By Leonard Calabrese, DO
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A 55-year-old man with a 30-year history of plaque-type psoriasis developed disease covering 75 percent of his body surface area (BSA) after being diagnosed with HIV in 2004. His physicians avoided immunosuppressants for his psoriasis and instead used a combination of narrowband ultraviolet B phototherapy and acitretin 10 to 30 mg daily, but improvement was mild at best. The patient was diagnosed with Kaposi sarcoma (KS) in 2008; imiquimod 5 percent cream halted its progression.
The patient’s HIV and KS were stable, but his psoriasis remained significant. A number of reports have shown that biologics are safe and effective in treating HIV-associated psoriasis, so we began treating him with ustekinumab in July 2016. His first dose of 45 mg led to almost complete clearance with no change in KS at four weeks, the time of his second ustekinumab dose. Every 12 weeks, the patient received an additional dose until his final follow-up in October 2017. His psoriasis remained nearly cleared, and KS lesions and CD4 counts remained stable with no negative impact on viral load or opportunistic infections. My colleagues Anthony Fernandez, MD, PhD, Cassandra Calabrese, DO, D.M. Wang and I published this report in Clinical and Experimental Dermatology.
(a–d) Patient in May 2016, just before initiation of ustekinumab treatment. Kaposi sarcoma (KS) lesions are denoted by arrows. (e–h) Patient in September 2017, after 15 months of ustekinumab treatment. The KS lesions were unchanged compared with before initiation of ustekinumab treatment. Image and caption originally appeared in Clinical Experimental Dermatology.
Biologics for immunocompromised patients
Patients with immunological dysfunction can experience cutaneous diseases, including psoriasis vulgaris and KS. KS is the most common tumor associated with HIV and is an incurable and potentially fatal malignancy. Psoriasis is often refractory to standard treatments in patients with HIV.
A growing collection of case reports and series supports the use of biologic agents for HIV-associated psoriasis, including ustekinumab, an IL-12/IL-23 inhibitor. Because IL-12 is a proinflammatory cytokine that has been explored as a treatment for HIV-associated KS, use of a drug that inhibits IL-12 could potentially promote KS progression. Significantly, our patient’s KS remained stable after 16 months.
Our case is the first reported that treats an HIV-positive patient with both severe psoriasis and KS with ustekinumab and suggests that the biologic may be a safe and effective treatment for patients with HIV-associated KS and psoriasis.
Dr. Calabrese is Director of the R.J. Fasenmyer Center for Clinical Immunology at Cleveland Clinic.