Chronic Nasolabial Fold Seborrheic Dermatitis Successfully Controlled With Crisaborole

May 2018 | Volume 17 | Issue 5 | Editorials | 577 | Copyright © May 2018

Dede Liu MD,a Peter Chow BS,b Sarah Strawn MD,a Anand Rajpara MD,a Ting Wang MD,a and Daniel Aires MD JDa

aUniversity of Kansas Medical Center, Kansas City, KS bUniversity of Kansas School of Medicine, Kansas City, KS

Chronic Nasolabial Fold Seborrheic Dermatitis Successfully Controlled With Crisaborole
Seborrheic dermatitis is a chronic inflammatory dermatosis characterized by redness and scaling and is typically seen in the brows, nasolabial folds, and chest.1 Topical antifungals such as ketoconazole can be helpful, but resistant seborrheic dermatitis often requires topical steroids or steroid sparing agents such as tacrolimus.2 The exact cause and pathogenesis of seborrheic dermatitis is not known. However, inflammation is known to play a role. The disease has a preference for body sites with increased or larger sebaceous glands (ie, face, scalp). Sebaceous glands create an environment favorable for growth of lipid dependent fungi such as Malassezia. Multiple seborrheic dermatitis treatment studies have demonstrated a connection with Malassezia, but mechanisms remain elusive.6 Because it is unclear that seborrheic dermatitis patients have higher Malassezia counts than controls, an alternative explanation posits that anti-fungals exert a local anti-inflammatory effect. 7Seborrheic dermatitis might result from a host’s immune response to Malassezia or its by-products such as lipase, free fatty acids, or reactive oxygen species.8 Malassezia or its byproducts have been hypothesized to induce inflammatory cytokine production in keratinocytes.10 A factor that can cause localized inflammation is the lipase activity of Malassezia, which can generate fatty acids from skin lipids.9 Additionally, seborrheic dermatitis skin biopsies demonstrate upregulation of inflammatory interleukins, natural killer cells, as well as complement activation.8 Phosphodiesterase 4 (PDE4) is involved in the regulation of pro-inflammatory cytokines through its degradation of cAMP. PDE4 activity has been previously discovered to be increased in the inflammatory cells of atopic dermatitis and thus targeting and inhibiting PDE4 reduces the local production of inflammatory mediators.5 This has led to the creation of Crisaborole 2% ointment, a novel PDE4 inhibitor that reduces local inflammation, and is newly approved for treatment of atopic dermatitis.3,4 We hypothesized that Crisaborole may show utility in seborrheic dermatitis via reducing the inflammatory component. We report a case of chronic bilateral nasolabial fold seborrheic dermatitis in a 50-year-old man who was previously treating it with over-the-counter CeraVe moisturizer BID. During the treatment period CeraVe was continued BID to both nasolabial folds, while Crisaborole was applied twice per week to the right nasolabial fold only. After four weeks the scale and erythema was notably reduced on the right nasolabial fold treated with Crisaborole (Figure 2) versus the untreated left (Figure 1) nasolabial fold. Larger trials will be needed to replicate this.


The authors have no conflicts of interest to declare.Figure1Figure2