Seborrheic Dermatitis

Etiology

There are multiple factors associated with the development of SD, and their disparate nature has led to many proposals about its cause and pathogenesis. The onset of SD appears linked to the interplay of normal microscopic skin flora (especially Malassezia spp.), the composition of lipids on the skin surface, and individual susceptibility.[3][4] Neither the level of sebum produced nor the amount of yeast appears to be significant factors.[5]

Epidemiology

The worldwide prevalence of SD is around 5%, but most of its noninflammatory variant, dandruff, is probably closer to 50%.[6] SD affects all ethnic groups in all regions globally.[7] The prevalence of SD is bimodal, with a peak in the first 3 months of life and from adrenarche to a second peak after the fourth decade. In Australian preschool children, SD prevalence was approximately 72% at 3 months, then fell rapidly with an overall incidence of 10%. Furthermore, the Rotterdam Study data analysis found that 14% of middle-aged and elderly adults had SD.[8] In patients with HIV-AIDS, however, 35% of those with early HIV infection have SD, and the prevalence reaches 85% in patients with AIDS.[9]

Risk factors

Risk factors for the development of SD include:

• Age 
• Male sex 
• Increased sebaceous gland activity 
• Immunodeficiency, including:[10]
• Lymphoma
• Renal transplantation
• HIV-AIDS
• Neurological and psychiatric diseases, including[11]:
• Parkinson disease [12]
• Stroke
• Alzheimer dementia
• Major depression
• Autonomic dysfunction
• Exposure to drug treatment, including:
• Dopamine antagonists
• Immunosuppressants
• Psoralen and psoralen plus ultraviolet A (PUVA)
• Lithium
• Low ambient humidity aandlow ambient temperature 

Pathophysiology

The proposed Mechanisms for the Pathogenesis of SD include:

• Disruption of the skin’s microbiota
• An impaired immune reaction to Malassezia spp. associated with a diminished T-cell response and activation of complement 
• The increased presence of unsaturated fatty acids on the skin surface 
• Disruption of cutaneous neurotransmitters  
• Abnormal shedding of keratinocytes
• Epidermal barrier disturbances associated with genetic factors [13]

The role of Malassezia spp. also includes the degradation of sebum and consumption of saturated fatty acids, disrupting the lipid balance on the skin surface.[14] Further evidence for the involvement of Malassezia spp. includes their isolation from SD lesions and the significant resolution of SD with antifungal treatment.

Histopathology

The dermatopathology of SD is nonspecific, but the surface and infundibular epidermis usually show a superficial perivascular infiltrate of lymphocytes, acanthosis, focal spongiosis, and focal parakeratosis.[15][14] "Shoulder parakeratosis" refers to scale-crust accumulation around the infundibular ostia, which is appreciated in patients. Malassezia spp. may be present in the stratum corneum.

Histological progression from acute to chronic SD characteristically demonstrates a transition from spongiosis to psoriasiform hyperplasia and the development of a lichenoid lymphocytic infiltrate. Severe SD is often associated with keratinocyte necrosis, focal interface destruction, and leukocytoclasia.

History and Physical

The distribution of lesions is the most important clinical feature of SD, with lesions occurring in areas where the skin is rich in sebaceous glands, especially on the scalp and face.[16] ISD is generally asymptomatic, but atopic dermatitis frequently coexists. On the other hand, pruritus is common in ASD, especially with scalp lesions, and patients regularly report burning, but there is usually no history of atopic dermatitis. SD characteristically demonstrates folliculocentric salmon-colored papules and plaques with a fine white scale and a yellowish crust often described as a greasy scale crust. It may present in one or more locations, with less scaling on flexural surfaces, and with lesions whose margins tend to be poorly defined.

The mildest form of SD is a noninflammatory variant commonly called pityriasis capitis or sicca.[14] It affects the scalp and "beard region" and is associated with the shedding of small light-colored flakes of skin, often seen on a background of dark clothing as "dandruff." The sudden onset of severe SD should be a red flag for the presence of HIV-AIDS, with early recognition and diagnosis of HIV-AIDS significantly improving long-term outcomes. Common clinical presentations include reddening of the face, scaling, and dandruff. On darker skin, there may be persistent dyschromia with variable hyper- and hypo-pigmentation.

Other conditions associated with Malassezia spp. may be present, including pityriasis versicolor and Pityrosporum or Malassezia folliculitis in adults and neonatal cephalic pustulosis.[17] Lesions on the anterior chest tend to have a psoriasiform morphology but frequently have a petaloid appearance, with such annular lesions commonly observed on the face in darker skin phenotypes. A pityriasiform variation (with a collarette scale mimicking pityriasis rosea) is rare.

ASD

The face, scalp, and chest are the sites most commonly involved in ASD, with around 88%, 70%, and 27% of cases developing lesions in these areas, respectively.[18] On the head and neck, SD is characteristically symmetrical and involves the central third of the face, including the malar region, the center of the forehead, the eyebrows (especially their medial aspects), the postauricular area, and the external ear canal. SD characteristically affects the nasolabial and alar folds, and blepharitis is a common finding with the involvement of the anterior (lash) line.

Psoriasis requires differentiating from SD in adults.[19] It is characterized by indurated red papules and plaques with a sharply defined margin and a loose, silvery lamella scale. The nails may show psoriatic changes, and the Auspitz sign is positive. The existence of sebopsoriasis as a separate clinical entity has come into dispute.[11]

ISD

ISD usually appears in the second week of life and tends to last 4 to 6 months. It can be present in the same facial distribution as that of ASD, the diaper region, the skin creases of the neck, and the axillae. The rash is usually not itchy or painful, and the infants look content, but parents may be distressed. It is generally mild and self-limiting. A common presentation known as cradle cap refers to an adherent yellowish scale-crust that arises on the crown and front of the scalp, developing from a bran-like scale, serous ooze, and a greasy crust, to create a firm mass that may progress to involve the whole scalp.[20]

Pityriasis amiantacea may be present in ISD.[21] It represents a set of clinical findings that may occur in older infants or young children but is not specific to seborrheic dermatitis.[22] Typically, there are thick, silvery, or yellow scales enveloping scalp hairs and binding them in tufts, and can also be present in scalp psoriasis, atopic dermatitis, and tinea capitis. Atopic dermatitis is important in the differential diagnosis of ISD. It tends to be pruritic and prone to weeping and typically occurs on the face and limb flexures (elbow and knee) and spares the trunk. The child tends to be upset by the rash, and scratch marks are common.

Evaluation

It is not necessary to routinely investigate SD, but HIV serology should be expedited in cases of severe SD, especially where the onset is sudden.[23] Clinical features of Parkinson disease require recognition in elderly patients. The patient’s medications require a review as well.

The following tests may be helpful in the diagnosis of SD and its associated pathologies:

• Potassium hydroxide (KOH) examination of skin scrapings
• Swab for microscopy, culture, and sensitivities
• Histology and direct immunofluorescence
• HIV serology; Venereal Disease Research Laboratory (VDRL)
• Serum zinc levels
• Antinuclear antibodies (ANA); extractable nuclear antigens (ENA); erythrocyte sedimentation rate (ESR)

Treatment / Management

The approach to treating SD varies according to the patient’s age and the distribution and severity of the condition. Discussing good general skincare practices, including using a soap substitute and appropriate moisturizing, is essential.[24] Treatments should address the underlying disease process and any secondary features, especially the hyperkeratotic scale, Staphylococcal infection, and associated symptoms, particularly pruritus. 

A Danish expert group recommended that authorities adopt topical antifungals as first-line treatment and agreed that topical corticosteroids and calcineurin inhibitors should only be used for significant symptoms and to manage moderate to severe flare-ups.[25] In ISD, removing the scale crust in the cradle cap and dealing with parental anxiety are important considerations.[26] Sorbolene cream or lotion and a soft-bristled toothbrush can soften and remove the cradle cap scales. On the other hand, it is crucial to relieve itch and discomfort in ASD. (A1)

A typical formulary should include antifungals, keratolytics, antipruritics, and antiinflammatories (topical corticosteroids and calcineurin inhibitors). Moreover, treatment rotation may be more effective and associated with fewer adverse reactions than persisting with monotherapy. For scalp and nonscalp SD treatment, evidence supports topical 1% to 2% ketoconazole, 1% ciclopirox, 1% zinc pyrithione, and 1% hydrocortisone.[27] Intermittent use of a mild topical corticosteroid and imidazole antifungal combination is convenient and can be very effective, but a potent corticosteroid may be necessary for the short-term treatment of scalp ASD. (B3)

Shampoos usually contain combinations of agents such as pine or coal tar (antipruritic/keratolytic), salicylic acid (keratolytic), sulfur (antimicrobial/keratolytic), and sulfacetamide (antiinflammatory/antibacterial). The patient can apply these to the scalp and nonscalp regions and wash them off after 5 to 10 minutes. Given the lack of safety and efficacy data to inform such treatment, care should be taken when using topical salicylic acid, selenium, or zinc for treating ISD. Still, topical ketoconazole has been shown to be safe in infants, with minimal systemic absorption detected.

Side effects associated with topical corticosteroids should be mitigated by intermittent use of site-appropriate potencies or steroid-sparing preparations such as topical 1% pimecrolimus. Another strategy is to employ the inherent antiinflammatory effect of the topical antifungals, estimated to be equivalent to 1% hydrocortisone.[28] 

Oral treatment should be a consideration for generalized or refractory disease, and the standard of care utilizes the antifungal and antiinflammatory properties of ketoconazole (monitor liver function; Black Box warning), itraconazole (check for CYP450 drug interactions; can worsen heart failure), and fluconazole (adjust the dose according to renal function). Itraconazole has the greatest antiinflammatory effect, whereas oral terbinafine may be more effective than oral fluconazole in severe SD. Low-dose isotretinoin is noninferior to the topical standard of care but is commonly associated with significant mucocutaneous side effects.[29](B2)

Itraconazole is safe and effective for controlling the flares of SD and preventing relapses.[28] It has also been shown to improve the quality of life in patients with moderate-to-severe SD.[30] However, given the absence of high-quality safety and efficacy data, a specialist team review is recommended before commencing oral treatment for ISD. In HIV-AIDS, antiretroviral treatment frequently improves SD, and SD may improve with L-dopa therapy in Parkinson disease.[31] Future therapies for SD could target improving skin barrier function or restoring the skin’s surface lipid composition.(B2)

Typical Formulary

Topical Creams, Ointments, and Lotions

• 2% salicylic acid + 2% sulfur in sorbolene cream or emulsifying ointment [32]
• 2% ketoconazole cream
• 1% clotrimazole + 1% hydrocortisone cream
• 10% sulfacetamide + 5% sulfur lotion [33]
• Betamethasone dipropionate 0.05% lotion
• 0.03% and 0.1% tacrolimus ointment
(A1)

Shampoos

• 1% zinc pyrithione
• 1% to .5% selenium sulfide
• 2% ketoconazole
• 1% ciclopirox
• 5% coal tar + 2% salicylic acid
• 0.1% and 0.03% tacrolimus

Oral Medication

• Itraconazole
• Fluconazole
• Terbinafine

Differential Diagnosis

Important considerations in the differential diagnosis of ASD include:

Scalp

• Psoriasis: Mostly nonpruritic and tends to affect the occipital and frontal regions, whereas SD tends to affect the vertex and parietal regions
• Eczema (contact): Due to the use of different shampoos and hair dye
• Darier disease: Yellowish-brown clusters of rough dome-shaped papules in seborrheic distribution; acanthosis; peculiar odor 

Face

• Psoriasis: Rarely occurs in isolation; pitted nails 
• Lupus erythematosus (LE): Discoid LE is associated with skin atrophy and scarring alopecia
• Rosacea: Look for erythema and telangiectasia; may cause meibomianitis along the posterior lid line
• Acne vulgaris: Look for comedones (hallmark feature)
• Staphylococcal blepharitis (anterior lash line)
• Eczema (contact): Eyelids commonly involved (versus irritant eczema [dry, scaly skin] or allergic eczema [swollen, vesicular skin rash])
• Darier disease: Nail changes 

Trunk

• Psoriasis: Sharply-defined red plaques with a loose, silvery lamella scale
• Pityriasis rosea: Herald spot; collarette scale; Christmas tree distribution
• Pityriasis versicolor: Not symmetrical; hypo- or hyperpigmentation
• Subacute LE: Photosensitive distribution
• Eczema (nummular): Intense pruritus
• Tinea corporis: Raised leading edges and central clearing; uncommon in infants
• Erythema annulare centrifugum: Recurrent polycyclic lesions that slowly expand and disappear
• Darier disease: Greasy wart-like papules and plaques
• Grover disease (transient acantholytic dermatosis): Acanthosis
• Drug reaction: Drug history (neuroleptic; immunosuppressant; PUVA; lithium)
• Parapsoriasis: Elderly; very slow growing; resistant to treatment
• Pemphigus foliaceus: Fragile, painful blisters; Nikolsky sign is positive
• Secondary syphilis: Lesions on the palms and soles; a history of chancre

Intertriginous Areas

• Psoriasis (inverse): Sharply-defined border
• Dermatitis (Contact) Itchy; vesicular
• Tinea cruris: Advancing border; very uncommon in infants
• Erythrasma: Coral-red fluorescence under Wood Lamp
• Candidiasis: Satellite lesions; obesity; a history of immunodeficiency
• Hailey-Hailey disease (familial benign pemphigus): Acanthosis

Important considerations in the differential diagnosis of ISD include:

Cradle Cap

• Tinea capitis: Look for broken hairs or “black dots”; very uncommon in adults
• Impetigo: Yellow, honey-colored crusting

Diaper Region

• Irritant contact dermatitis: Tends to spare the skin folds
• Candidiasis: Either secondary or from colonization with fecal yeast; look for satellite lesions
• Infantile psoriasis: Sharply-defined red plaques with silver scale
• Histiocytosis X (Langerhans cell histiocytosis): Tends to be confined to the skin folds with a purpuric rash on the body
• Acrodermatitis enteropathica: Look for periorificial involvement and check zinc levels

Prognosis

ISD usually affects the scalp and is mild and self-limiting, whereas ASD presents a chronic pattern of skin disease characterized by relapses and remissions.

ASD is very controllable but not curable. Although the disease does take a toll on the well-being of patients, timely management can help increase the quality of life.[34]

Complications

SD usually takes a benign course, and serious complications are very rare. The intertriginous areas and eyelids are prone to secondary bacterial infections, especially during acute flares, and the diaper region is particularly prone to overgrowth with Candida spp.

Erythroderma has been reported in immunosuppressed neonates with generalized ISD, but it is more frequently a feature in adults with HIV-AIDS. However, research has not firmly established that SD causes erythroderma per se, given its predilection for sebaceous-rich skin.[11][17] The most common problems associated with both ISD and ASD relate to misdiagnosis of the condition.[35]