Immune checkpoint inhibitors increase the risk of psoriasis

Abstract

Patients with cancer treated with immune checkpoint inhibitors (ICIs) had a 2-fold increased risk of developing psoriasis, according to an observational, national cohort study conducted in Taiwan.¹

The results are based on a cohort of 135,230 Taiwanese patients with stage III/IV cancer who received neoplastic medications for cancer between January 2019 and June 2021; 3188 were eligible to receive ICIs, including programmed cell death 1 (PD-1) and programmed cell death ligand 1 (PD-LI) inhibitors (ICI users), and 132,042 were eligible for non-ICIs (controls).

With an average follow-up of 18 months (or 197,107 person-years), 295 patients (0.2%) were diagnosed with psoriasis.

The increased risk of psoriasis among the ICI users and those treated with chemotherapy or targeted agents (non-ICI users) was 5.76 and 1.44 cases per 1000 person-years, respectively, per the as-started analysis (i.e., intention-to-treat analysis), with a hazard ratio of 3.31 (95% CI, 1.93–5.68).

Consistent findings were found via an on-treatment analysis, which showed 16.13 and 2.35 cases per 1000 person-years for ICI users and non-ICI users, respectively.

The study was conducted to clarify the risk of psoriasis in patients with cancers treated with ICIs because of the growing use of ICIs to treat cancer and frequent immune-related adverse effects often reported with their usage. Given the nonrandomized design of the study, investigators used a statistical method called inverse probability of treatment weighting to adjust for confounding in observational trials.

Commenting on the study, Jason Luke, MD, an associate professor of medicine at the University of Pittsburgh and UPMC Hillman Cancer Center, calls the findings somewhat new but not especially surprising or novel considering the long-standing recognition of a link between anti–PD-1 agents and dermatologic issues, particularly in patients with melanoma.

He notes that people are increasingly recognizing the potential long-term toxicities associated with anti–PD-1 agents, such as chronic fatigue and now psoriasis. “Monitoring for these and early intervention are therefore important to maximize quality of life,” he says. “This being said, access to these medicines should not be limited for patients given they have the potential for long-term disease control of metastatic disease.”

Citing the well-established association between various human leukocyte antigen haplotypes and rheumatologic diseases, he notes that the study did not address the association between ethnicity (or germline genetics) and immunotherapy-related dermatologic toxicity. Dr Luke also notes that the generalizability of the results is not clear because of the different genetic background of people in Taiwan with respect to, for example, people in the United States or those with a predominantly Caucasian heritage. “The ability to apply these data directly in the USA may be unclear,” he says, adding that he does not see the results affecting the standard practice of care in the United States.

“The results do not in any way change how we might use immunotherapy for melanoma, but it is reasonable to be particularly cognizant to monitor for psoriasis-like clinical presentation and to educate patients surrounding this potential risk,” he says.

Dr Luke emphasizes the need to educate physicians, patients, and family members about the risk of immune-related side effects from an immune checkpoint blockade, particularly dermatologic adverse events, which, he says, “remain a very important aspect to optimizing patient outcomes.”

“These data should not be taken to mean, however, that the availability of these potentially curative agents should be limited in any patient,” he says.