Dermatitis

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© Springer Nature Switzerland AG 2020
A. Tosti et al. (eds.)Hair and Scalp Treatmentshttps://doi.org/10.1007/978-3-030-21555-2_12



12. Seborrheic Dermatitis



Daniel Asz-Sigall1   and Antonella Tosti2


(1)
National University of Mexico, Department of Onco-dermatology and Trichology Clinic, Mexico City, Mexico

(2)
Fredric Brandt Endowed Professor of Dermatology, Dr. Phillip Frost Department of Dermatology and Cutaneous Surgery, University of Miami Miller School of Medicine, Miami, FL, USA

 



 

Daniel Asz-Sigall


Keywords

Seborrheic dermatitisDandruffSebaceous glandMalassezia spp.Epidermal barrierTreatmentAntifungalsAnti-inflammatory agentsOral isotretinoin


Introduction


Seborrheic dermatitis (SD) is a common chronic inflammatory skin disease that manifests itself as scaly reddish-brown patches on the sebaceous gland-rich regions. The disease typically occurs in healthy persons, but its prevalence is very high (34–83%) in immunocompromised patients (HIV) as well as in patients with neurological disorders. SD is more frequent in men and more severe in cold and dry climates as well as during periods of increased stress. Infant SD presents with thick white-yellow greasy scales on the scalp; it is usually benign and resolves spontaneously. In adolescents and adults, it typically presents as scaly greasy erythematous patches on the scalp, nasolabial folds, ears, eyebrows, and anterior chest. The pathogenesis of the disease is not well understood; however, the following predisposing factors have been identified: fungal colonization, sebaceous gland activity, individual susceptibility, aberrant epidermal barrier function, and genetic predisposition. Malassezia spp. yeasts (Figs. 12.1 and 12.2) cause a nonspecific immune response that begins a cascade of skin changes in the stratum corneum, releasing lipases and free fatty acids. This phenomenon causes stratum corneum hyperproliferation (scaling), inflammation, and an incomplete corneocyte differentiation, which alters the skin barrier and impairs its function [1–15].

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Fig. 12.1

Smear with Gram stain shows abundant yeasts (100×)


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Fig. 12.2

Malassezia spp . can be isolated if Dixon’s agar culture is performed


Diagnostic Procedures and Laboratories Required Before Starting Treatment


SD clinical diagnosis is based on history, location, and appearance of the skin lesions. Scalp dermoscopy is a very useful diagnostic procedure and shows increased numbers of arborizing vessels (Fig. 12.3), erythema, yellow greasy scales (Fig. 12.4), small pustules, and excoriations. In uncertain or non-responding cases, a skin biopsy must be performed. Histopathology of acute or subacute patches shows superficial perivascular and perifollicular inflammatory infiltrates (lymphocytes and histiocytes) in association with spongiosis, psoriasiform hyperplasia, and parakeratosis around the follicular openings (“shoulder parakeratosis”). In chronic lesions, there is marked psoriasiform hyperplasia with parakeratosis and venules dilation, and differently from psoriasis, the sebaceous glands are preserved and enlarged [1–16].

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Fig. 12.3

Increased number of arborizing vessels (dermoscopy 70×)


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Fig. 12.4

Abundant yellow greasy scales in a severe case (dermoscopy 70×)


Treatment Strategy: A General Introduction


Seborrheic dermatitis is a chronic disease, and the principal goals of treatment are to clear the visible signs, reduce associated symptoms (erythema and pruritus), promote normalization of skin structure and function, and maintain disease remission with long-term therapy. Given that Malassezia proliferation, as well as local skin irritation and inflammation, is the primary pathogenic mechanism; first-line treatment involves topical antifungal and anti-inflammatory (steroidal and non-steroidal) agents. Second-line topical treatments include selenium sulfide, keratolytic agents, and phototherapy. Oral treatment with antifungals and isotretinoin is reserved for severe or refractory cases. Alternative options include aloe vera and tea tree oil among others (Table 12.1). Treatment selection depends on disease topography, drug efficacy, side effects, and patient age [1–15


Table 12.1

Scalp seborrheic dermatitis treatment options








































































First-line treatments


 Topical


  A. Antifungals


  B. Anti-inflammatory agents


   a. Corticosteroids


   b. Non-steroidal anti-inflammatory agents


    1. Bisabolol


    2. Glycyrrhetinic acid


    3. Climbazole/piroctone olamine


    4. Promiseb®


    5. Lactoferrin


Second-line treatments


 Topical


  A. Selenium sulfide


  B. Keratolytic agents


   a. Coal tar


   b. Salicylic acid/lipohydroxy acid


   c. K301


  C. Phototherapy


 Systemic


  A. Itraconazole


  B. Terbinafine


  C. Fluconazole


  D. Pramiconazole


  E. Isotretinoin


Third-line treatments


 Topical


  A. Aloe vera


  B. Borage and tea tree oils


  C. Quassia amara


  D. Solanum chrysotrichum


  E. Homeopathic mineral medicine


  F. Vitamins



Modified from Borda LJ, Perper M, Keri JE. Treatment of seborrheic dermatitis: a comprehensive review. J Dermatolog Treat. 2018;24:1–12

].

First-Line Treatments


Topical Antifungals


Antifungal agents decrease the population of Malassezia spp. on the affected skin and have anti-inflammatory properties. Topical azoles (ketoconazole 2%, clotrimazole 1%, miconazole 2%, and sertaconazole 2%) alter the permeability of the fungal cell wall by blocking cytochrome P450, terbinafine 1% is an allylamine with fungicidal activity on the cell membrane, ciclopirox olamine 1% inhibits the metal-dependent enzymes inside the fungal cell, and zinc pyrithione has antifungal and antibacterial properties. Commercial products include shampoos that must be applied daily or 3–4 times per week during the shower and left for 5 minutes before rinsing. Lotions must be applied daily or 3–4 times per week, leaving them overnight (Table 12.2). Possible side effects include contact dermatitis, pruritus, burn sensation, and xerosis [1, 2, 17–22].


Table 12.2

Scalp seborrheic dermatitis treatment regimensa



















































Drug

Formulation

Instructions for use

Topical antifungals

Ciclopirox 1–1.5%


Ketoconazole 1–2%


Zinc pyrithione 1–2%


Shampoo or lotion

Daily or 3–4 times per week for 4 weeks or until clinical remission


Maintenance therapy: once or twice per week for several months to prevent relapse


Non-steroidal anti-inflammatory agents

Piroctone olamine, bisabolol, glycyrrhetic acid, lactoferrin, and Promiseb®


Shampoo or lotion

Daily or three to four times per week for 4 weeks or until clinical remission


Maintenance therapy: once or twice per week for several months to prevent relapse


Low-potency topical corticosteroids (classes I–II)


Class I potency Hydrocortisone 1%


Class II potency


Desonide 0.05% Lotion

Daily for 2–4 weeks and then decrease


High-potency topical corticosteroids (class III–IV)

Class III potency


Fluocinolone acetonide 0.01%


Class IV potency


Clobetasol propionate 0.05%


Shampoo or lotion

Daily for 2 weeks and then decrease


Second-line treatments

Selenium sulfide 2.5%


Shampoo or lotion

Daily or 3–4 times per week for 4 weeks or until clinical remission


Maintenance therapy: once or twice per week for several months to prevent relapse


Keratolytics

Tar 1–2%, salicylic acid 3%


Shampoo or lotion

Daily or 3–4 times per week for 4 weeks or until clinical remission


Maintenance therapy: once or twice per week for several months to prevent relapse


Systemic antifungals


Itraconazole 100 mg caps

200 mg/day for 1 week, then 200 mg/day for 2 days/ per month for 2–3 months


Terbinafine 250 mg caps

Continuous: 250 mg/day for 4–6 weeks. Intermittent: 250 mg/day for 12 days a month for 3 months


Fluconazole 150 mg caps

50–300 mg weekly for 2–4 weeks


Oral isotretinoin

 

5–10 mg/day or three times per week for several months



aAdapted from Ref. [4]


Topical Anti-inflammatory Agents


Corticosteroids

They are the most effective drugs in clearing SD signs and symptoms (inflammation, erythema, and pruritus). They can be used alone or in combination with antifungal agents; however, their prolonged use is not recommended due to possible side effects (telangiectasias, hypertrichosis, atrophy, and perioral dermatitis). Prescribe a weak-moderate topical corticosteroid (classes I and II) daily for 2–4 weeks. The authors prefer a lotion versus a shampoo to avoid unnecessary exposure of other body areas. Treatment is then gradually discontinued [1, 2, 23–25].


Non-steroidal Anti-inflammatory Agents

These drugs inhibit Malassezia species growth through their anti-inflammatory, antimycotic, keratolytic, and antioxidant effects. They are usually combined with other compounds in shampoos and lotions and are applied daily or 3–4 times per week. These drugs are generally well-tolerated, effective, viable, and safe. Adverse effects may include pricking sensation, stinging, itching, burning, erythema, and viral gastroenteritis [1, 2, 26–28].



Bisabolol


Monocyclic sesquiterpene alcohol with antioxidant and anti-inflammatory properties that downregulates the human polymorphonuclear neutrophils’ release. In SD, it has an anti-inflammatory effect more specific than corticosteroids and anti-fungal drugs but is probably not very potent in monotherapy [1, 2, 28, 29].



Glycyrrhetinic acid


It is an ingredient of the black licorice with anti-microbial and anti-inflammatory properties. It inhibits the 11-β-hydroxysteroid hydroxygenase enzyme in the steroid metabolism, potentiating the anti-inflammatory effects [1, 2, 30].



Climbazole/piroctone olamine


Piroctone olamine is an ethanolamine salt with antifungal properties which creates iron ion complexes in the fungal cell membrane, and climbazole is an imidazole antifungal agent that blocks P-450 [1, 2, 26, 31, 32].



Promiseb®


This combines many active ingredients (e.g., glycyrrhetinic acid and piroctone olamine) to enhance the anti-inflammatory and anti-fungal activity against SD [1, 2, 33].



Lactoferrin


The precise mechanism of action is not well understood yet, but it is believed to modulate the migration, maturation, and function of immune cells, iron binding, and interactions with other compounds [1, 2, 34].


Second-Line Treatments


Selenium Sulfide


Heavy metal salt with antifungal properties that promote the shedding of the infected stratum corneum. It is indicated in shampoo at 2.5% daily or 3–4 times per week for 4–8 weeks. Adverse effects include pruritus, burning sensation, and hair/scalp discoloration. Other effective alternatives include precipitated sulfur 3% and colloidal sulfur 5% [35, 36].


Keratolytic Agents


Coal Tar

A complex mixture of phenols, polycyclic aromatic hydrocarbons, and heterocyclic compounds with antifungal, anti-inflammatory, anti-itch, and keratolytic properties. Commercial presentations include shampoos and lotions to be applied 2–3 times per week for 4–8 weeks. Side effects include skin irritation, sun sensitivity, allergic reactions, and skin discoloration. Its use in pregnancy and breastfeeding is not recommended [37–40].


Salicylic Acid/Lipohydroxy Acid (LHA)

Its mechanism of action includes exfoliation, stimulation of epidermal renewal, and antimicrobial properties against Malassezia spp. Apply daily or 3–4 times per week for 4–8 weeks for scale removal [41].


K301

Topical solution with a mixture of urea, propylene glycol, and lactic acid with keratolytic, exfoliating, anti-fungal, and hydrating properties. It is applied daily during 4 weeks and then three times per week for another month. Adverse effects included smarting pain, redness, burning, rash, itching, eczema, and ulceration [42].


Phototherapy


UVB therapy is useful in some inflammatory skin conditions by inducing immunosuppression, T cell apoptosis, and reducing cell proliferation. There is not an established phototherapy regimen in DS, but the administration of narrow-band UVB three times per week has proved to be effective until signs disappear completely. Home devices are available for the scalp and can be utilized in association with antifungals and anti-inflammatory treatments [43–46].


Systemic Treatment


Itraconazole


A triazole with high keratinophilic and lipophilic properties and a good safety profile. This drug also has an anti-inflammatory effect inhibiting the 5-hypoxygenase metabolite synthesis. The recommended treatment includes 100 mg twice per day for 1 week followed by pulse administration of 200 mg/day during the first 2 days of the months for 2–3 months. Side effects include nausea, vomiting, diarrhea, headache, stomach discomfort, or dizziness; however, these are rare with pulse treatment [47–51].


Terbinafine


Antimycotic with antioxidant and anti-inflammatory properties against dermatophytes, molds, dimorphic fungi, and other pathogenic yeasts. The recommended dose is 250 mg per day for 4–6 weeks or as intermittent treatment (250 mg/day for 12 days a month for 3 consecutive months). Adverse effects include mild tachycardia, insomnia, gastrointestinal discomfort, migraine, cutaneous rash, hypogeusia, and hyposmia [52–54].


Fluconazole


Broad-spectrum bistriazole derivative that inhibits dermatophytes, yeasts, and dimorphic fungi. It has been demonstrated to be effective in the sebum excretion at a dose of 150 mg or 300 mg per week for 4–8 weeks. Adverse effects include elevated liver function tests and nausea [55–57].


Ketoconazole


Not indicated for DS because of hepatotoxicity risk and testosterone metabolic alterations [58].


Pramiconazole


It is a triazole antifungal agent that inhibits ergosterol synthesis and which has broad activity against Candida sp., dermatophytes, and Malassezia sp. This drug has the best activity against Malassezia spp. due to its high affinity toward cytochrome P450. A single daily dose of 200 mg for 1–4 weeks improves erythema, itching, and desquamation. Adverse events include diarrhea and gastrointestinal discomfort [59–61].


Isotretinoin


Oral isotretinoin decreases the sebum secretion by reducing the sebaceous gland size and stimulating basal sebocyte apoptosis. This drug also has anti-inflammatory properties as it reduces the interleukin production, Toll-like receptor 2 activity, and polymorphonuclear cell migration. Low doses of this drug (5–10 mg/day or three times per week) for several months may be considered as a treatment option for moderate to severe seborrhea. This drug requires effective contraception in women [62–66].


Third- and Fourth-Line Treatments


Aloe vera


Aloe vera has anti-inflammatory, antibacterial, and antifungal properties. This plant has been used widely for the prevention of seborrheic dermatitis and other fungal infections, wound healing, and anesthetic purposes [67, 68].


Borage and Tea Tree Oil (Topical Essential Oils)


Borage oil contains approximately 25% of gamma-linolenic acid (GLA) which is one of the several essential amino acids involved in skin barrier restoration. Tea tree oil (TTO) is obtained from Melaleuca alternifolia leaves and has antimicrobial, anti-inflammatory, antifungal, antioxidant, and anti-skin cancer properties. Terpinen-4-ol is the tea tree oil’s major component which reduces the production of tumor necrosis factor, interleukin-1 (IL-1), IL-8, IL-10, and prostaglandin E2. Tea tree oil is a possible allergen, and contact dermatitis is a possible side effect [69–73].


Quassia amara


It is a small tree from South America with high levels of active phytochemicals (triterpenoid quassinoids) and antimicrobial, anti-inflammatory, and antifungal properties [74].


Solanum chrysotrichum


The main component of this plant (steroidal saponins) has demonstrated antifungal properties against yeast and dermatophytes [75, 76].


Homeopathic Mineral Medicine


Low doses of oral homeopathic medication (potassium bromide, sodium bromide, nickel sulfate, and sodium chloride) are an alternative therapy for SD. Adverse effects are minimal and include stomach discomfort, stomach pain, and nausea [77].


Vitamins


Some nutrients such as essential fatty acids, vitamins A, E, and D, vitamins B1, B2, and B6, niacin, biotin, vitamin C, selenium, zinc, and iron may play a role in the treatment of SD. Biotin (vitamin H) is essential for the long-chain fatty acid synthesis; nicotinamide regulates the cellular inflammation and zinc the sebum production (epithelial differentiation with anti-inflammatory, antibacterial, and antiandrogen properties) . Biotin’s recommended dose is 5–10 mg/day. Patients should be informed to discontinue the drug a few days before laboratory exams as its intake can interfere with lab results [78–84].


Treatment Selection


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Mar 23, 2021 | Posted by in Dermatology | Comments Off on Dermatitis

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