Treating Seborrheic Dermatitis: Review of Mechanisms and Therapeutic Options
July 2013 | Volume 12 | Issue 7 | Original Article | 796 | Copyright © 2013
Neal Bhatia MD
Division of Dermatology, Harbor UCLA Medical Center, Los Angeles, CA
Seborrheic dermatitis is one of those conditions that dermatologists and patients alike tend to find a routine for, and in many cases those routines are hard to break. And, unlike the new treatment paradigms for eczema, acne, and even actinic keratoses, combination therapies for addressing the disease process typically have not been a part of the approach to treating seborrheic dermatitis. However, with the advent of new therapies and vehicles as well as a better understanding of how neutrophils and free oxygen radicals impact inflammation,1 there are new options to maintain and control the disease process of seborrheic dermatitis to minimize flares. Although the needs of the scalp, face and chest are different, as are the variations in skin types, the fundamental mechanisms of the inflammatory process are often the same. If it is understood that seborrheic dermatitis is histologically classified as a papulosquamous disorder with paucineutrophilic and lymphocytic infiltrates,1 and if the trigger and etiologic agent most likely is Malassezia furfur,2 then the ideal mechanisms of action of therapies should be directed as such.
J Drugs Dermatol. 2013;12(7):796-798.
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Application of Mechanism of Action
Is there another dermatosis besides seborrheic dermatitis that we treat with either steroids or antifungals, or even both in combination? This tells us that with seborrheic dermatitis, it is unclear whether inflammation or the contribution of M. furfur is the primary target of our treatment regimen, which mechanism of the pathogenesis is the main actor, and if the inflammation is primary or directed at the target pathogen. Intuitively, the application of a steroid would result in local reduction of the Th1 cellular response, which would allow a fungal element to have an easier time of serving as a pathogen; yet, it is not often that steroids create breakthrough flares or eruptions. Consider how seborrheic dermatitis can be more aggressive in infants, patients with Parkinson’s disease, and AIDS patient populations— each of these patient groups experience some level of immune compromise, so the response against M. furfur is diminished. In that regard, an agent that provided the benefits of without the known consequences of steroids would be a better long-term option.
Conversely, we use antifungal therapies such as ciclopirox, which induces activity against free radical oxygen species and acts to chelate iron and other minerals to promote cell death, or the azole family, which work against cell membrane synthesis by inhibiting ergosterol. There are other active ingredients, or even added ingredients, that have anti-mycotic activity against M. furfur and other yeasts.3 For example, propane-1,2-diol, commonly known as propylene glycol, has been demonstrated to have both antimicrobial and keratolytic properties, which allows for utility both alone and with other anti-fungal agents.4 Glycyrrhetinic acid, the ingredient in black licorice, has more broad-spectrum anti-microbial activity and anti-inflammatory actions and is structurally similar to cortisol, but its main medicinal purposes to date have taken advantage of the mineralcorticoid properties in hypertension management.5 Glycyrrhetinic acid has been shown to have potent inhibition of 11-B-hydroxysteroid hydroxygenase, the enzyme necessary for the conversion of hydrocortisone in normal steroid metabolism. From this observation, there is a potentiation of the anti-inflammatory activity of hydrocortisone and prednisolone, enough to suggest its utility as an adjunct if administered at appropriate levels clinically. In addition, glycyrrhetinic acid can have dose-dependent inhibition on the classic pathway of the complement cascade, which in turn would directly impact chemotaxis, tissue destruction, immune complex formation and other important inflammatory responses.5
The question to ask is: Can the anti-fungal activity against the mycelia forms of M. furfur (in the yeast phase known as Pityrosporum ovale)3 be enough to slow down or minimize the inflammatory process? To that end, is it likely that the conventional use of azoles and other antifungals do not have sufficient anti-inflammatory activity, and may represent incomplete therapy when used alone and independent of vehicle?
The same question should be asked about monotherapy with steroids, since the short-term benefits alleviate the symptoms but do not affect the actual process of the disease to prevent flares and relapse. Is comparison of steroid monotherapy to another agent that could be incorporated as both therapy and maintanence enough to change the approach to management?6
The non-steroidal alternatives have been considered by many to be viable options to steroids in the treatment of seborrheic dermatitis. The calcineurin inhibitor pimecromilus, formulated as a 1% cream, has been shown in comparative trials to be as effective as hydrocortisone 1% cream or ketoconazole 2% cream in the treatment of seborrheic dermatitis, although with more frequent adverse effects.7 In a single-blind trial, tacrolimus 0.1% ointment reduced symptoms of seborrheic dermatitis as effectively as hydrocortisone 1% cream, with more rapid clearing and higher ratings from patients.]8