areas of skin. Causes of seborrheic dermatitis include Malassezia furfur (formerly known as Pityrosporum ovale), as well as genetic, environmental, hormonal, and immune-system factors. Medical therapy for seborrheic dermatitis includes antifungal agents, corticosteroids, and lithium salts.

Historical Perspective

Seborrheic dermatitis was first described by Unna in 1887. In 1894, a hypothesis was made by Unna and Sabouraud that causative agents responsible for seborrheic dermatitis include yeast Malessezia, bacteria, or both as they were obtained in high quantities in cultures obtained from the affected patients. In 1984, Shuster studied the disease and discovered seborrheic dermatitis can be treated with oral ketoconazole which was further supported by numerous studies.[1]There have been several terms used for seborrheic dermatitis such as seborrheic eczema, dermatitis seborrhoides, seborrhea oleosa (Von Hebra), steatorrhagia, seborrhagia, and flux sebacea (Rayer). Terms in the past have included morbus Unna, hyperhidrosis oleasa (Unna; increased sweat and oil), crusta lactea in infants (milk crust, cradle cap), napkin dermatitis, and eczema flannelairepityriasis sicca (dandruff, seborrhea/pityriasis capitis), pityriasis amiantacea (thick scalp involvement), and seborrhea blepharitis (seborrheic blepharitis, marginal blepharitis of the eyelids).[2]

Classification

There is no established classification system for seborrheic dermatitis.However, it may be classified according to the site involved, age group, symptoms, etiology and severity into 5 subtypes[3][4][5][6][7]

Classification by Anatomy

There is no established classification system for seborrheic dermatitis. However, seborrheic dermatitis can be classified on the basis of following factors:[8][3][9][10]

Localised

  • Scalp: In infants its called Cradle Cap. Its the most common presentation in infants and appear as red yellow plaques coated by thick greasy scales, commonly appearing in first three months of age. In adults, presentation of disease is mild desquamation to honey coloured crusts which can extend to involve forehead called "corona seborrheica"
  • Face: It most commonly involves eyelids, eyebrows and nasolabial folds. Eyes are involved resulting in blephritis.
  • Retroauricular: lt invloves crusting, oozing and fissuring in the affected area. It may also involve external ear resulting in otitis externa.
  • Body folds: It usually affects axilla, breast folds, inguinal area and genital area. May progress to fissuring and secondary infection.
  • Upper Chest: It is mostly seen in adults. Affected areas may present with one of the following presentation.
    • Pityriasiform: It is usually in the form oval macules and patches ranging from 5-15mm in size which tend to involve intertriginous areas.
    • Petaloid type: It appears as small papules with oily scales which enlarges to become patches giving it an appearance of petals of flower, hence the name.
  • Trunk: common in infants and most common site of involvement is lower abdomen.

Generalized: mostly seen in infants associated with leiner's disease and children with severe immunodeficiency. It usually is associated with diarrhea and failure to thrive and may resolve in few weeks.[11]

Classification by Age

  • Infantile: seen in first three months of life. It is mostly a self limited disease in children.
  • Adults: occurs most commonly between 30-60 years of age. In adults, it usually appears as chronic relapsing condition involving various parts of the body.

Classification by Symptomic Presentation

  • Non pruritic: This type is most commonly seen in infants.
  • Pruritic: This type is seen in older children and adults. This type is common with scalp involvement.

Classification by Etiology

Exact cause of seborrheic dermatitis is unknown. However, following causes may be related to pathogenesis of seborrheic dermatitis.

  • Idiopathic : No known cause
  • Infectious: Caused by fungus named Malassezia based on its response to antifungal agents.
  • Autoimmune/Inflammatory: One hypothesis suggests it as a primary inflammatory dermatoses resulting in increased apoptosis, scaling and inflammation in epidermis.

Classification by Severity

  • Mild to moderate disease: seen in immunocompetent individuals.
  • Severe disease: Immunocomprised patients have more extensive disease which is mostly unresponsive to treatment.

Pathophysiology

Despite high prevalence of seborrheic dermatitis, there remains controversy between different pathological mechanisms causing seborrheic dermatitis. Following proposed mechanisms may play a role in pathogenesis of seborrheic dermatitis.However, patients with seborrheic dermatitis may have normal sebum production and in some individuals increased sebum production does not cause seborrheic dermatitis.[12] [13][14][15][11]

Pathogenesis

  • Complete pathogenesis of seborrheic dermatitis is not fully understood. However, studies have demonstrated strong correlation between presence of fungal yeast named Malassezia and response to antifungals in patients with seborrheic dermatitis.[16]
  • Malassezia is a lipophilic yeast found on the skin of both healthy individuals and seborrheic dermatitis patients. The exact mechanism of disease process in individuals having seborrheic dermatitis is not established but it is thought that host reaction to Malassezia or its metabolites causing inflammatory reaction may have a significant role in the process. Two species of Malassezia named Malassezia globosa and Malassezia restricta may have a stronger association with the development of seborrheic dermatitis.[13].
  • Another proposed mechanism for seborrheic dermatitis may indicate that lipid layer of fungus Malassezia when disrupted leads to an inflammatory response resulting in increased production of pro inflammatory cytokines such as IL-6 and IL-7 and decreased production of IL-10. [7]
  • Another hypothesis states that host immune response to Malassezia is not responsible for causing the disease.[17] The main cause for seborrheic dermatitis may be irritant rather than immune response, due to production of certain metabolites such as nitrates, reactive oxygen species and lipases.[14]Malasseziais seen to have lipase activity, which when act on human triglycerides causes release of unsaturated fatty acids such as arachidonic acid. These metabolites causes abnormal proliferation and differentiation of stratum corneum leading to signs and symptoms of seborrheic dermatitis.[18]

Genetics

Accordig to some studies, there is no genetic predisposition for seborrheic dermatitis.[19]. However, certain studies may show genetic causation to seborrheic dermatitis resulting from mutations in certain genes coding zinc finger proteins which is normally expressed in keratinocytes.[20]

Associated factors

Some other associated factors implicated in pathogenesis of seborrheic dermatitis include following

  • Sabaceous gland activity

It is stated that sebum gland activity may correlate with seborrheic dermatitis but increased sebum production does not have a role in seborrheic dermatitis. It is supported by the fact that there is increased incidence of seborrheic dermatitis after birth in infants, teens at puberty and during third and fourth decades, all related to increased sebum gland activity at these times.[15]However, patients with seborrheic dermatitis may have normal sebum production and in some individuals increased sebum production does not cause seborrheic dermatitis.[21]

  • Immune response

Seborrheic dermatitis is strongly related to immunosuppression and HIV/AIDS. Elevated levels of certain HLA antigens such as HLA-AW30, HLA-AW31, HLA-A32, HLA-B12 and HLA-B18 and increased levels of total serum IgA and IgG antibodies have been detected in SD patient implying an immune mediated pathological mechanism.[14][22][23]

  • Epidermal barrier dysfunction

Abnormalities in stratum corneum such as corneocyte shape and corneodesmosomes, and disrupted lipid lamellar structure causing disruption of epidermal barrier permeability may cause alteration in intercellular lipids and desquamation process leading to increased flaking and itching.[24]

  • Neurogenic and other factors

Seborrheic dermatitis in patients of parkinsonism is under neuro-endocrinological rather than pure neurological regulation supported by the fact that patients with unilateral parkinsonism present with bilateral seborrheic dermatitis. One possible explanation for this may be increase in levels of α-melanocyte stimulating hormone (α-MSH) levels. seborrheic dermatitis in these patients respond to L-dopa treatment.[23]

Gross Pathology

Superficial flaking and redness are characteristic findings of seborrheic dermatitis. Flakes usually occur in patches on scalp and tend to move about scalp over time.[25]

  • Seborrheic dermatitis showing erythema on face

    Seborrheic dermatitis showing erythema on face

  • Scalp showing redness and crusting

    Scalp showing redness and crusting

Microscopic Histopathology

Histopathological findings of seborrheic dermatitis can be divided into three types based on the following types, [22][26]

  • Acute

Focal mild spongiosis with superficial crust containing neutrophils centered on a follicle, mild edema of papillary dermis, dilatatiuon of blood vessels in superficial vascular plexus with mild infiltration of lymphocytes, histiocytes and occasional neutrophils are characteristic findings of seborrheic dermatitis.

  • Subacute

In addition to findings mentioned above, there is also some psoriasiform hyperplasia in subacute form of seborrheic dermatitis. This type may show presence of yeast like organisms in the surface keratin.

  • Chronic

Extensive psoriasiform hyperplasia and minimal spongiosis are characteristic findings seen in this type. This type resembles psoriasis and might be difficult to differentiate from psoriasis but presence of follicular crusting favours seborrheic dermatitis.

  • Chronic Seborrheic dermatitis.

    Chronic Seborrheic dermatitis.

  • Acute dematitis showing papillary edema with neutrophil infiltration.

    Acute dematitis showing papillary edema with neutrophil infiltration.

Causes

The cause of seborrhoeic dermatitis remains unknown, although many factors have been implicated.

  • The widely present yeast, Malassezia furfur (formerly known as Pityrosporum ovale), is involved,[27][28] as well as genetic, environmental, hormonal, and immune-system factors.[29][30]
  • A suggestion that seborrhoeic dermatitis is an inflammatory response to this yeast has yet to be proven.[31] Those afflicted with seborrhoeic dermatitis have an unfavourable epidermic response to the infection, with the skin becoming inflamed and flaking.
  • In children, excessive vitamin A intake can cause seborrhoeic dermatitis.[32] Lack of biotin,[33] pyridoxine (vitamin B6)[33][34] and riboflavin (vitamin B2)[33] may also be a cause.

Differentiating Seborrheic dermatitis from Other Diseases

Differential diagnosis of seborrheic dermatitis can be classified into two types by age group[35][36][37][18][38][39][26]

Differential diagnosis in Infants

Differential diagnosis in Adults

Epidemiology and Demographics

Epidemiology

Seborrheic dermatitis is one of the most common skin disorders in general population but prevalence estimate of the condition is difficult due to lack of diagnostic criteria and grading system for severity.[40]

Prevalence

Worldwide, the prevalence of seborrheic dermatitis is estimated to be 11000 cases per 100,000.[19] Prevalance rate varies among individuals based on the following factors:

  • The prevalence rate of disease increases when mild cases are also involved.
  • The prevalence of seborrheic dermatitis is higher in patients with HIV with 35000 per 100,000 in early diagnosis and 85000 per 100,000 with full blown AIDS.[41]The cause of increased prevalance in patients with seborrheic dermatitis is resistant to treatment.
  • Regarding exposure to solar UV radiation, there is higher prevalence seen among those directly exposed to UV radiation which includes large percentage of mountain guides among general population.[42]

Incidence

Seborrheic dermatitis has a biphasic incidence, which involves occurence in infants between age range of 2-12 weeks and second incidence peak occuring later in life during adulthood between age groups of 40 to 60 years of life.[43]. Incidence of seborrheic dermatitis is affected by the following factors:

  • The incidence of seborrheic dermatitis is higher in patients with HIV with 35000 per 100,000 in early diagnosis and 85000 per 100,000 with full blown AIDS.[41][44]

Demographics

Following demographic factors may significantly affect the incidence and prevalence of seborrheic dermatitis:

Age

Seborrheic dermatitis commonly affects three age groups.[44][45][22]

  • First incidence peak is seen in infants around three to four months of age, which usually resolves in 12 months
  • Second incidence peak seen around puberty.
  • Third incidence peak is seen after age 50 with highest prevalence seen among age group ranging 33-44 years of age.[46]
  • Age groups showing lowest prevalence of clinical disease is seen in individuals younger than 12 years.[47]

Gender

Males are more commonly affected with seborrheic dermatitis than females.[48]

Race

There may be racial predilection for seborrheic dermatitis as only few cases are seen in African Americans. If seborrheic dermatitis is seen in this population, it leads to high suspicion of HIV in affected individuals.[49]

Risk Factors

Most common risk factors for Seborrheic dermatitis are[50][18]

Other risk factors include

  • Stress[54]
  • Patients treated with psoralene and ultravoilet light A for psoriasis are seen to have a predisposition for seborrheic dermatitis.
  • Male population is more prone to develop seborrheic dermatitis as compared to females.[55]
  • Obesity, diabetes Mellitus and other endocrine disorders causing alteration in glucose metabolism.[56]
  • Seasonal changes such as low temperature and decreased humditiy may have a significant role in seborrheic dermatitis flare ups[57]
  • Drugs such as haloperidol deconate, lithium and chlorpromazine are associated with increased risk of disease in some patients.

Screening

There are no screening guidelines for seborrheic dermatitis.[58]

Natural History, Complications, and Prognosis

Natural History

Complications

Common complications of Seborrheic dermatitis include the following[59][44][60][61][62][11]

  • Side effects to inflammation may include temporary hair loss. If severe outbreaks go untreated for long periods of time, permanent hair loss may result due to damaged hair follicles.
  • Secondary bacterial infection may occur aggravating erythema, exudate and increase in local discomfort.
  • Blephritis involving meibomian glands can cause abcess formation.
  • Otitis Externa can result from involvement of external ear due to maceration of skin due to extcessive itching.
  • Severe seborrheic dermatitis or generalised seborrheic erythroderma can occur with immunosuppression including HIV or cardiac failure.

Prognosis

  • Prognosis of Seborrheic dermatitis is excellent in infants as it is a self limited disease and usually resolves in few months after birth. However, in adults it is a recurrent condition with no permanant cure. In conditions where patient is immunocompromised such as HIV or malignancy it is refractory to treatment.[63][64]

Diagnosis

There are no definitive diagnostic criteria for seborrheic dermatitis. Diagnosis of seborrheic dermatitis is primarily clinical based on history and physical examination findings.[65]

History

Obtaining complete history is important in making diagnosis of seborrheic dermatitis as it will give an insight into cause and associated risk factors for the disease. In addition to symptoms of seborrheic dermatitis presence of any of the following conditions are suggestive of below mentioned etiologies[66][67][68][18] [69][70][71]

Symptoms

Symtoms can be divided into following categories based on age[19][72]

Infants

Infants usually present in the first few months of life with following symptoms. Symptoms can be divided into following types depending on extent of involvement.

  • Localised
    • Redness and flaking are the main presenting complaints of infantile seborrheic dermatitis.
    • It may involve scalp and face which are the most common sites to get involved. Other sites involved include retroauricular area, nasolabial folds, cheeks, eyebrows and eyelids.
    • Pruritis is usually mild in infants having localised seborrheic dermatitis.
    • Areas involving neck, axilla or body folds may present with redness without flaking giving it a glistening look.
    • Napkin or diaper area involvement is not rare in infants.
  • Generalised
    • Few cases may present with generalised involvement such as lower abdomen, groin and pubic area. Generalised and more severe forms may raise the suspicion for underlying immunosupressive condition.
    • Seborrheic dermatitis self resolves in few months and rarely presents after 12 months. In cases where it is suspected after 12 months should raise the suspicion for an alternative diagnosis.

Adults

Symptoms of seborrheic dermatitis may overlap with other skin conditions such as psoriasis, candidiasis, contact dermatitis, atopic dermatitis but most common symptoms of seborrheic dermatitis are divided into two types based on extent of involvement.[19]

  • Localised
    • It involves macules, thin plaques, or red patches involving scalp, face, nasolabial folds, anterior hairline, eyebrows, glabella region of the forehead, melolabial folds, ears (including the external canals, anterior auricular region, retroauricular region), central chest (sternum area), and genital region
    • Pruritis is usually present in adult form and depends on severity of disease.
    • Mild disease may present with fine scales with no itching.
    • More severe disease presents with visible signs of inflammation such as redness and yellow to white crusting or scaling.
    • Involvement of eyes is common causing redness, itching and yellow crusting of eye lashes (Blephritis).
    • In cases where ears are involved, repeated itching leads to skin trauma causing secondary bacterial infection resulting in fever and ear pain.
  • Generalised
    • Patients with HIV or other immunosupressive conditions such as malignancies usually present with more severe disease which is resistant to treatment. It may present on unusual sites in this case such as extremities.[73][74]


Physical Examination

Age Site

involved

Local

Examination

Image
Infants General Appearance Infant looks healthy with good apatite and sleep.
Scalp Fine scaling in mild cases

Thick greasy scales with erythema in severe cases.

Face Face may present with scaly salmon colored scales.
Neck, axilla and body Folds Non scaly moist glistening appearance of lesions which tend to appear confluent.
Trunk Trunk involvement is seen in severe cases. However, diaper area gets commonly involved

which presents with erythema and maceration of skin with edema of surrounding skin. Secondary bacterial and candidal infections are common in these cases.

Generalised It is most commonly seen in Leiner's disease which is an immunosuppressive condition.

It may involves unusual site such as extremities and trunk with scaling and erythematous red patches. Scaling and crusting usually spreads to involve other parts of the body with extensive peeling of skin.

Adults General appearance Adults may present with healthy outlook in mild cases or may present in considerable distress

due to widespread involvement esp in cases with underlying diseases associated with seborrheic dermatitis such as HIV, malignancy, parkinsonism.

Scalp Mild desquamation to honey coloured crusting of scalp and hair causing alopecia.
Face/Retroauricular

areas

Erythema and scaling may spread to malar region in a butterfly situation. Yellowish scaling between eyelashes

and eyelids causing blephritis with honey colored crusting on free margins.

Upper Chest SD presents as petalloid or pityriasiform.

Petalloid: Small reddish follicular or perifollicular papules that may colace forming patches resembling petals of flower Pityriasiform: Common on skin tension lines and intertriginous areas and presents as oval scaly macules and patches. This type involves extensive involvement of the body.

Body Folds Lesions usually present as moist, macerated and erythematous lesions. May lead to fissuring and secondary infection.
SD in

Immuno suppression

It may presents as extensive scaling and erythema involving unusual sites such as extremities and is refractory to treatment. It is usually seen in children and adults with immunosuppression such as HIV/AIDS.

General Appearance

Infants look generally healthy with good apatite and sleep.

Skin

  • Thick greasy scales involving scalp, forehead and vertex.
  • Involvement of face may present with scaly, salmon coloured plaques.
  • Areas involving neck, axilla or body folds may present with non scaly, moist look and usually tend to appear as confluent skin lesions.
  • Diaper area involovement presents as erythema and maceration of skin with edema of surrounding area. Secondary bacterial and candidal infection is common in theses cases[75]

Head

Head involvement involves fine scaling in mild cases and erythematous patches with marked crusting showing signs of inflammation in severe cases.

Ear

Neck

Trunk

Extremities

Genitals

Adults

Imaging Findings

Other Diagnostic Studies

Treatment

Medical Therapy

The mainstay of treatment for seborrheic dermatitis is supportive. Depending on age, it can be divided into following types:

Infantile

In infants seborrheic dermatitis(Cradle Cap) is self limited disease in most cases and resolves in few months. The mainstay of treatment is supportive and divided into two types depending on severity of disease.[76]

  • Mild
  • Education and reassurance of parents
  • Use of simple skin measures such as application of emollients such as baby oil or mineral oil to loosen scales and frequent shampooing using non-medicated shampoos and removing scales frequently.
  • Severe and persistant
  • In severe cases or cases having extensive involvement of the body, short course of topical corticosteroids (1% hydrocortisone) and antifungal agent (2% ketoconazole) have equal efficacy of treatment as demonstrated by studies.[77][78]

Adults

There is no curative treatment for seborrheic dermatitis as it is a chronic recurring condition. The mainstay of treatment is supportive to control the acute flares of disease. Supportive treatment includes use of topical and oral glucorticoids, zinc pyrithione, selenium sulfide (1%–2.5%), imidazoles (1%–2% ketoconazole shampoo, creams, lotions, or foams), ciclopirox (cream, gel, and shampoo), salicylic acid (shampoos, creams), coal tar (creams, shampoos), or mild detergents.[79][80][81]

Depending on severity of disease, treatment can be divided into following types:

  • Mild
  • Treatment modality for mild cases of scalp disease is topical antifungals such as azoles, zinc pyrithione, selenium sulfide (1%–2.5%), imidazoles (1%–2% ketoconazole shampoo, creams, lotions, or foams), ciclopirox (cream, gel, and shampoo), salicylic acid (shampoos, creams), coal tar (creams, shampoos. Topical use of (low, moderate and high potency) corticosteroids requiring overnight application, Baker's P&S solution, tar shampoo, or salicylic acid (ointment or shampoo, is usually reserved for thick and severe scaling.[82]
  • Other effective treatments include coconut oil compound (ointment combination of coal tar, salicylic acid and sulfur).
  • Moderate to Severe
  • Treatment modalities for severe seborrheic dermatitis involving scalp may include systemic use of glucocorticoids((prednisolone 0.5 mg/kg body weight/day) for 7 days.
  • Seborrheic dermatitis involving face, trunk and ears may require short courses of low potency topical corticosteroids to suppress initial inflammation.[82]
  • Long term use of corticosteroids is discouraged due to potential adverse effects.
  • Topical use of calcineurin inhibitors(pimecrolimus and tacrolimus) have both antifungals and antinflammatory properties and can be used safely.[83]
  • Topical antifungals(ketoconazole, miconazole, fluconazole, itraconazole, econazole, bifonazole, climbazole, ciclopirox, and ciclopiroxolamine) have shown favourable outcomes in controlling the acute flares of seborrheic dermatitis.[84]
  • Oral antifungals and oral turbinafine are reserved for severe and refractory conditions not responding to topical treatment.[85][86]
  • Aluminium acetate solution may have a role in seborrheic dermatitis externa as a maintainence therapy.
  • The mainstay of treatment for seborrheic blephritis is use of warm to hot compresses followed by washing with non medicated baby shampoos and debridement of thick scales by using cotton tip.
  • Severe cases respond to ophthalmic ointment soultion containing sodium sulfacetamide. Fluconazole may have a role in patients with seborrheic dermatitis.[87]
  • Other treatment modalities which may have a role in severe and refractory disease include isotretinoin in low doses for 3-5 months and use phototherapy with narrowband ultraviolet B or psoralen plus ultraviolet A. Phototherapy treatment is not effective in patients with thick hair.[88][89]
  • Lithium succinate or gluconate topical preparations may have a role in seborrheic dermatitis involving areas other than the scalp, probably due to their antiinflammatory properties.[90][91][92]

Following are the preffered treatment regimens for treatment of seborrheic dermatitis:[93]

  • 1. Antifungal agents
  • Preferred regimen (1): Ketoconazole 2% in shampoo, foam, gel, or cream
  • Scalp: Twice/week for clearance THEN once/week or every other week for maintenance
  • Other areas: From bid to twice/week for clearance THEN from twice/week to once every other week for maintenance
  • Preferred regimen (2): Bifonazole 1% in shampoo or cream
  • Scalp: 3 times/week for clearance
  • Other areas: qd for clearance
  • Preferred regimen (3): Ciclopirox olamine (also called ciclopirox) 1.0% or 1.5% in shampoo or cream
  • Scalp: Twice to 3 times/week for clearance THEN once/week or every 2 week for maintenance
  • Other areas: Twice daily for clearance THEN qd for maintenance
  • 2. Corticosteroids
  • Scalp: Twice weekly in a short- contact fashion (up to 10 min application, then washing)
  • Preferred regimen (5): Desonide 0.05% lotion bid on scalp and other areas
  • 3. Lithium salts

Plant-based treatments

Main article: phytotherapy

The World Health Organization mentions Aloe vera gel as a yet to be scientifically proven traditional medicine treatment for Seborrhoeic dermatitis.[94]

Surgery

Surgical intervention is not recommended for the management of seborrrheic dermatitis.

Prevention

Related Chapter

External Links

References

  1. ↑ Shuster S (1984). "The aetiology of dandruff and the mode of action of therapeutic agents". Br J Dermatol. 111 (2): 235–42. PMID 6235835.
  2. ↑ Low, R. Cranston, and H. W. Barber. "Discussion on the etiology of seborrhoea and seborrhoeic dermatitis." The British Medical Journal (1922): 752-757.
  3. ↑ 3.0 3.1 Dessinioti C, Katsambas A (2013). "Seborrheic dermatitis: etiology, risk factors, and treatments: facts and controversies". Clin Dermatol. 31 (4): 343–51. doi:10.1016/j.clindermatol.2013.01.001. PMID 23806151.
  4. ↑ Dessinioti, Clio, and Andreas Katsambas. "Seborrheic dermatitis: Etiology, risk factors, and treatments:: Facts and controversies." Clinics in dermatology 31.4 (2013): 343-351.
  5. ↑ ===Classification by Anatomical Location===Peyri, J., and M. Lleonart. "Clinical and therapeutic profile and quality of life of patients with seborrheic dermatitis." Actas Dermo-Sifiliográficas (English Edition) 98.7 (2007): 476-482.
  6. ↑ name="pmid6220754">Burton JL, Pye RJ (1983). "Seborrhoea is not a feature of seborrhoeic dermatitis". Br Med J (Clin Res Ed). 286 (6372): 1169–70. PMC 1547390. PMID 6220754.
  7. ↑ 7.0 7.1 {{cite journal| author=Thomas DS, Ingham E, Bojar RA, Holland KT| title=In vitro modulation of human keratinocyte pro- and anti-inflammatory cytokine production by the capsule of Malassezia species. | journal=FEMS Immunol Med Microbiol | year= 2008 | volume= 54 | issue= 2 | pages= 203-14 | pmid=: 18752620 | doi=10.1111/j.1574-695X.2008.00468.x | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?
  8. ↑ Schwartz RA, Janusz CA, Janniger CK (2006). "Seborrheic dermatitis: an overview". Am Fam Physician. 74 (1): 125–30. PMID 16848386.
  9. ↑ Dessinioti, Clio, and Andreas Katsambas. "Seborrheic dermatitis: Etiology, risk factors, and treatments:: Facts and controversies." Clinics in dermatology 31.4 (2013): 343-351.
  10. ↑ ===Classification by Anatomical Location===Peyri, J., and M. Lleonart. "Clinical and therapeutic profile and quality of life of patients with seborrheic dermatitis." Actas Dermo-Sifiliográficas (English Edition) 98.7 (2007): 476-482.
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  12. ↑ name="pmid6220754">Burton JL, Pye RJ (1983). "Seborrhoea is not a feature of seborrhoeic dermatitis". Br Med J (Clin Res Ed). 286 (6372): 1169–70. PMC 1547390. PMID 6220754.
  13. ↑ 13.0 13.1 {{cite journal| author=Tajima M| title=[Malassezia species in patients with seborrheic dermatitis and atopic dermatitis]. | journal=Nihon Ishinkin Gakkai Zasshi | year= 2005 | volume= 46 | issue= 3 | pages= 163-7 | pmid=16094289 | doi= | pmc= | url=http://www.ncbi.nlm.nih.gov/entrez/eutils/elink.fcgi?
  14. ↑ 14.0 14.1 14.2 Faergemann J, Bergbrant IM, Dohsé M, Scott A, Westgate G (2001). "Seborrhoeic dermatitis and Pityrosporum (Malassezia) folliculitis: characterization of inflammatory cells and mediators in the skin by immunohistochemistry". Br J Dermatol. 144 (3): 549–56. PMID 11260013.
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