Seborrheic dermatitis

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Jesus Rosario Hernandez, M.D. [2]; Aysha Aslam, M.B.B.S[3]

Synonyms and keywords: Seborrheic eczema; Seborrhea; Cradle cap

Overview

Seborrheic eczema (also known as Seborrheic dermatitis, seborrhea) is a skin disorder affecting the scalp, face, and trunk. Seborrheic dermatitis causes flaky, itchy, red skin and temporary hair loss. It particularly affects the sebum-gland rich areas of skin. Causes of seborrheic dermatitis include Malassezia furfur (formerly known as Pityrosporum ovale) as well as genetic, environmental, hormonal, and immune-related factors. Medical therapy for seborrheic dermatitis includes antifungal agents, corticosteroids, and lithium salts.

Historical Perspective

• In 1887, seborrheic dermatitis was first described by Unna.
• In 1894, a hypothesis was made by Unna and Sabouraud that causative agents responsible for seborrheic dermatitis include yeast Malassezia, bacteria, or both as they were obtained in high quantities in cultures obtained from the affected patients.
• In 1984, Shuster discovered that seborrheic dermatitis can be treated with oral ketoconazole..

Classification

There is no established classification system for seborrheic dermatitis. However, it may be classified according to the anatomical location, age group, symptoms, etiology and severity.

Classification by Anatomy

Seborrheic dermatitis may be classified on the basis of anatomical location into following types:

• Localized
  • Scalp: Most common presentation in infants known as cradle cap
  • Face: Most commonly involves eyelids, eyebrows, and nasolabial folds
  • Retroauricular
  • Body folds: Commonly affects axilla, breast folds, and inguinal area
  • Trunk: May be seen in severe cases and most common site of involvement is lower abdomen
  • Upper Chest: Most commonly seen in adults
    • Pityriasiform: Oval macules and patches.
    • Petaloid type: Small papules with oily scales may enlarge to become patches resembling petals of flower.

• Generalized: Mostly seen in infants; it is associated with Leiner's disease and children with severe immunodeficiency.

Classification by Age

• Infantile: Occurs in first three months of life.
• Adults: Occurs most commonly between 30-60 years of age.

Classification by Symptomatic Presentation

• Non pruritic: Most commonly occurs in infants
• Pruritic: Most commonly occurs in older children and adults

Classification by Etiology

• Idiopathic
• Infectious
• Autoimmune / Inflammatory

Classification by Severity

• Mild to moderate disease: Occurs in immunocompetent individuals
• Severe disease: Occurs in immunocompromised individuals

Pathophysiology

The exact pathophysiology of seborrheic dermatitis remains unclear. However, several mechanisms are hypothesized to play a role in pathogenesis of seborrheic dermatitis.

Pathogenesis

Hypotheses regarding the pathogenesis of seborrheic dermatitis include:

Hypotheses related to Malassezia :

• A strong correlation between presence of the fungal yeast Malassezia and response to antifungals in patients with seborrheic dermatitis.

• Malassezia is a lipophilic yeast found on the skin of both healthy individuals and seborrheic dermatitis patients. It is thought that host reaction to Malassezia or its metabolites causes an inflammatory reaction that may have a significant role in the process..

• Another proposed mechanism for seborrheic dermatitis suggests that a disrupted lipid layer of Malassezia leads to an increased production of pro inflammatory cytokines such as IL-6 and IL-7, and decreased production of IL-10.

• Malassezia is seen to have lipase activity, which acts on cutaneous triglycerides causing a release of unsaturated fatty acids such as arachidonic acid. These metabolites may cause abnormal proliferation and differentiation of the stratum corneum leading to signs and symptoms of seborrheic dermatitis.

Other Hypotheses

• Sebaceous gland activity

Sebum gland activity may correlate with seborrheic dermatitis.

• Immune response

Elevated levels of HLA-AW30, HLA-AW31, HLA-A32, HLA-B12 and HLA-B18 and increased levels of total serum IgA and IgG antibodies have been detected in seborrheic dermatitis patients. This implies an immune mediated pathological mechanism.

• Epidermal barrier dysfunction

Abnormalities in stratum corneum that may be associated with seborrheic dermatitis include:

• Corneocyte shape
• Corneodesmosomes
• Disrupted lipid lamellar structure

• Neurogenic and other factors

Patients with parkinsonism may have increase levels of α-melanocyte stimulating hormone (α-MSH) levels and seborrheic dermatitis in these patients respond to L-dopa treatment

Genetics

There is no specific genetic cause for seborrheic dermatitis..

Associated conditions

• Parkinsonism
• Epilepsy
• Depressive mood disorder
• Traumatic brain injury
• Spinal cord injury
• HIV
• Lymphoma
• Downs syndrome

Gross Pathology

Superficial flaking and redness are characteristic findings of seborrheic dermatitis.

• 

  Seborrheic dermatitis showing erythema on face. - By Roymishali - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=27267929

• 

  Upper chest showing redness and crusting. - Adapted from Dermatology Atlas.

Microscopic Histopathology

Histopathological findings of seborrheic dermatitis may be categorized into the following stages:

• Acute

• Focal mild spongiosis with superficial crust containing neutrophils.
• Edema of papillary dermis.
• Dilatation of blood vessels in superficial vascular plexus with infiltration of lymphocytes, histiocytes.

• Subacute

• Psoriasiform hyperplasia.
• Keratin showing presence of yeasts.

• Chronic

• Extensive psoriasiform hyperplasia
• Minimal spongiosis
• Follicular crusting

Causes

The cause of seborrheic dermatitis remains unknown; however, the following factors may have been implicated:

• Malassezia furfur (formerly known as Pityrosporum ovale).
• Excessive vitamin A
• Lack of biotin,
• pyridoxine (vitamin B6)
• riboflavin (vitamin B2)

Differentiating Seborrheic dermatitis from Other Diseases

Symptoms of seborrheic dermatitis may overlap with other skin conditions such as psoriasis, candidiasis, contact dermatitis, and atopic dermatitis. Differential diagnosis of seborrheic dermatitis may be classified into two types by age group:

Differential diagnosis in Infants

• Atopic dermatitis
• Candidiasis
• Dermatophytosis
• Diaper dermatitis
• Langerhans cell histiocytosis
• Psoriasis
• Pityriasis amiantacea
• Rosacea
• Tinea capitis
• Zinc deficiency
• Vitamin B deficiency

Disease	Rash Characteristics	Signs and Symptoms	Associated Conditions	Images
Cutaneous T cell lymphoma/Mycosis fungoides	Premycotic phase: A scaly, red rash in areas of the body that usually are not exposed to the sun. This rash does not cause symptoms and may last for months or years. Patch phase: Thin, erythematous, eczema-like rash. Plaque phase: Small raised bumps (papules) or hardened lesions on the skin, which may be erythematous. Tumor phase: Tumors form on the skin. Infection secondary to ulcers.	Epidermal atrophy or poikiloderma Generalized itching (pruritus) Pain in the affected area of the skin Insomnia Red (erythematous) patches scattered over the skin of the trunk and the extremities Tumor-like lobulated outgrowths form on the skin in the latter phase of the disease Weight loss Lymphadenopathy Malaise and fatigue Anemia May progress to Sezary syndrome (skin involvement plus hematogenous dissemination)	Sezary syndrome	By Bobjgalindo - Own work, GFDL, https://commons.wikimedia.org/w/index.php?curid=7139812
Pityriasis rosea	Pink or salmon in color, which may be scaly; referred to as "herald patch" Oval shape Long axis oriented along the cleavage lines Distributed on the trunk and proximal extremities Squamous marginal collarette and a “fir-tree” or “Christmas tree” distribution on posterior trunk Secondary to viral infections Resolves spontaneously after 6-8 weeks	Preceded by a prodrome of: Sore throat Gastrointestinal disturbance Fever Arthralgia	Infection by any of the following: HHV-6 HHV-7 HHV-8	By James Heilman,MD - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=16305230
Pityriasis lichenoides chronica	Recurrent lesions are usually less evenly scattered than in cases of psoriasis Brownish red or orange-brown in color Lesions are capped by a single detachable, opaque, mica-like scale Often leave hypopigmented macules	High fever Malaise Myalgias Paraesthesia Pruritus	Infection by any of the following: Epstein-Barr virus (EBV) Toxoplasma gondii Human immunodeficiency virus (HIV)
Nummular dermatitis	Multiple coin-shaped eczematous lesions Commonly affecting the extremities (lower>upper) and trunk May ooze fluid and become dry and crusty	Often appears after a skin injury, such as a burn, abrasion (from friction), or insect bite Lesions commonly relapse after occasional remission or may persist for long periods Pruritus	Associated with: Dry skin Emotional stress Allergens (rubber chemicals, formaldehyde, neomycin, chrome, mercury, and nickel) Staphylococcus infection Seasonal variation Alcohol Drugs Atopy
Secondary syphilis	Round, coppery, red colored lesions on palms and soles Papules with collarette of scales	Fever Generalized lymphadenopathy Sore throat Patchy hair loss Headache Weight loss Myalgia Fatigue	Associated with: Condylomata lata Corona verinata Positive VDRL test	By James Heilman,MD - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=16305230
Bowen’s disease	Erythematous, small, scaly plaque, which enlarges erratically over time Scale is usually yellow or white and it is easily detachable without any bleeding Well-defined margins	Pruritus Pain Bleeding lesions	Associated with: Erythroplasia of Queyrat (Bowen's disease of the penis) Squamous cell carcinoma Solar radiation and ultraviolet (UV) exposure Radiotherapy Immunosuppression Arsenic exposure Human papilloma virus (HPV) type 16 Merkel cell polyomavirus Sjögren’s syndrome	By Klaus D. Peter, Gummersbach, Germany - Own work (own photograph), CC BY 3.0 de, https://commons.wikimedia.org/w/index.php?curid=6839115
Exanthematous pustulosis	Numerous small, primarily non-follicular, sterile pustules, arising within large areas of edematous erythema	Fever Leukocytosis Intracorneal, subcorneal, and/or intraepidermal pustules with papillary dermal edema containing neutrophils and eosinophils	Associated with: Antibiotics (penicillins, sulfonamides, tetracyclines) Carbamazepine Calcium channel blockers (Diltiazem) Hydroxychloroquine	By See below - (2010). "Acute generalized exanthematous pustulosis: an unusual side effect of meropenem". Indian J Dermatol 55 (2): 176–7. DOI:10.4103/0019-5154.62759. PMID 20606889. PMC: 2887524., CC BY 1.0, https://commons.wikimedia.org/w/index.php?curid=52979729
Hypertrophic lichen planus	Classically involves shin and ankles and is characterized by hyperkeratotic plaques and nodules covered by a scale Lesions may transform into hyperkeratotic thickened, elevated, purplish or reddish plaques and nodules	Chronic pruritus Scaling May be asymptomatic	Associated with Hepatitis C virus infection	Di James Heilman, MD - Opera propria, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=11509003
Sneddon–Wilkinson disease	Flaccid pustules that are often generalized and have a tendency to involve the flexural areas Annular configuration	Pruritus May be asymptomatic	Associated with: Monoclonal gammopathy, usually an IgA paraproteinemia Crohn's disease Osteomyelitis Adalimumab
Small plaque parapsoriasis	Erythematous plaques with fine scaly surface May present with elongated, finger-like patches Symmetrical distribution on the flanks Known as digitate dermatosis	Lesions may be asymptomatic May be mildly pruritic May fade or disappear after sun exposure during the summer season, but typically recur during the winter	May progress to mycosis fungoides
Intertrigo	Red and fleshy looking lesion in skin folds Itching Oozing May be sore	Pruritus Musty odor	Associated with: Infections (Fungal, bacterial, viral) Allergies Diabetes Obesity	Source: https://www.cdc.gov/
Langerhans cell histiocytosis	Scaling and crusting of scalp	Pathological fractures Visceromegaly (hepatomegaly, spleenomegaly) Chronic cough Dyspnea Lymphadenopathy	Associated with: Diabetes insipidus Pancytopenia
Tinea manuum/pedum/capitis	Scaling, flaking, and sometimes blistering of the affected areas Hair loss with a black dot on scalp in case of tinea capitis	Pruritus KOH preparation of the lesions confirms fungal infection	Associated with: Diabetes Immunosupression Intimate contact with infected person May lead to asthma exacerbation
Seborrheic dermatitis	Papulosquamous, scaly, flaky, itchy, and red rash found particularly at sebaceous gland-rich areas of the body	Pruritus	Associated with: AIDS Stress Fungal infection Fatigue Sleep deprivation Change of season Parkinson's disease Biotin deficiency	By Roymishali - Own work, CC BY-SA 3.0, https://commons.wikimedia.org/w/index.php?curid=27267929

Differential diagnosis in Adults

• Systemic lupus erythematosus
• Candidiasis
• Erythrasma
• Contact dermatitis
• Psoriasis
• Tinea versicolor
• Tinea corporis
• Secondary syphilis
• Pemphigus foliaceus
• Rosacea

Epidemiology and Demographics

Epidemiology

Worldwide, the prevalence of seborrheic dermatitis is estimated to be 11000 cases per 100,000. Prevalence of seborrheic varies among individuals based on the following factors:

• Higher reporting of mild cases
• Higher in patients with HIV with 35000 per 100,000 in early diagnosis and 85000 per 100,000 with full blown AIDS
• Higher prevalence seen among those directly exposed to UV radiation

• The exact incidence of seborrheic dermatitis is unknown

Demographics

Age

Seborrheic dermatitis demonstrates a tri-modal age distribution as follows:

• The first incidence peak is seen in infants around three to four months of age, which usually resolves within 12 months
• The second incidence peak is seen around puberty.
• The third incidence peak is seen after age 50 with the highest prevalence seen among ages 33-44 years.
• Age groups showing lowest prevalence of clinical disease is seen in individuals younger than 12 years.

Gender

Males are more commonly affected with seborrheic dermatitis than females.

Race

• Seborrheic dermatitis is rarely seen in African Americans.
• If seborrheic dermatitis is seen in this population, it leads to high suspicion of HIV in affected individuals.

Risk Factors

The most common risk factors for seborrheic dermatitis include:

Immunosuppression

• Organ transplant recipients
• HIV/AIDS
• Malignancies such as lymphoma

Neurologic and psychiatric cases

• Parkinsonism
• Depression
• Tardive dyskinesia
• Traumatic brain injury
• Epilepsy
• Facial nerve palsy
• Spinal cord injury

Genetic disorders

• Downs syndrome
• Hailey-Hailey Disease
• Cardiofaciocutaneous syndrome
• Mutation in (ZNF750) coding a zinc finger protein (C2H2)

Other risk factors

• Stress
• Treatment with psoralene and UV-A
• Male gender
• Obesity
• Diabetes mellitus
• Seasonal changes such as low temperature and decreased humditiy
• Drugs such as haloperidol deconate, lithium and chlorpromazine

Screening

There are no screening guidelines for seborrheic dermatitis.

Natural History, Complications, and Prognosis

Natural History

• The symptoms of seborrheic dermatitis usually develop in the first three months in infants. It may resolve without treatment in most cases in few months and rarely presents after 12 months.
• In adults, symptoms of seborrheic dermatitis usually develop in the second and third decade of life, and start with symptoms such as redness, scaling and crusting on affected areas. However, occurrence of seborrheic dermatitis is highly variable and it may present after 50 years of age.
• The course of disease is highly variable among individuals despite treatment. Some cases present with more frequent relapses than others.

Complications

Common complications of seborrheic dermatitis include:

• Temporary or permanent hair loss
• Secondary bacterial infection
• Blepharitis
• Abscess of meibomian glands
• Otitis externa
• Extensive involvement of body

Prognosis

• The prognosis of seborrheic dermatitis is excellent in infants; it is a self limited disease and usually resolves within few months after birth.
• In adults, it is a recurrent condition with no permanent cure.

Diagnosis

There is no definitive diagnostic criteria for seborrheic dermatitis. Diagnosis of seborrheic dermatitis is primarily clinical; it is based on history and physical examination findings.

History

Obtaining complete history is important in making diagnosis of seborrheic dermatitis as it will give an insight into cause and associated risk factors for the disease. In addition to symptoms of seborrheic dermatitis, patients may present with symptoms of one of the following associated conditions:

• Parkinsonism
• Epilepsy
• Depressive mood disorder
• Traumatic brain injury
• Spinal cord injury
• HIV
• Lymphoma
• Downs syndrome
• Hailey-Hailey Disease
• Diabetes mellitus

Symptoms

Symptoms of seborrheic dermatitis may be categorized according to age as follows:

Infants

Infants usually present in the first few months of life. Symptoms can be divided into following types depending on extent of involvement.

• Localized
  • Redness and flaking
  • Pruritis
  • Most common sites involved are scalp and face
  • Other sites involved include retroauricular area, nasolabial folds, cheeks, eyebrows and eyelids
  • Napkin or diaper area involvement

• Generalized
  • Few cases may present with generalized involvement such as lower abdomen, groin and pubic area.

Adults

The most common symptoms of seborrheic dermatitis may be divided into two types based on extent of involvement:

• Localized
  • Macules, thin plaques, or red patches(scalp, face, nasolabial folds, anterior hairline, eyebrows, glabella region of the forehead, melolabial folds, ears, central chest, and genital region)
  • Pruritis
  • Fine scaling (mild cases)
  • Redness and yellow to white crusting or scaling (severe disease)
  • Redness, itching and yellow crusting of eye lashes (Blepharitis).
  • Repeated itching of ear causing secondary bacterial infection resulting in fever and ear pain.

• Generalized
  • Patients with HIV or other immunosupressive conditions such as malignancies usually present with more severe disease involving unusual sites such as extremities.

Physical Examination

Physical examination may be divided into two types according to age group:

Age	Site involved	Local Examination		Image
Infants	General Appearance	Infants often looks healthy with a good appetite and sleep habits.
	Scalp	Fine scaling in mild cases. Thick greasy scales with erythema in severe cases.
	Face	Face may present with scaly salmon colored scales.
	Neck, Axillae and Body Folds	Non-scaly moist glistening appearance of lesions which tend to appear confluent.
	Trunk	Trunk involvement is seen in severe cases. However, the diaper area iscommonly involved which presents with erythema and maceration of skin with edema of surrounding skin. Secondary bacterial and candidal infections are common in these cases.
	Generalized	Most commonly seen in Leiner's disease, which is an immunosuppressive condition. It may involve unusual sites such as extremities and trunk with scaling and erythematous patches. Scaling and crusting usually spreads to involve other parts of the body with extensive peeling of skin.
Adults	General appearance	Adults may present with a healthy general appearance in mild cases or may present in considerable distress due to widespread involvement especially. Patients may appear ill in cases with underlying diseases associated with seborrheic dermatitis such as HIV, malignancy, or parkinsonism.
	Scalp	Mild desquamation to honey coloured crusting of the scalp causing alopecia.
	Face/Retroauricular areas	May present as a "butterfly rash". Malar erythema and scaling in a symmetrical pattern . Yellowish scaling between eyelashes and eyelids causing blepharitis with honey colored crusting on free margins.
	Upper Chest	SD presents as petalloid or pityriasiform. Petalloid: Small reddish follicular or perifollicular papules that may coalesce forming patches resembling petals of flower. Pityriasiform: Common on skin tension lines and intertriginous areas and presents as oval scaly macules and patches. This type involves extensive involvement of the body.
	Body Folds	Lesions usually present as moist, macerated, and erythematous lesions. May lead to fissuring and secondary infection.
SD of Immunosuppression		It may present as extensive scaling and erythema involving unusual sites such as extremities and is refractory to treatment. It is usually seen in children and adults with immunosuppression such as HIV/AIDS.

Imaging Findings

There are no imaging findings associated with seborrheic dermatitis.

Other Diagnostic Studies

There are no other diagnostic studies for seborrheic dermatitis.

Treatment

The mainstay of treatment for seborrheic dermatitis is medical therapy. Depending on age and severity of symptoms the treatment may be categorized as follows:

	Severity	Acute Therapy	Maintainence Therapy
Infants	Mild	Education and reassurance of parents. Application of emollients such as baby oil or mineral oil. Frequent shampooing using non-medicated shampoos. Removal of scales.	Self limited, resolves in few months
	Moderate to Severe	Use of Topical corticosteroids (1% hydrocortisone) and antifungal agent (2% ketoconazole)	Topical corticosteroids and antifungal agent. Look for alternative diagnosis.
Adults	Mild	No curative treatment. Topical antifungals such as azoles, zinc pyrithione, selenium sulfide (1%–2.5%), imidazoles (1%–2% ketoconazole shampoo, creams, lotions, or foams), ciclopirox (cream, gel, and shampoo), salicylic acid (shampoos, creams), coal tar (creams, shampoos) Topical azoles such as ketoconazole, miconazle Topical use of (low, moderate and high potency) corticosteroids Keratolytic agents: Lipohydroxy acid, propylene glycol. Coconut oil compound (ointment combination of coal tar, salicylic acid and sulfur).	Using of 1% ciclopirox shampoo once or twice weekly for 4 weeks. Using 2% ketoconazole such as once a week or twice a week. Aluminium acetate solution (seborrheic dermatitis externa).
	Moderate to Severe	Topical azoles such as ketoconazole, miconazole (Scalp) Short courses of low potency topical corticosteroids (face, trunk and ears) Lithium succinate or gluconate] topical preparations (Non scalp SD) Fluconazole (Seborrheic blepharitis) Oral antifungals and oral terbinafine ( refractory cases) Calcineurin inhibitors suh as tacrolimus ( non scalp SD)	0.1% tacrolimus ointment twice daily for up to 4 weeks. Isotretinoin in low doses for 3-5 months and phototherapy with narrowband ultraviolet B or psoralen plus ultraviolet A(refractory cases). Systemic use of glucocorticoids (prednisolone 0.5 mg/kg body weight/day) for 7 days (severe).

The following are the preferred treatment regimens for seborrheic dermatitis:

• 1. Antifungal agents

• Preferred regimen (1): Ketoconazole 2% in shampoo, foam, gel, or cream

• Scalp: Twice/week for clearance THEN once/week or every other week for maintenance
• Other areas: From bid to twice/week for clearance THEN from twice/week to once every other week for maintenance

• Preferred regimen (2): Bifonazole 1% in shampoo or cream

• Scalp: 3 times/week for clearance
• Other areas: qd for clearance

• Preferred regimen (3): Ciclopirox olamine (also called ciclopirox) 1.0% or 1.5% in shampoo or cream

• Scalp: Twice to 3 times/week for clearance THEN once/week or every 2 week for maintenance
• Other areas: Twice daily for clearance THEN qd for maintenance

• 2. Corticosteroids

• Preferred regimen (1): Hydrocortisone 1% in cream areas other than scalp qd or bid
• Preferred regimen (2): Betamethasone dipropionate 0.05% in lotion scalp and other areas qd or bid
• Preferred regimen (3): Clobetasol 17- butyrate 0.05% in cream areas other than scalp qd or bid
• Preferred regimen (4): Clobetasol dipro- pionate 0.05% in shampoo

• Scalp: Twice weekly in a short- contact fashion (up to 10 min application, then washing)

• Preferred regimen (5): Desonide 0.05% lotion bid on scalp and other areas

• 3. Lithium salts

• Preferred regimen: Lithium succinate AND Zinc sulfate Oin

Plant-based treatments

Main article: Phytotherapy

The World Health Organization mentions Aloe vera gel as a yet to be scientifically proven traditional medicine treatment for Seborrhoeic dermatitis.

• Arctium lappa (Burdock) oil
• Chelidonium majus (Celandine)
• Glycyrrhiza glabra (Licorice)
• Melaleuca (Tea tree) species
• Plantago (Plantain) species
• Symphytum officinale (Comfrey)
• Zingiber officinale (Ginger) root juicetreatment containing 8% Lithium succinate AND 0.05% Zinc sulfate

• Preferred regimen: Lithium gluconate 8% in gel bid on areas other than scalp

Surgery

Surgical intervention is not recommended for the management of seborrrheic dermatitis.

Prevention

Primary Prevention

There is no established method for prevention of seborrheic dermatitis.

Secondary Prevention

Secondary prevention strategies following seborrheic dermatitis include:

• Using of 1% ciclopirox shampoo once or twice weekly for 4 weeks. Shampooing once weekly or once every two weeks decreases the relapse rate of seborrheic dermatitis.
• Using 2% ketoconazole such as once a week or twice a week may decrease relapse of seborrheic dermatitis.
• Ketoconazole 2% shampoo may have greater prophylactic effect against relapse than selenium sulfide.