Resident Rounds. Part III A. Serendipitous Improvement in Moderate to Severe Acne in Psoriasis Patients Treated With Ustekinumab: A Two-Case Series

June 2013 | Volume 12 | Issue 6 | Feature | 710 | Copyright © 2013

J. Daniel Jensen MD,a Thy Huynh BS,a Jennifer Cafardi MD,b and Naveed Sami MDa

aDepartment of Dermatology, University of Alabama at Birmingham, Birmingham, AL bThe Skin Cancer Center, Cincinnati, OH

Abstract

No abstract available

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CASE 1

A 24-year old Caucasian male with a history of unspecified seizure disorder presented for evaluation and treatment of psoriasis and acne. The patient had a several year history of moderate-to-severe psoriasis which had been treated with etanercept 50 mg twice weekly in conjunction with numerous other topical therapies, including corticosteroids, vitamin D analogues, and calcineurin inhibitors. The patient also had a several year history of moderate-to-severe acne which consisted of deep-seated erythematous papules and pustules on the face, back, and chest. He had been treated with oral doxycycline 100 mg twice daily as well as topical tretinoin 0.1% cream and benzoyl peroxide-clindamycin gel without an optimal response. We were unable to decrease the dosage of the doxycycline since his acne vulgaris was still active despite the maximum optimal dosage for almost two years.

Etanercept was discontinued due to lack of efficacy and ustekinumab 45 mg subcutaneously was initiated according to recommended dosing protocol for the treatment of psoriasis. Interestingly, four to six weeks after beginning ustekinumab therapy, the patient’s acne had cleared remarkably. There were decreased numbers of inflammatory papules and pustules on the face and no lesions on the chest or back. The dosage of doxycycline was tapered to 40 mg (oral), and from thenceforth, the patient remained largely acne free while experiencing only mild acne flares during the week prior to each ustekinumab injection.

CASE 2

A 25-year old Caucasian female with no other medical history presented for evaluation and treatment of long-standing psoriasis. The patient also had a history of moderate acne vulgaris composed of erythematous papules on the perioral face, which was not actively being treated at the time of presentation. The psoriasis had been treated with methotrexate and etanercept previously, and the patient was unable to tolerate the side effects of those medications, resulting in their discontinuation. She had also been treated with topical steroids and vitamin D analogues in addition to biologic therapy.

The patient began therapy with ustekinumab 45 mg subcutaneously according to recommended dosing protocol. Three weeks following her first ustekinumab injection, the patient noticed complete clearing of her acne, with mild acne recurrence in the week prior to each subsequent ustekinumab injection.

Note: Due to the unanticipated improvement in these patient’s acne symptoms, photographs are not available for these cases.

DISCUSSION

Ustekinumab is a human monoclonal antibody directed against interleukin (IL)-12 and IL-23 with specific binding activity to the p40 subunit of both cytokines.1 Griffiths et al demonstrated the superiority of ustekinumab to etanercept, a tumor necrosis factor (TNF) inhibitor, over 12-week period in a phase 3 trial.2 This biologic is approved for treatment of moderate-to-severe plaque psoriasis in the United States.

We discovered serendipitous improvement of moderate-tosevere acne vulgaris with use of ustekinumab in our psoriatic patients. Both patients began treatment with ustekinumab after discontinuing methotrexate or etanercept due to lack of efficacy or unfavorable side effects. Evaluating the pathogenesis of acne vulgaris, a multifactorial inflammatory disease of the pilosebaceous unit, yields insight into the potential molecular mechanism by which ustekinumab results in acne improvement.

Propionibacterium acnes is normal skin flora that contributes to the pathogenesis of acne vulgaris and has been shown to be significantly increased in pilosebaceous follicles of acne patients.3 Studies have suggested that P. acnes triggers cytokine production via induction of toll-like receptor (TLR)-2, a transmembrane protein with pathogen-associated molecular patterns that mediate responses to peptidoglycans of Gram-positive microorganisms. 4-5 Activation of TLR-2 via P. acnes induces the release of proinflammatory cytokines IL-8 and IL-12p40 from primary human monocytes and keratinocytes.4-5 IL-8 acts as neutrophil chemotactic factor inducing neutrophils to release lysosomal

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