DERMATITIS (ECZEMA)

Eczema or dermatitis is an inflammatory skin reaction in response to an antigen stimulation. Eczema is Greek word , which means "to boil out" or "to effervesce". Baer describes eczema as a pruritic papulovesicular reaction, which is associated in its acute phase with erythema and edema, and in its chronic phase by thickening, lichenifecation, scaling, and retaining some of its papulovesicular features. Dermatitis constitutes more than thirty per cent of clinical dermatology. Classification of Eczema There are different classifications of eczema, which are sometimes confusing and therefore most authors prefer the word dermatitis. In spite that all cases of eczema is dermatitis, not all cases of dermatitis is considered as eczema since dermatitis means skin inflammation. Classification of eczema is sometimes arbitrary depending on the causative triggering factors. Eczema may be classified into: endogenous, which is due to processes originating within the body or exogenous eczema that is, mediated by exogenous factors. 1. Endogenous Eczema The term endogenous eczema implies that the eczematous condition is not due to exogenous or external environmental factors, but is mediated by processes originating within the body. In some conditions, however, there are both external and internal precipitating factors. Endogenous eczema includes: Atopic dermatitis Seborrheic dermatitis Nummular (Discoid) Pompholyx (dyshidrotic) Metabolic eczema or eczema associated with systemic diseases. Juvenile planter dermatoses Eczematous drug eruption Stasis dermatitis 2. Exogenous eczema This type of eczema is due to different exogenous factors that include the following: Primary irritant dermatitis Allergic contact dermatitis Photo allergic dermatitis Polymorphous light eruption. Infective dermatitis 3. Unclassified types of eczema Neurodermatitis (Lichen simplex chronicus) Nodular prurigo Eczema can be also classified according to the course and clinical picture in to: Acute eczema Sub acute eczema Chronic eczema

Atopic Dermatitis
Keith A. Knoell, MD* and Kenneth E. Greer, MD*

Definition
Atopic dermatitis (AD) or atopic eczema is a chronically relapsing, pruritic, exanthematous dermatosis of uncertain etiology that is characterized primarily by an allergic diathesis as well as erythema, oozing, crusting, excoriations, lichenification, and dehydration of involved skin surfaces (Figs 1 and 2). Affected infants typically are fussy from sleep deprivation because of pruritis and often are uncomfortable, are fretful, and may not eat well. Older children who have severe atopic eczema frequently are asthenic and may have difficulties at school. Onset occurs at approximately 2 to 3 months of age, and the disease may persist, with periodic exacerbations and remissions, into adulthood. Sites predisposed to rash change with growth and development. The face primarily is involved in infants (Fig 1); extensor areas of the body are affected more commonly by age 10 months (Fig 2); and lesions are located predominantly on the flexor surfaces, antecubital and popliteal fossa, and neck in older children and adolescents. Spread to other areas may occur in severe cases. This disorder is diagnosed primarily on clinical grounds, and treatment consists of removal of precipitating factors, antibiotic coverage, rehydration of the stratum corneum, and topical anti-inflammatory therapy.

Epidemiology
Regional variations in the prevalence of AD have been documented. In the western part of the world, the prevalence has been estimated at approximately 10%, up to a 20% prevalence has been reported in parts of Russia, and the prevalence is believed to be only 4.3% in Finland. Further, certain populations who migrate from areas of low disease prevalence, such as West India or Asia, to areas of high prevalence, such as London or southern California, respectively, have experienced an increased incidence of AD. Overall, males and females are affected with equal incidence and severity, and clear racial and ethnic predilections have not been established. Seasonal variation does play a role in the prevalence, with exacerbations occurring primarily in the winter. Although a clear genetic predisposition has not been identified, there usually is a family history of either atopic eczema, asthma, or seasonal allergic rhinitis.

Etiology and Precipitating Factors

The etiology of AD has not been fully elucidated, but it has been suggested that both genetic and environmental factors play a role in its genesis. Although a genetic linkage for AD has not yet been identified, clinical observations do suggest a hereditary basis for the disease. Recently, it has been shown that the prevalence of atopic eczema in children is approximately 60% with one affected parent and approaches 80% with two affected parents. It also has been reported that nearly 40% of patients have at least one firstdegree relative who has AD. Studies of twins have shown a very high degree of concordance of AD in monozygotic compared with dizygotic twins. Several genodermatoses, including icthyosis vulgaris, Netherton syndrome, Wiskott-Aldrich syndrome, and Bruton agammaglobulinemia, also are associated with AD. Environmental factors, including contact irritants and allergens, climate, sweating, aeroallergens, microbial organisms, certain foods, and stress/psyche, all have been shown to trigger AD in susceptible individuals (Table 1). Contact irritants and allergens (eg, soaps, solvents, wool clothing, mechanical irritants, detergents, preservatives, perfumes) compromise the integument, creating inflammation, irritation, and a portal of entry for further environmental insult. The threshold for pruritis is lowered, and a fierce cycle of itching and

scratching ensues, resulting in additional cutaneous damage. Similar changes occur with maceration from sweating and the drying effects of low humidity. Aeroallergens, including the house dust mite (Dermatophagoides pteronyssinus), molds, pollen, and dander, may induce eosinophilia and elevated levels of immunoglobulin E (IgE), leading to increased histamine release from IgE-activated mast cells and elevated activity of the Th2 immune system. Microbial agents such as Staphylococcus aureus, Pitysporum yeasts, Candida organisms, and Trichophyton also may exacerbate AD through direct cutaneous damage, formation of superantigen, and elevation of IgE with an associated allergic response. Foods such as eggs, milk, soy, nuts, fish, shellfish, and wheat also can precipitate an allergic response, although this type of hypersensitivity usually fades by 1 year of age. Stress has been shown to precipitate the itch scratch cycle. It is also important to consider the contribution of maladaptive behavior patterns involving intentional scratching as a mode for continued worsening of disease. Other psychophysiologic mechanisms that trigger AD may involve the actions of substance P, adenylcyclase-cyclic adenosine monophosphate, or vasoactive intestinal peptide at activated cutaneous nerve endings.

Pathophysiology
It has been proposed that dysregulation of the immune system plays a vital role in the pathogenisis of AD. Normally, there is a balance between the activities of the Th1 cell immune response, which involves secretion of the cytokines interferongamma and interleukin-2, and those of the Th2 cell immune response, in which interleukin-4 and interleukin-5 are secreted. Actions of cytokines of the Th1 system include stimulation of immune cytotoxicity, antiviral activity, and antitumor activity; upregulation of major histocompatability complex I and II cell surface proteins; increased expression of adhesion molecules; blocking of interleukin-4 activity (interferon gamma); stimulation of the differentiation of T lymphocytes and proliferation and immunoglobulin secretion of B lymphocytes; and upregulation of natural killer cell cytotoxicity (interleukin 2). Cytokines of the Th2 system are associated primarily with promotion of IgE production from B lymphocytes, differentiation of CD-4 T lymphocytes, suppression of Th1 cell activities, and stimulation of proliferation and differentiation of B lymphocytes. A positive correlation between the development of AD and increased levels of serum IgE has been observed. Upregulation of interleukin-4 and downregulation of interferongamma, with increased eosinophils and elevated levels of IgE-activated mast cells, also have been reported in this disease. Furthermore, administration of cyto-kines of the Th1 immune response to atopic individuals has resulted in clinical improvement in disease severity. It has been suggested that these changes, when taken together, indicate a possible hyperactive Th2 cell response that may be a fundamental aberration in atopic eczema. Disturbances in fatty acid metabolism might be involved in the pathogensis of AD. Deficiencies of omega-6 fatty acids have been observed in plasma and adipose tissues and formed blood elements of patients who have AD and in the human milk of mothers of some affected infants. Additionally, there is an overall increased incidence of AD among infants fed formula diets that are relatively poor in concentrations of omega-6 fatty acids compared with human milk. In vitro studies have shown that PGE1 and PGE2, major metabolites of omega-6 fatty acid biosynthesis, can suppress blood mononuclear cell synthesis of IgE. Furthermore, evidence suggests that PGEs are necessary for optimal efficacy of thymic hormone stimulation of Th1 cell activities.
Pathophysiology*

Hyperactive Th2 subset Thelper cells (associated with promotion of IgE production from B lymphocytes, differentiation of CD-4 T lymphocytes, suppression of Th1 cell activities, stimulation of proliferation, and differentiation of B lymphocytes) Increased levels of serum IgE Upregulation of interleukin-4 Downregulation of interferongamma Increased eosinophils Elevated levels of IgEactivated mast cells Disturbances in fatty acid metabolism/deficiencies of omega-6 fatty acids in plasma, adipose tissues, and formed blood elements

Clinical Manifestation
The natural history of the illness may be described under the different age groups: Infancy In infancy, at between two months to two years of age, a child may develop an itchy erythemathous rash on the cheeks. The rash may develop into minute epidermal vesicles which can rupture and produce moist crusted areas. It may then rapidly extend to other parts of the body like the scalp (cradle cap), neck, forehead, wrists, buttocks, diaper areas and extremities. Sometimes it becomes generalized causing erythroderma and desquamation. In the acute stage when the lesion is moist, exudation may be marked with associated secondary effects of scratching and rubbing. Infection results in crusts, pustules and indurations. In the chronic stage, the indurations take on a characteristic lichenified appearance with dry lesions and xerosis. In older children, this usually appears at the cubital and popliteal fossae. In most instances, the skin symptoms disappear towards the end of the second year. However, in some cases, it progresses into the childhood phase. Childhood In the childhood phase, the rashes are usually less acute, less exudattive, drier and more papular. The lesions occur at classical locations like the antecubital and popliteal fossae, wrists, eyelids, face and collar regions. Lichenified, slightly scaly or infiltrated patches may intermingle with isolated, excoriated papules over the exposed parts. Pruritis is a constant feature and many cutaneous changes are secondary to it. About 60-70% resolve before adulthood. Adolescence and adulthood In the adolescent and adult stage, the lesions may appear as localised erythematous, scaly, papular or vesicular patches. Or they may appear in the form of pruritic, lichenified patches. They usually involve the antecubital and popliteal fossae, the front and sides of the neck, the forehead, and around the eyes. The hands and wrists are frequently involved. Hyperlinearity of the palm is a manifestation of ichthyosis vulgaris which accompanies 30-40% of cases. At times the eruption is generalized, being severe in the flexures, and consists mostly of lichenification. These lesions arc papular, dry, slightly elevated and flattopped that tend to coalesce to form lichenified, slightly scaly plaques with excoriation. The plaques are erythematous and hyperpigmented. With trauma from scratching, the plaques may become exudative and crusted when infected. The skin is usually dry and has a tendency to become thickened. Widespread involvement results in disseminated neurodermatitis with a leather quality skin with exaggerated markings. Pruritis is again the symptom that causes the skin changes.

Diagnostic of Atopic Dermatitis

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As no biochemical criteria exist that may firmly establish the certainty diagnosis of atopic dermatitis, clinical criteria must be reverted to. The universally accepted criteria are those postulated in 1983 by Hanifin and Rajka, which are presented. These criteria have been examined by a number of investigators, and their reliability has been fully validated. Major Criteria: At least 3 of the following: 1. Pruritis 2. Personal or family history of atopy (asthma, allergic rhinitis, atopic dermatitis) 3. Chronic or chronically relapsing dermatitis 4. Typical morphology and distribution A. Face and extensors in early childhood B. Flexures with lichenification in adolescence Minor Criteria: At least 3 of the following: 1. Xerosis 2. Hand/foot dermatitis 3. Cheilitis 4. Elevated serum IgE 5. Immediate (type 1) skin test reactivity 6. Facial pallor/facial erythema 7. Perifollicular accentuation 8. Tendency to skin infections (ie, Staphylococcus aureus and herpes simplex) 9. Icthyosis, keratosis pilaris, or hyperlinear palms 10. Early age of onset 11. Anterior neck folds 12. Recurrent conjunctivitis 13. Anterior subcapsular cataracts 14. Keratoconus 15. Pityriasis alba 16. Sensitivity to emotional factors 17. Food intolerance 18. Pruritis with sweating 19. Intolerance of wool 20. Orbital darkening 21. Nipple eczema 22. Dennie Morgan fold/lower eyelids 23. White dermographism
Proposed by Hanifin JM, Rajka G. Acta Derm Venereol Suppl (Stockh). 1980;92:4447.

Management of AD (JM Spergel, 2000)

1. Moisturizers are the first line of topical therapy for AD, and are important to reduce and prevent the dry itchy skin of AD. Petroleum products such as Vaseline or hydrated petrolatum are the best moisturizers. Non-perfumed skin creams can also be effective. Moisturizers should be applied to the skin immediately after a tepid bath (while the skin is still moist). 2. Tar preparations may act as antiprurutics, disinfectants, antiinflammatory and desquamating agents when put in the bath or applied topically, and are often beneficial in both the acute and chronic phases of AD.

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Avoidance of irritants is crucial to controlling AD. A mild non-perfumed soap should be used and excessive scrubbing should be avoided. All cotton clothing and bedding are less irritating than synthetic or wool fabrics. In a subset of patients with atopic dermatitis, allergens can trigger a flare of AD should be avoided. However, diagnosis of food or inhalant allergies in patients with atopic dermatitis can be difficult since skin testing may yield false positive results. In order to clarify whether a food is a trigger for atopic dermatitis, double blind placebo controlled food challenges or elimination diets are required. Additionally, some recent studies have demonstrate that food allergen avoidance in neonates from families with a history of atopy will prevent some cases of AD . Infections can worsen AD, and should be treated early with topical and/or oral antibiotics, antifungals, or anti-viral agents. Early Staphylococcus aureus infections can be treated with topical antibacterial agents such as mupirocin (Bactroban ). For more widespread infection, oral anti-Staphylococcal agents such as dicloxacillin, erythromycin, or cephalexin should be prescribed. Intravenous or oral anti-viral agents are beneficial in decreasing severity and duration of the eruption and should be used for eczema herpeticum. Emotional stress can exacerbate atopic dermatitis. Children with AD often have disrupted sleep and daytime behavioral difficulties associated with insufficient sleep. Also, AD patients were more depressive and psychomatic-prone than normal controls and suggest that some patients with atopic dermatitis should be treated both dermatologically and psychiatrically . Hypnotherapy has been useful for some patients with intense pruritus and sleep abnormalities. In addition, the intense itching and skin appearance can lead to stress for the family and patient. Lay organizations such as the Eczema Association for Science and Education (EASE), the Food Allergy Network, and the Asthma and Allergy Foundation of America (AAFA) provide patients with information and support. This is emphasized by an enlightening piece written by Irene Crosby entitled My skin is only the top layer of the problem. Topical steroid ointments or creams are needed for acute flares of atopic dermatitis. Topical steroids should not be the sole treatment for atopic dermatitis, but should be used in conjunction with other forms of therapy, especially emollients. For acute flares a potent topical steroid, such as the diflorinated or the fluorochlorinated preparations, should be used for 7 to 10 days and then replaced with a low to midpotency topical steroid for 2 to 3 weeks until the lesions have resolved. Severely affected patients may require chronic use of a low potency topical steroid in conjunction with lubricants. Fluorinated steroids should not be chronically applied to the face, genitals, axillae, inguinal region, or skin folds and they should not be used in infants. Excessive or prolonged use of high potency topical steroids can lead to local atrophy. Significant systemic absorption is a potential hazard of topical steroids. Antihistamines may be helpful especially at night to control the itching associated with atopic dermatitis. Hydroxyzine or cetirizine and diphenhydramine are frequently prescribed. Nonsedating antihistamines such as astemizole, loratidine, terfenadine occasionally provide relief for patients. Topical doxepine has recently been shown to be effective in reducing pruritis in AD, however, may cause localized stinging and drowsiness. Topical diphenhydramine should be avoided because of low efficacy and high likelihood of skin sensitization. In spite of the above therapies, some patients have recalcitrant or severe AD. For such patients with severe disease, short term phototherapy using ultraviolet radiation (UVB or PUVA) is often beneficial . However, the usefulness of this therapy is limited by the long term risks, inconvenience and expense. A recent study has shown that cyclosporin (5 mg/kg per day) is an effective short term therapy for refractory AD. Recombinant IFN-g has shown promising preliminary results for patients with severe AD and may be appropriate
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for chronic therapy. [. Recent trials of topical tacrolimus (FK-506) ointment have shown promising results and additional studies are now underway . As the immunology of atopic dermatitis is better understood, specific cytokine or cytokine receptor antagonists may be important therapies for severe disease.

Prognosis
In most cases, the prognosis is good for children who have AD. Frequent follow-up is important early in the disease course to assess responsiveness to treatment and parental compliance with treatment regimens in younger children. Bath oil soaks with daily applications of moisturizers and avoidance of precipitating factors should be continued during the maintenance period. Antibiotics and steroids should be reserved for disease flares, and antihistamines may be used on an as-needed basis. Most cases of atopic eczema resolve by adulthood, although 20% to 40% of atopic children remain atopic as adults. For these patients, good treatment habits developed early in life will provide the framework for long-term successful disease control. NUMMULAR DERMATITIS (Discoid Eczema) Nummular dermatitis is a chronic eczematous lesion that is caused by different known and unknown factors. The condition may be preceded by atopic dermatitis. The lesion may appear as a separate entity as annular, coin-like or discoid lesions on the extensor surface of the extremities, trunk and the buttocks. This type of eczema appears mainly in older age groups . Predisposing Factors Insect bites : the papular and urticarial lesions may become chronic in neglected untreated cases or by the repeated severe itching and excoriation. Late manifestation of atopic dermatitis :Discoid eczema may appear at the end stage of chronic atopic eczema Irritating agents : irritants whether external such as topical sensitizing creams, detergents, metal or internal allergens may cause nummular dermatitis. Dryness of the skin: dryness of skin due to different factors such as excessive bathing , using harsh and medicated strong alkaline soaps. In older age groups the skin usually tends to be drier. Psychosomatic disorders may be considered an important predisposing factor. Autosensitisation. Drug reaction. Drug reaction due to different drugs such as sulfonamides and methyldopa, where the fixed drug lesion may appear on the previous eczematized site . Clinical Features Acute type Skin lesions are annular or coin-shaped papulo vesicular patches or plaques on an erythematous base. Oozing surface of the lesion may occur with excessive excoriation due to itching or rubbing followed by secondary bacterial infection. One of the characteristic features of nummular dermatitis is that the patches that seem to be dormant may become active again, particularly if treatment is discontinued. Chronic type Atopic dermatitis in childhood is liable to become discoid eczema later on. Cases of chronic discoid eczema have usually an atopic history. In the chronic stage , the lesions are dry and excoriated coin shaped. These are single or multiple lesions and may be accompanied by severe itching which usually increases with different irritating factors such as emotional stress.
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Secondary lesions may follow later on involving the limbs or the trunk. The course of this type of eczema is very chronic and has the characteristic of relapse and remission, where after healing of the lesions, new recurrent eruption occurs at the same older site . Treatment Elimination of the irritating factor if possible . Mild topical steroid alone or combined with an antibiotic or salicylic acid (Locosalene, diprosalic, salidecoderm) in an ointment base especially in dry lesions . Antihistamine preparation such as Citrizine is given for few days preferably at bedtime, where itching is more severe at night and to combat the possibility of sedation especially with old sedating antihistamines. Corticosteroids orally or parentally are rarely indicated in nummular eczema. DYSHIDROTIC ECZEMA (Pompholyx) Dyshidrotic eczema is a deep vesicular skin reaction involving the fingers, the interdigital spaces and the feet. The vesicles have a characteristic morphological appearance as that of sago grains. The condition is rare in young age groups and more common in adults . Predisposing Factors Excessive sweating . Hormonal imbalance . Psychosomatic factors. Occlusion of the areas for a long time as by keeping the feet non-aerated by the socks and shoes most of the day such as in athletes Drugs such as Penicillin, Aspirin. Primary irritants due to nickel , dichromate , perfumes and strong detergents can be considered among the precipitating factors . Bacterial or fungal infection is blamed as a triggering factor also. Meanwhile, bacterial and fungal infections, usually secondarily infect the dyshidrotic areas. Clinical Features The lesions are vesicular and usually symmetrical accompanied with mild or severe itching. Excoriation of the lesions is not uncommon. The vesicles of dyshidrotic eczema involute spontaneously and do not rupture as in other vesicular skin lesions. Treatment Most cases resolve spontaneously . Treatment and correction of the predisposing factors such as hyperhidrosis. Severe eczematized cases need antihistamine and topical steroid cream . Creams are preferred than ointments in these cases as cream is less occlusive than ointments . Dusting powder between the toes may help to keep the skin dry.

Seborrhoeic Dermatitis
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, 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 disease and in AIDS. 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 may come from its lipase activityreleasing inflammatory free fatty acidsand from its ability to activate the alternative complement pathway. The etiology of seborrheic dermatitis remains unknown, although many factors, including hormonal, have been implicated. This chronic inflammatory skin disorder is generally confined to areas of the head and trunk where sebaceous glands are most prominent. When seborrheic dermatitis occurs in the neonatal period, it usually disappears by six to 12 months of age, suggesting that it may be a response to maternal hormone stimulation.1 Seborrheic dermatitis frequently affects persons in postpuberty. Additional evidence of hormonal influence is provided by research demonstrating that the human sebocyte responds to androgen stimulation.2 Pityrosporum ovale, a lipophilic yeast of the Malassezia genus, has been implicated in the development of this condition.3 It has been suggested that seborrheic dermatitis is an inflammatory response to this organism, but this remains to be proved.4 P. ovale is present on all persons. Why some persons develop seborrheic dermatitis and others do not is unclear. The colonization rate of involved skin by this organism may be lower than that of uninvolved skin. 3 Nonetheless, the fact that seborrheic dermatitis responds to antifungal medications is strongly suggestive of the role of yeast in this disorder. Genetic and environmental factors, as well as other comorbid diseases, may predispose specific populations to the development of seborrheic dermatitis. Although seborrheic dermatitis affects only 3 percent of the general population, the incidence in persons with acquired immunodeficiency syndrome may be as high as 85 percent. The exact mechanism whereby human immunodeficiency virus infection promotes an atypical and explosive onset of seborrheic dermatitis (and other common inflammatory skin disorders) is unknown, but many factors have been explored, including CD4-positive T lymphocyte counts, 5 P. ovale density6 and nutritional factors.

Clinical Manifestations
Seborrheic dermatitis typically affects areas of the skin where sebaceous glands appear in high frequency and are most active. The distribution is classically symmetric, and common sites of involvement are the hairy areas of the head, including the scalp (Figure 1), the scalp margin (Figure 2), eyebrows, eyelashes, mustache and beard. Other common sites are the forehead (Figure 3), the nasolabial folds (Figure 4), the external ear canals (Figure 5) and the postauricular creases. Seborrhea of the trunk may appear in the presternal area (Figure 6) and in the body folds, including the axillae, navel, groin, and in the inframammary and anogenital areas. Figure 7 illustrates the typically symmetric distribution of seborrheic dermatitis. One of the characteristics of seborrheic dermatitis is dandruff, characterized by a fine, powdery white scale on the scalp. Many patients complain of the scalp itching with dandruff, and because they think that the scale arises from dry skin, they decrease the frequency of shampooing, which allows further scale accumulation. Inflammation then occurs and their symptoms worsen.

Treatment
General Treatment Overview Hygiene issues play a key role in controlling seborrheic dermatitis. Frequent cleansing with soap removes oils from affected areas and improves seborrhea. Patients should be counseled

that good hygiene must be a lifelong commitment. Outdoor recreation, especially during summer, will also improve seborrhea, although caution should be taken to avoid sun damage. Pharmacologic treatment options for seborrheic dermatitis include antifungal preparations (selenium sulfide, pyrithione zinc, azole agents, sodium sulfacetamide and topical terbinafine) that decrease colonization by lipophilic yeast and anti-inflammatory agents (topical steroids). Suggested products are listed in Table 1. For severe disease, keratolytics such as salicylic acid or coal tar preparations may be used to remove dense scale; then topical steroids may be applied. Other options for removing adherent scale involve applying any of a variety of oils (peanut, olive or mineral) to soften the scale overnight, followed by use of a detergent or coal tar shampoo. As a last resort in refractory disease, sebosuppressive agents such as isotretinoin (Accutane) may be used to reduce sebaceous gland activity. Treatment of Scalp and Beard Areas Many cases of seborrheic dermatitis are effectively treated by shampooing daily or every other day with antidandruff shampoos containing 2.5 percent selenium sulfide or 1 to 2 percent pyrithione zinc. Alternatively, ketoconazole shampoo may be used.10 The shampoo should be applied to the scalp and beard areas and left in place for five to 10 minutes before rinsing. A moisturizing shampoo may be used afterward to prevent dessication of the hair. After the disease is under control, the frequency of shampooing with medicated shampoos may be decreased to twice weekly or as needed. Topical terbinafine solution, 1 percent, has also been shown to be effective in the treatment of scalp seborrhea.11 If the scalp is covered with diffuse, dense scale, the scale may first be removed by applying warm mineral oil or olive oil to the scalp and washing several hours later with a detergent such as a dishwashing liquid or a tar shampoo. 12 An alternative is an overnight application of a coal tar-keratolytic combination or phenol-saline solution with or without occlusion with a plastic shower cap followed by shampooing in the morning.

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