Seborrheic Dermatitis from Journal

Selden T. Seborrheic Dermatitis Clinical presentation. United States. 2012 [Diakses pada 6 Januari 2013]. Diakses dari http://emedicine.medscape.com/article/1108312-overview#a0101.

Seborrheic dermatitis is a papulosquamous disorder patterned on the sebum-rich areas of the scalp, face, and trunk. In addition to sebum, this dermatitis is linked to Malassezia,[1] immunologic abnormalities, and activation of complement. It is commonly aggravated by changes in humidity, changes in seasons, trauma (eg, scratching), or emotional stress. The severity varies from mild dandruff to exfoliative erythroderma. Seborrheic dermatitis may worsen in Parkinson diseaseand in AIDS.[2, 3] Pathophysiology Seborrheic dermatitis is associated with normal levels of Malassezia but an abnormal immune response. Helper T cells, phytohemagglutinin and concanavalin stimulation, and antibody titers are depressed compared with those of control subjects. The contribution of Malassezia species to seborrheic dermatitis may come from its lipase activityreleasing inflammatory free fatty acidsand from its ability to activate the alternative complement pathway.[4] Frequency International The prevalence rate of seborrheic dermatitis is 3-5%, with a worldwide distribution. Dandruff, the mildest form of this dermatitis, is probably far more common and is present in an estimated 15-20% of the population. Age The usual onset occurs with puberty. It peaks at age 40 years and is less severe, but present, among older people. In infants, it occurs as cradle cap or, uncommonly, as a flexural eruption or erythroderma.[5] History Intermittent, active phases of seborrheic dermatitis manifest with burning, scaling, and itching, alternating with inactive periods. Activity is increased in winter and early spring, with remissions commonly occurring in summer.

Active phases of seborrheic dermatitis may be complicated by secondary infection in the intertriginous areas and on the eyelids. Candidal overgrowth is common in infantile napkin dermatitis. Such children may have a diaper dermatitis variant of seborrheic dermatitis or psoriasis. Generalized seborrheic erythroderma is rare. It occurs more often in association with AIDS, [2,
3]

congestive heart failure, Parkinson disease, and immunosuppression in premature infants.

Physical The scalp appearance of seborrheic dermatitis varies from mild, patchy scaling to widespread, thick, adherent crusts. Plaques are rare. From the scalp, seborrheic dermatitis can spread onto the forehead, the posterior part of the neck, and the postauricular skin, as in psoriasis. Note the images below. Seborrheic dermatitis affecting the scalp line and the eyebrows with red skin and scaling. Courtesy of Wilford Hall Medical Center Dermatology slide files. Seborrheic dermatitis may affect any hairbearing area, and the chest is frequently involved. Courtesy of Wilford Hall Medical Center Dermatology Teaching slides. Seborrheic dermatitis skin lesions manifest as branny or greasy scaling over red, inflamed skin. Hypopigmentation is seen in blacks. Infectious eczematoid dermatitis, with oozing and crusting, suggests secondary infection. A seborrheic blepharitis may occur independently. Distribution follows the oily and hair-bearing areas of the head and the neck, such as the scalp, the forehead, the eyebrows, the lash line, the nasolabial folds, the beard, and the postauricular skin. An extension to submental skin can occur. Presternal or interscapular involvement is more common than nonscaling intertrigo of the umbilicus, axillae, inframammary and inguinal folds, perineum, or anogenital crease, which also may be present. Two distinct truncal patterns of seborrheic dermatitis can occasionally occur. An annular or geographic petaloid scaling is the most common. A rare pityriasiform variety can be seen on the trunk and the neck, with peripheral scaling around ovoid patches, mimicking pityriasis rosea. Note the image below. African Americans and persons from other darker-skinned races are susceptible to annular seborrheic dermatitis, also called petaloid seborrheic dermatitis or seborrhea petaloides. Sarcoidosis, secondary syphilis, and even discoid lupus may be in the differential in such cases. Courtesy of Jeffrey J. Meffert, MD

Causes Malassezia organisms are probably not the cause but are a cofactor linked to a T-cell depression, increased sebum levels, and an activation of the alternative complement pathway. Persons prone to this dermatitis also may have a skin-barrier dysfunction.[6, 7] Because seborrheic dermatitis is uncommon in preadolescent children, and tinea capitis is uncommon after adolescence, dandruff in a child is more likely to represent a fungal infection. A fungal culture should be completed for confirmation. Various medications may flare or induce seborrheic dermatitis. These medications include auranofin, aurothioglucose, buspirone, chlorpromazine, cimetidine, ethionamide, fluorouracil, gold, griseofulvin, haloperidol, interferon alfa, lithium, methoxsalen, methyldopa, phenothiazines, psoralens, stanozolol, thiothixene, and trioxsalen.[8, 9] Laboratory Studies A clinical diagnosis of seborrheic dermatitis is usually made based on a history of waxing and waning severity and by the distribution of involvement upon examination. Procedures A skin biopsy may be needed in persons with exfoliative erythroderma, and a fungal culture can be used to rule out tinea capitis, although tinea capitis in the adult is rare. Histologic Findings Dermatopathologic findings of seborrheic dermatitis are nonspecific. Hyperkeratosis, acanthosis, accentuated rete ridges, focal spongiosis, and parakeratosis are characteristic. Psoriasis is distinguished by regular acanthosis, thinned rete ridges, exocytosis, parakeratosis, and an absence of spongiosis. Neutrophils may be seen in both diseases. Medical Care Early treatment of flares is encouraged. Behavior modification techniques in reducing excoriations are especially helpful with scalp involvement. Topical corticosteroids may hasten recurrences, may foster dependence because of a rebound effect, and are discouraged except for short-term use. Skin involvement responds to ketoconazole, naftifine, or ciclopirox creams and gels.[11,
12, 13]

Alternatives include calcineurin inhibitors (ie, pimecrolimus,

tacrolimus),[14, 15, 16]sulfur or sulfonamide combinations, or propylene glycol. [17, 18, 19, 20, 21] Class IV or

lower corticosteroid creams, lotions, or solutions can be used for acute flares. Systemic ketoconazole or fluconazole may help if seborrheic dermatitis is severe or unresponsive.[22] Combination therapy has been recommended.[23] Dandruff responds to more frequent shampooing or a longer period of lathering. Use of hair spray or hair pomades should be stopped. Shampoos containing salicylic acid, tar, selenium, sulfur, or zinc are effective and may be used in an alternating schedule.[24,
25]

Overnight occlusion of tar, bath oil, or

Baker's P&S solution may help to soften thick scalp plaques. Derma-Smoothe F/S oil is especially helpful when widespread scalp plaques are present. Selenium sulfide (2.5%), ketoconazole, and ciclopirox shampoos may help by reducingMalassezia yeast scalp reservoirs.[26, 27, 28] Shampoos may be used on truncal lesions or in beards but may cause inflammation in the intertriginous or facial areas. Siadat et al reported that 1% metronidazole gel is effective for seborrheic dermatitis of the face.
[29]

Some suggest using a nonsteroidal cream.[30] Bikowski recommends azelaic acid.[31] Seborrheic

blepharitis may respond to gentle cleaning of eyelashes with baby shampoo and cotton applicators. The use of ketoconazole cream in this anatomical region is controversial. Ketoconazole topical Available as ketoconazole cream 2% (Nizoral), ketoconazole foam (Extina), ketoconazole shampoo 2% (Nizoral 2%; prescription only in United States), ketoconazole shampoo 1% (Nizoral A-D Shampoo; over-the-counter in United States) Imidazole broad-spectrum antifungal agent. Inhibits synthesis of ergosterol, causing cellular components to leak, resulting in fungal cell death. Corticosteroids Class Summary Have anti-inflammatory properties and cause profound and varied metabolic effects. Also modify body's immune response to diverse stimuli. Betamethasone topical (Valisone) Medium-strength topical corticosteroid for body areas. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Affects production of lymphokines and has inhibitory effect on Langerhans cells.

Desonide For inflammatory dermatosis responsive to steroids. Decreases inflammation by suppressing migration of polymorphonuclear leukocytes and reversing capillary permeability. Keratolytics Class Summary Cause cornified epithelium to swell, soften, macerate, and then desquamate. Coal tar shampoo (DHS Tar, MG217, Theraplex T, Psoriasin); Scytera foam Inhibits deregulated epidermal proliferation and dermal infiltration; antipruritic and antibacterial. Immunosuppressants Class Summary Exert anti-inflammatory affect by inhibiting T-lymphocyte activation. Safer than topical steroids for prolonged use or in skin folds. Tacrolimus ointment (Protopic) Nonsteroidal anti-inflammatory agent. Should not cause steroid-type skin atrophy. Currently indicated only for atopic dermatitis in immunocompetent patients 2 y. Pimecrolimus (Elidel cream 1%) Nonsteroidal anti-inflammatory agent. Should not cause steroid-type skin atrophy. Currently indicated only for atopic dermatitis in immunocompetent patients 2 y. Use cream sparingly to avoid maceration in skin folds.

VI. DIAGNOSIS Diagnosis dermatitis seboroikdapat ditegakkan berdasarkan : A. Kelainan kulit yang terdiri dari eritema dan skuama yang berminyak dan agak kekuningan batasnya agak kurang tegas (skuama dapat halus atau kasar)1 B. Predileksi dermatitis seboroik terdapat pada bagian tubuh yang banyak terdapat kelenjar sebasea (kelenjar minyak) yaitu daerah kepala (kulit kepala, telinga bagian luar, saluran telinga, kulit di belakang telinga), wajah (alis mata, kelopak mata, glabellla, lipatan nasolabial, dagu), badan bagian atas (daerah presternum, daerah interskapula, areolla mammae, umbilikus, lipatan paha, daerah anogenital) .6

Leiners Disease atau disebut juga erythroderma desquamativum merupakan kelainan kulit dengan gangguan sistem imun yang terjadi pada bayi baru lahir dan ditandai oleh dermatitis seboroik generalisata, diare berulang, infeksi lokal pada kulit, anemia dan kegagalan untuk berkembang, sehingga bayi dengan gejala-gejala ini harus dievaluasi. Erythroderma desquamativum (Leiners Disease) merupakan komplikasi dermatitis seboroik pada bayi (dermatitis seborrhoides infantum). Kelainan kulit pada Leiners Disease berupa eritema universal disertai skuama yang kasar pada daerah kulit kepala, wajah. Sangat cepat menyebar ke bagian lain dari tubuh