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.
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.
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