Seborrheic dermatitis 

Salient features

• Seborrheic dermatitis is a common inflammatory skin disease affecting various age groups.
• Infantile and adult forms
• Erythematous, greasy, scaling patches and plaques appear on scalp, face, ears, chest, and intertriginous areas.
• Severe forms, like generalized erythroderma, rarely occur.
• Etiology is unclear but may be related to abnormal immune mechanism, active sebaceous glands, abnormal sebum composition, Malassezia (Pityrosporum) spp. and individual susceptibility.
• Can be a cutaneous sign of HIV infection
• Treatment is based on symptomatic control.    

 

Introduction

Seborrheic dermatitis is a common mild chronic eczema typically confined to skin regions with high sebum production and the large body folds. Although its pathogenesis is not fully elucidated, there is a link to sebum overproduction (seborrhea) and the commensal yeast Malassezia.

 

Epidemiology

The incidence of SD 2 to 5% of the general population and notably peaks in three age groups, in infancy between 2 weeks and 12 months of age, during adolescence, and between age 30 and 60 years during adulthood. This observation, together with the fact that SD occurs only in seborrhoeic areas, already raise the question whether these incidence peaks correlate with defined environmental, microbial and/or hormonal (eg androgen) changes in the skin milieu. Men are afflicted more often than women in all ages. Extensive and therapy-resistant seborrheic dermatitis is an important cutaneous sign of HIV infection.

 

Etiology and pathogenesis

Etiologic links with active sebaceous glands, abnormal sebum composition, and Malassezia furfur (Pityrosporum ovale). The cause of seborrhoeic dermatitis is not completely understood. It is associated with proliferation of various species of the skin commensal malassezia, in its yeast (non-pathogenic) form. The inflammation seen in seborrheic dermatitis may be irritant, caused by toxic metabolites (such as the fatty acids oleic acid, malssezin, and indole-3-carbaldehyde), lipase, and reactive oxygen species.^.

 

 

WORKING HYPOTHESIS

 

 

In contrast to the conventional Malassezia‐centric view of SD etiology, the working hypothesis is that intrinsic factors of the host—such as defective epidermal barrier (①) and/or changes in the amount or composition of sebum (②)—may be the root cause of seborrhoeic dermatitis (SD). These changes can be brought about, for example by genetic predisposition, host immune function, neuroendocrine factors, nutrition, medication and environmental factors. Once these changes have occurred, they may provide favorable conditions for the commensal Malassezia to over colonize the area and become the dominant species, alter skin microbiota (③), and for yeast metabolites such as oleic acid to penetrate the defective barrier and elicit a rather non‐specific inflammatory response (④). Defects in host immune response to or clearing of microbes may bypass the initial epidermal or sebaceous abnormalities. Recruitment of more immune cells to the site of disruption and release of pro inflammatory cytokines and chemokines could further disrupt epidermal differentiation and barrier function, cause further imbalance of the skin microbiota, and to allow more yeast metabolites and yeast to penetrate the epidermal layers, thus trigger sustained inflammation in a vicious circle. The role of γδ T cells is currently unknown in human SD. Restoration of barrier function (①), modulating sebaceous activity (②), and modulating host immune activity (④) in combination with antifungal treatment (③) may provide more effective intervention to break the vicious cycle of SD

 

Environmental factors

SD is more common and severe in cold and dry climates in winter and improves with sun exposure.

 

Seborrheic dermatitis: Parts of the body typically affected 

 

 

 

Clinical Features

 

Seborrheic dermatitis is defined by clinical parameters, including:

  

·       Red sharply demarcated patches or thin plaques covered with bran-like flaky greasy adherent scales.

·       A predilection for areas rich in active sebaceous glands – scalp, facial creases, ears, presternal region and large body folds (inguinal, inframammary, and axillary). Less commonly involved sites include interscapular, umbilical, perineum, and the anogenital crease.

 

·       A mild course with little or moderate discomfort.

Seborrheic dermatitis is most often limited in extent, but generalized and even erythrodermic forms can occur, albeit rarely.

 

Clinical patterns of seborrhoeic dermatitis

Adult

 

Scalp

 

Dandruff

Inflammatory—may extend onto non-hairy areas (e.g. post auricular)

 

Face (may include blepharitis and conjunctivitis)

 

Trunk

 

Petaloid

Pityriasiform

Flexural

Eczematous plaques

Follicular

Generalized (may be erythroderma)

Infantile

 

Scalp (cradle cap)

Trunk (including flexures and napkin area)

 

Adult seborrheic dermatitis

In adults, seborrheic dermatitis is generally found on the scalp and, usually of milder intensity, on the face; less often, lesions occur on the central upper chest and the intertriginous areas. Erythrodermic seborrheic dermatitis has been described as a rarity.

 

There are several morphological variants of seborrhoeic dermatitis in the adult form.

 

Scalp

Dandruff (Pityriasis simplex capillitii) is a common condition and is usually the mildest form and the earliest manifestation of seborrhoeic dermatitis. Most individuals periodically experience a diffuse, slight to moderate, fine dry white scaling of the scalp and terminal hair-bearing areas of the face (beard area), but without significant erythema or irritation. Scales accumulate visibly on dark clothing; this is dandruff. This common condition may be considered the mildest form of seborrheic dermatitis of the scalp. They tend to attribute this condition to a dry scalp and consequently avoid hair washing. Avoidance of washing allows more scales to accumulate and inflammation may occur. As a result yellow bran-like flaky greasy adherent scales may occur on an inflamed base. Patients with minor amounts of dandruff should be encouraged to wash every day or every other day with antidandruff shampoos.

In seborrheic dermatitis of the scalp, there is inflammation and pruritus in addition to dandruff. The vertex and parietal regions are predominantly affected, but in a more diffuse pattern than the discrete plaques of psoriasis. Towards the forehead, the erythema and scaling are usually sharply demarcated from uninvolved skin, with the border either at the hairline or slightly transgressing beyond it ("corona seborrhoica").  Pruritus is usually moderate but may be intense, particularly in patients with male pattern alopecia; folliculitis, furuncles, and meibomitis are not uncommon complications, elicited by scratching and rubbing.

In chronic cases there may be some degree of hair loss, which is reversible when the inflammation is suppressed.

 

Behind the ears there may be redness and greasy scaling, and a crusted fissure often develops in the fold and these greasy scales and crusts may extend into the adjacent scalp. Both sides of the pinna, the periauricular region, and the sides of the neck may be involved.

 

Face

 

Seborrheic dermatitis of the facial skin is often strikingly symmetric, affecting the forehead, medial portions of the eyebrows, the glabella, eyelashes, upper eyelids, nasolabial folds and lateral aspects of the nose, usually in association with involvement of the scalp. Lesions are yellowish-red, with a typical bran-like scale. Hypo pigmentation may be a prominent feature in dark‐skinned individuals.

 

Inflammation of the anterior eyelid margin (anterior blepharitis) may occur in SD and presents as redness of the lids margin with flaky debris on the eyelashes, typically near the base. When this loose debris falls into the eye, it results in conjunctival irritation and red eye.

 

 

Trunk

 

On the trunk, several forms of seborrhoeic dermatitis occur. Commonest is the petaloid form (so-called because the lesions are petal-shaped). This is often seen in men on the front of the chest and in the interscapular region. The initial lesion is a small, red follicular papule, covered by a greasy scale. More often, extension and confluence of the follicular papules gives rise to a figured eruption, consisting of multiple circinate patches, with a fine branny scaling in their centers, and with dark-red papules with larger greasy scales at their margins.

A rarer form, involving the trunk and limbs, is the so-called

pityriasiform type. This is a generalized erythematosquamous eruption, somewhat similar to, but more extensive than, pityriasis rosea. In particular it involves the neck up to the hair margin. It is not particularly pruritic, and it resolves spontaneously, although somewhat more slowly than does pityriasis rosea. In some patients the lesions may become psoriasiform.

 

 

Flexures

 

In the flexures, notably in the axillae, the groins, the anogenital and submammary regions, and the umbilicus, seborrhoeic dermatitis presents as an intertrigo, with diffuse, sharply marginated glazed erythema with less scale. Crusted fissures develop in the folds, and with sweating, secondary infection and inappropriate treatment, a weeping dermatitis may extend far beyond them.

 

All show a tendency to chronicity and recurrence. Occasionally, seborrhoeic dermatitis may become generalized, resulting in erythroderma.

 

Adult seborrheic dermatitis has a chronic relapsing course. Patients feel well and systemic signs are absent. Extensive and severe seborrheic dermatitis, however, should raise the suspicion of underlying HIV infection. Among patients with seborrheic dermatitis tested for HIV infection, 2% were found to be positive, frequently in a late stage of their disease. In patients with Parkinson disease, seborrheic dermatitis is a common finding, along with seborrhea. Its severity, however, is not correlated with that of the Parkinson disease. The facial immobility of patients with Parkinson disease might result in a greater accumulation of sebum on the skin, resulting in a permissive effect on the growth of Malassezia. Seborrheic dermatitis may be more common in patients with other causes of immobility such as cerebrovascular accidents. Rebound flares of seborrheic dermatitis can follow tapers of systemic corticosteroids.

 

 

Infantile seborrheic dermatitis

 

 

Infantile SD presents primarily with cradle cap and/or napkin dermatitis. This form usually begins about one week after birth with a peak incidence at 3 months of age, and may persist for several months. It corresponds to the time when neonates produce sebum, which then regresses until puberty. Initially, mild greasy scales adherent to the vertex and anterior fontanelle regions which may later extend over the entire scalp. Inflammation with erythema and oozing may finally result in a coherent scaly and crusty mass covering most of the scalp (“cradle cap”). Lesions of the axillae, inguinal creases, neck, and retroauricular folds are often acutely inflamed, oozing, sharply demarcated, and surrounded by satellite lesions. Superinfection with Candida spp. or occasionally bacteria (e.g. group A Streptococcus) can occur. A disseminated eruption of scaly papules with a psoriasiform appearance (“psoriasiform id reaction”) may develop on the trunk, proximal extremities, and face in association with exuberant or superinfected seborrheic dermatitis, especially of the diaper area.

 

Diagnosis

 

The diagnosis is usually made on clinical grounds without the need for diagnostic tests. HIV testing should be considered in any patient with severe seborrhoeic dermatitis, particularly in a patient involved in high-risk activities.

 

Differential Diagnosis

 

Infantile seborrheic dermatitis is distinguished from atopic dermatitis by its earlier onset, different distribution pattern, and, most importantly, by the absence of pruritus, irritability and sleeplessness. In contrast to atopic dermatitis, infants with seborrheic dermatitis generally feed well and are content. 

 

Irritant diaper dermatitis is confined to the diaper area and tends to spare the skin folds. 

 

Candidiasis of the diaper area can result from colonization with fecal yeast and some infants have seborrheic dermatitis with a superimposed candidal infection.

 

Infantile psoriasis may be difficult to distinguish from psoriasiform seborrheic dermatitis. Although psoriasiform diaper dermatitis can represent the initial manifestation of psoriasis, many affected infants do not subsequently develop psoriasis elsewhere.

 

When scalp scaling is present in prepubertal children, the possibility of tinea capitis due to Trichophyton tonsurans should be considered.

Pityriasis amiantacea is a localized or diffuse inflammatory condition of the scalp characterized by large plates of thick asbestos-like silvery scales firmly adherent to both the scalp and hair tufts. This condition can occur at any age, especially adolescents and young females. Alopecia may result and is generally non scarring unless secondary scalp infection occurs. Concomitant bacterial skin infection, mostly Staphylococcus, may result in scarring alopecia, so early and appropriately treatment is necessary.  Young females commonly have concomitant post auricular scales and fissures.

 

The most common skin diseases associated with pityriasis amiantacea are psoriasis (35%), and eczematous conditions like seborrheic dermatitis and atopic dermatitis (34%). Up to a third of the affected children and adolescents eventually develop psoriasis.+

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A number of entities are included in the differential diagnosis of adult seborrheic dermatitis. Distinction of seborrheic dermatitis of the scalp from psoriasis can be difficult. ++The controversial term sebopsoriasis is often used in patients when there appears to be an overlap of psoriasis and seborrheic dermatitis. It tends to localize to the scalp, face, and presternal chest as seen with seborrheic dermatitis. However, the plaques of psoriasis tend to be thicker and palpable, brighter pink color with silvery white scale, more circumscribed and discrete, less pruritic, and unassociated with seborrhea. In addition, features of psoriasis may be found elsewhere.

 

Dry scaling of the scalp, along with dry brittle hair (as opposed to greasy hair), is a symptom of xerotic skin (e.g. in atopic dermatitis), frequently mistaken for (and mistreated as) seborrheic dermatitis.

 

Lichen simplex of the nape of the neck occurs in females, and can mimic seborrhoeic dermatitis. The thickened plaques in this condition are, however, intensely irritable.

 

Seborrheic dermatitis of the face may closely resemble both early rosacea and the butterfly lesions of systemic lupus erythematosus. Lupus erythematosus rarely affects the nasolabial folds and often has a clearly demonstrable photo distribution. Notably, seborrheic dermatitis and rosacea frequently coexist.

 

The differential diagnosis of seborrheic dermatitis of the trunk includes pityriasis rosea (but in this latter entity the lesions are ellipsoid in shape, have collarette-like scaling, and there is no predilection for the central chest). The lesions of pityriasiform type of seborrhoeic dermatitis are more widely distributed, and there is no herald patch.

 

The brown scaly lesions of pityriasis versicolor are flatter, more extensive, and less symmetrical than the lesions of petaloid seborrhoeic dermatitis of the trunk. Microscopy of scrapings quickly establishes the diagnosis.

In the flexures, microscopic examination of scrapings from the advancing margin, and examination under Wood’s light will exclude ringworm infections, candidiasis and erythrasma.

 

 

Clinical course and prognosis

 

Generally SD in adults and adolescence has a chronic and recurrent relapsing course. Consequently the primary goal of treatment should be control of symptoms like pruritus, erythema, and scales, rather than cure of the disease. Also patients should be informed that they need to prepare for a future re-outbreak and avoid aggravating factors of SD. However, ISD has a benign, self-limited course; ISD spontaneously disappears by 6-12 months of age. Severe exacerbation with exfoliating dermatitis may occur, albeit rarely, but its prognosis is usually favorable. ISD does not progress to adulthood.

 

 

Management

 

Summary of NICE recommendations for the treatment of SD (The National Institute for Health and Care Excellence)

Type of seborrhoeic dermatitis	First line therapy	Second line therapy	Additional therapy
Scalp and beard	2% ketoconazole shampoo twice a week for a month, then once or twice a week for symptom control	Medicated shampoos with zinc pyrithione, coal tar or salicylic acid	Topical keratolytic or mineral/olive oil for the removal of scale and crust Potent topical corticosteroid scalp application for 4 weeks if there is severe scalp itch
Face and body in adults	Ketoconazole 2% cream o.d./b.d., Use as above for at least 4 weeks, then less frequently	Mild topical corticosteroids for 1–2 weeks	Antifungal shampoo, e.g. 2% ketoconazole, as a body wash Hygiene measures for eyelid involvement using cotton buds moistened with baby shampoo
Severe	Review diagnosis, consider specialist referral, HIV testing
In infants	Removal of scalp crusts with baby shampoo and gentle brushing. Overnight soak of petroleum jelly or warmed vegetable oil if needed. Daily bathing with soap substitute	Topical imidazole cream: clotrimazole 1% cream b.d./t.d.s., econazole 1% cream b.d., miconazole 2% cream b.d.	Topical corticosteroids not routinely advised but may be used for certain infants with nappy rash

 

 

 

Seborrhoeic dermatitis can generally be suppressed, there is no permanent cure. Long‐term maintenance treatment may be required but some patients only use treatment intermittently for acute, symptomatic flares. Topical antifungals are the mainstay of therapy due to their safety in all ages. Ketoconazole have been the most heavily investigated topical agent in SD. New formulations may also improve patient choice, such as 2% ketoconazole foam, which was found to be popular and effective as a long‐term treatment of SD for up to 52 weeks. However, some strains of Malassezia globosa and M. restricta are resistant to azole antifungals and this may be associated with treatment failure. Ciclopiroxolamine, a broad spectrum antifungal and anti-inflammatory agent, and a newer azole such as sertaconazole are also effective topically in treating SD of the scalp as a shampoo and face as a cream.

 

Dandruff is usually treated by the frequent and regular use of medicated shampoos which act against Malassezia yeasts, including zinc pyrithione, ketoconazole and various tar shampoos; 1% terbinafine solution has also been shown to be effective.

 

For severe dandruff with persistent scaling or crusting, 5% salicyclic acid ointment may be useful. If secondary bacterial infection is present or suspected, oral erythromycin or flucloxacillin may be used.

 

Acute forms of seborrhoeic dermatitis on the face, trunk and ears are treated with topical corticosteroids in combination with antifungals for their additional anti‐inflammatory effects, with improved results compared with antifungal monotherapy, which can then be changed to ketoconazole cream for long-term control. Short courses of low potency topical glucocorticoids (Class IV or lower) should be used to suppress the initial inflammation. Hydrocortisone ointment (0.5%) is often effective. Ketoconazole cream (2%) is possibly a more logical therapy, which has been shown to be equally effective. Concerns about atrophy limit the long‐term use of corticosteroids, especially in delicate sites such as the eyelids. Topical calcineurin inhibitors are emerging as an effective alternative. Topical calcineurin inhibitors (pimecrolimus and tacrolimus) have anti-inflammatory and antifungal (tacrolimus) properties without the long-term side effects of topical corticosteroid use. They manifest good effects on SD by blocking calcineurin, thus preventing both inflammatory cytokines and signaling pathways in T lymphocyte cells. Studies of topical pimecrolimus and tacrolimus in SD have found that improvement occurred within 2 weeks and that if SD recurred after stopping treatment it was significantly less severe. Seborrheic dermatitis tends to relapse if a maintenance regimen is not instituted. As M. furfur has a slow proliferation rate, an interval of two to several weeks will pass until relapses appear. The intervals of topical therapy should follow this rhythm. Maintenance treatment with topical calcineurin inhibitors may be useful in preventing the relapse and twice weekly 0.1% tacrolimus has been reported to be effective for up to 10 weeks in adult facial SD. Adverse effects includes mild burning and irritation.

Patients with seborrheic blepharitis can be treated with warm compresses and washing with baby shampoo followed by gentle cotton tip debridement of thick scale. Avoid ocular glucocorticoids. Ophthalmic sodium sulfacetamide ointment can be used for resistant seborrheic blepharitis.

Other treatments reported to be of benefit in facial SD include 4% nicotinamide cream and metronidazole 0.75% gel, and these may be particularly useful in patients with coexistent acne/rosacea.

Frequent washing with soap and water is helpful, possibly because removal of lipid removes the substrate for the yeasts.

 

For unresponsive cases, oral itraconazole (100 mg daily for up to 21 days) is also effective or itraconazole 200mg for the first 7 days of the month for several months is a regime used to get clinical improvement.

 

Generalized seborrhoeic dermatitis usually responds to the medications listed above, but in recalcitrant cases systemic steroids may be required. A 1-week course of prednisolone 0.5 mg/kg body weight/day usually produces a rapid response, while cautioning the patient of side effects and informing them of potential rebound flares following discontinuation of the medication.

 

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Infantile seborrheic dermatitis (ISD)

The basic principles of treatment are the same for infants. When ISD involves the diaper areas, the use of superabsorbent disposable diapers with frequent changes prevent the aggravation of the symptoms. Soap and alcohol containing compounds are not recommended in cleaning the diaper lesions.

 

Infantile seborrheic dermatitis usually responds satisfactorily to bathing and application of emollients. Ketoconazole cream (2%) is indicated in more extensive or persistent cases. Short courses of low-potency topical corticosteroids may be used initially to suppress inflammation. Mild shampoos are recommended for the removal of scalp scales and crusts. Avoidance of irritation (e.g. the use of strong keratolytic shampoos including salicylic acid and selenium sulfide that are dangerous to neonates because of the possibility of the percutaneous absorption; and mechanical measures to remove the scales from the scalp) is important.

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Figure 22-7

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