Scalp psoriasis

The scalp is among the most commonly involved body regions and is frequently one of the first sites affected in patients with psoriasis. The particular vulnerability of the scalp to psoriasis may be due to multiple factors including lack of UV penetration to the skin, Malassezia proliferation caused by high sebum production, and koebnerization due to frequent brushing and styling of the hair. These same factors that predispose the scalp to the development of psoriatic plaques also make it especially difficult to treat (Kircik and Kumar 2010).

Psoriatic scalp lesions have variable morphology and distribution. Classically, they present as asymmetric, sharply demarcated plaques with overlying silver-white scale. These plaques can extend beyond hair margins to include the forehead, posterior neck, ear, and retroauricular skin (Crowley 2010). Patients often complain of scale shedding and pruritus. Most patients also report significant social and psychological distress, primarily due to pruritus and the appearance of these lesions, especially when they extend onto the face (Kircik and Kumar 2010).

Of note, mild scalp psoriasis may show only minimal scaling and can be difficult to diagnose (Johnson and Armstrong 2013). While scalp psoriasis and seborrheic dermatitis are both common and present with scaling, there are features that distinguish these disease entities. Psoriatic plaques are well defined and the scale is silver-white. In contrast, the scaly patches of seborrheic dermatitis are greasy, yellow, ill-defined, and more diffusely distributed on the scalp. Seborrheic dermatitis is more often seen on the central face of patients who complain of combination oily and dry skin. Autoimmune conditions that involve the scalp can also mimic psoriasis. While localized alopecia can be seen in psoriatic plaques on the scalp, it is non-scarring, and hair growth typically resumes when lesions improve. In contrast, discoid lupus erythematous (DLE), which may also present with scaly plaques on the scalp, causes a scarring alopecia. Dermatomyositis may also present with scaly, pink, pruritic patches on the scalp. Furthermore, involvement of the extensor surfaces of the knuckles, elbows, and knees may resemble psoriasis. However, scalp patches are usually more prominent posteriorly than anteriorly (Bolognia et al. 2014). It is important to consider atopic dermatitis and tinea capitis in a child with a scalp rash because both of these conditions are much more common than psoriasis in childhood.

Ultrapotent topical corticosteroids are first-line therapy for scalp psoriasis. They act rapidly, resulting in marked improvement often within 2 weeks of treatment initiation (Crowley 2010). Based on available evidence, clobetasol propionate and betamethasone dipropionate have the largest treatment effect of the steroids in these classes when used as monotherapies. Theoretical side effects of long-term use include local skin atrophy, folliculitis, and telangiectasia. These side effects were not observed in 2–4 week studies, although evidence is insufficient to draw conclusions about the safety of topical corticosteroids for greater than 8 weeks. These agents are best given as foams, gels, or solutions, as ointments and creams can be greasy, more difficult to apply, and thus unappealing to patients (Mason et al. 2013; Van de Kerkhof et al. 1998).

Topical calcipotriol can be used as an alternative first-line treatment. Side effects include burning, redness, dryness, and itching (Crowley 2010). They also have a slow onset of action compared to corticosteroids, which may make them unappealing to patients. While calcipotriol binds the vitamin D3 receptor and can alter bone and calcium metabolism, there are few reports of clinically significant alterations in the blood or urine calcium levels (Gooderham et al. 2014; Scott et al. 2001). Of note, these vitamin D3 analogues are inactivated at low pH and thus cannot be used with acidic topicals like salicylic acid (Warren et al. 2008).