INTRODUCTION
Dissecting cellulitis (DC) is a progressive disease that warrants prompt and adequate diagnosis and treatment to prevent scarring and irreversible hair loss. Since data on treatment options for DC are limited to case series and case reports, the relative efficacy of treatment options cannot be compared. This poses a challenge as there are no consensus guidelines on the therapeutic approach however, DC treatment often mirrors that for other follicular occlusion diseases. The use of systemic therapies such as isotretinoin, dapsone, and tumor necrosis factor (TNF) inhibitors (adalimumab and infliximab) has been described with varying degrees of efficacy.2-4 To the best of our knowledge, there has only been one report of an IL-23 inhibitor (guselkumab) used in the treatment of recalcitrant DC, which was described in a patient with concomitant hidradenitis suppurativa (HS).5 Studies of HS have shown increased levels of IL-23 within macrophages in lesional dermis, thus it was speculated that IL-23 may also be implicated in the pathogenesis of DC.6 This patient showed a favorable response, substantiating the role of IL-23 in the pathogenesis of DC and the shared pathogenesis of diseases of the follicular tetrad. In this novel approach, risankizumab, an IL-23 inhibitor, is used in recalcitrant DC with excellent and promising results.
CASE
A 65-year-old African American male presented to the dermatology clinic with a 13-year history of recurrent itchy bumps and persistent draining nodules on his scalp- clinical characteristics suggestive of DC. His past medical history was significant for congestive heart failure (ejection fraction of 45%), coronary artery disease, hyperlipidemia, hypertension, and non-alcoholic fatty liver disease. The patient was being followed by our clinic for approximately one year for treatment of recalcitrant DC. He was previously treated with topical clindamycin, doxycycline 100mg BID, intermittent intralesional triamcinolone, chlorhexidine gluconate, fluocinonide, and isotretinoin 30mg BID with minimal response.
At the time of the visit, the patient reported disease progression. Physical examination showed multiple tender, crusted lesions with suppurative drainage on the parietal and occipital scalp (Figure 1). Due to the inadequate response to previous therapy, and the severe mucocutaneous dryness he experienced on
At the time of the visit, the patient reported disease progression. Physical examination showed multiple tender, crusted lesions with suppurative drainage on the parietal and occipital scalp (Figure 1). Due to the inadequate response to previous therapy, and the severe mucocutaneous dryness he experienced on
