Continuing Education Activity
Seborrheic dermatitis (SD) is a common papulosquamous skin disease occurring predominantly in infancy and middle age, exhibiting distinct variations across these age groups.Characterized byfolliculocentric salmon-colored papules and plaques with a fine white scale and a yellowish crust (often described as a greasy scale-crust), SD manifests diversely across different body areas and maypresent inmultiple locations. Because it often resembles other dermatoses, SD necessitates accurate differentiation. Notably, flexural surfaces typically display lesser scaling, with poorly defined margins.
This activity delineates the nuanced manifestations of SD in infants, presenting as greasy scales on the scalp, reassuring clinicians about its typically mild, self-resolving nature within the first year of life. Conversely, the adult variant of SD showcases a relapsing and remitting disease pattern, significantly impacting quality of life.Emphasizing the importance of tailored management approaches for varying disease stages,the source discussion reviewshow distinct presentations of SD influence treatment decisions, thereby enhancing clinicians' skills in optimizing therapeutic outcomes.
Objectives:
Assess the burden ofSD from an epidemiological, clinical, and economic perspective and be aware of its potential to impair quality of life.
Identify the hypotheses concerned with understanding the diverse pathophysiological mechanisms underlying the development of SD.
Determine the various dermatoses that morphologically resembleSD and differentiate the latter from the rest based on characteristic clinical features.
Develop an evidence-based formulary for treatingSD that includes conservative measures, over-the-counter products, and prescription treatments that are age-appropriate and likely to improve compliance, along with facilitating the variation of treatment at home.
Introduction
Seborrheic dermatitis (SD) is a common inflammatory skin disease presenting with a papulosquamous morphology in areas rich in sebaceous glands, particularly the scalp, face, and body folds.[1]Two variants of SD reflect the condition's bimodal occurrence:infantile SD (ISD) and adult SD (ASD).
Infants are usually extensively affected by SD, whichoften appears as firm, greasy scales on the crown and frontal regions of the scalp that can cause significant parental anxiety. ISD occursduring the first3 months of life; it is mild, self-limiting, and, in most cases, resolvesspontaneously by the first year of life.
ASD, on the other hand, is characterized by a relapsingand remitting pattern of disease and isranked third behind atopicand contact dermatitis for its potential to impairpatients' quality of life.[2]
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 ofSD 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 first3 months of life and from adrenarche to a second peak after the fourth decade. In Australian preschool children, SD prevalence was approximately 72% at3 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 factorsfor the development of SD include:
Age
Male sex
Increased sebaceous gland activity
Immunodeficiency, including:[10]
Lymphoma
Renal transplantation
HIV-AIDS
Neurologicaland 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 ofSD 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 sebumand 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 andthe significant resolution of SD with antifungal treatment.
Histopathology
The dermatopathology ofSD 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 scalpand "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 versicolorand Pityrosporumor 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 arethesites most commonly involved in ASD, witharound 88%, 70%, and 27% of cases developing lesions in these areas, respectively.[18]On the headand 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 papulesand 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 mildand self-limiting. A common presentationknown ascradle 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]
Pityriasisamiantacea 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 pruriticand prone to weeping and typically occurs on the faceand 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
Histologyand direct immunofluorescence
HIV serology; Venereal Disease Research Laboratory (VDRL)
Serum zinc levels
Antinuclearantibodies (ANA); extractable nuclear antigens (ENA); erythrocyte sedimentation rate (ESR)
Treatment / Management
The approach to treating SDvaries according to the patient’s age and the distributionand 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 corticosteroidsand 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.
A typical formulary should include antifungals, keratolytics, antipruritics, and antiinflammatories (topical corticosteroidsand calcineurin inhibitors).Moreover, treatment rotation may be more effective and associated with fewer adverse reactions than persisting with monotherapy.For scalpand 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 corticosteroidand 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.
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 scalpand nonscalp regions and wash them off after 5to 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 antifungaland 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]
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.
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% tacrolimusointment
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 atrophyand scarring alopecia
Rosacea: Look for erythemaand 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]orallergic 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 edgesand 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 palmsand 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 diagnosisof 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 mildand self-limiting, whereas ASD presents a chronic pattern of skin disease characterized by relapsesand remissions.
ASD is very controllable but not curable.Althoughthe 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 areasand 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 SDcauses 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]
Deterrence and Patient Education
Parental education ishelpful in allaying anxiety associated with ISD, and well-informed adults can learn to be confident in managing their condition,
For ASD,patient educationrequires emphasizing that there is no cure, but the condition can be well-controlled and managed primarilyat home.[25]
Many treatments for SD are available without a prescription, over the counter at the pharmacy, or increasingly on supermarket shelves. Directing the patient to the selection of such products may save consultation time and associated costs.
Enhancing Healthcare Team Outcomes
SD is a difficult condition to manage in adults, and it is best done by an interprofessional team. A few important considerations:
Consider the impact of SD on psychosocial functioningand quality of life, and remember that SD may accompany neurological or psychiatric disease.[36]
The dermatologistand pharmacist can help to promote the appropriate use of topical corticosteroids and employ steroid-sparing alternatives.
New evidence suggests diet may play a role in SD, with a high fruit intake associated with a 25% lower risk of SD, whereas a "Western" diet was associated with a 47% increased risk of SD.[37]Proper diet counseling sessions with a dietician can help the patient.
Even though primary clinicians manage the condition, it is best to refer the complex patient to the dermatologist for guidance. Dermatology specialty–trained nurses can also help by counseling the patient, providing direction on medical management, and monitoring and charting treatment progress. A pharmacist should also be on the case, with assistance in selecting the most appropriate agents, verifying dosing, offering patient education, performing medication reconciliation, and informing the prescriber of any issues encountered. Close communication between interprofessional team members is vital for better patient management.
Review Questions
Figure
Infantile Seborrhoeic Dermatitis DermNet New Zealand
Figure
Seborrhoeic Dermatitis DermNet New Zealand
Figure
Seborrheic Dermatitis Contributed by S bhimji, MD
Figure
Seborrheic dermatitis Contributed by Dr. Hasnain Ali Syed
Figure
Seborrheic Dermatitis seen on the scalp extending to forehead. Contributed by Dr. Hasnain Ali Syed
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Disclosure: Dan Tucker declares no relevant financial relationships with ineligible companies.
Disclosure: Sadia Masood declares no relevant financial relationships with ineligible companies.