Increased psoriasis risk found in cancer patients treated with immune checkpoint inhibitors

Researchers from the National Defense Medical Center in Taiwan have identified an increased risk of psoriasis in patients with cancer undergoing immune checkpoint inhibitor (ICI) treatments, with implications for other immune-related adverse events.

Over the past decade, ICIs have become an increasingly important part of cancer immunotherapy. ICI therapies enhance the immune system’s ability to fight cancer cells but have been associated with adverse events. These events can result from a loss of T-cell tolerance, allowing the immune system to attack healthy organ tissues such as the skin, gastrointestinal tract, liver, lungs, and endocrine system.

In a study titled “Psoriasis Risk With Immune Checkpoint Inhibitors,” published in JAMA Dermatology, researchers analyzed data from the Taiwan National Health Insurance database and the Taiwan Cancer Registry, focusing on individuals who received antineoplastic medications for stage III and IV cancers. The team delved into the connection between ICIs and psoriasis, a skin disease characterized by red, scaly patches with significant physical and emotional impact on patients.

Of 135,230 patients (mean age 62.94 years; 45.1% female), 3,188 were classified as ICI users, while 132,042 received chemotherapy or targeted therapies and served as non-ICI users. The primary outcome measured was the incidence of psoriasis during the follow-up period.

ICI use was linked to a higher incidence of psoriasis at 5.76 cases per 1,000 person-years, compared to 1.44 cases in the non-ICI group. Using a statistical method to account for other factors, the researchers found that patients treated with ICIs were more than three times as likely to develop psoriasis (adjusted HR, 3.31) and over two times as likely when considering other risks (adjusted subdistribution HR, 2.43). These increased risks remained consistent across different study methods and additional analyses.

The researchers determined that ICIs, particularly those targeting programmed cell death protein 1 and its ligand PD-L1, essentially block the function of proteins that usually act as brakes on the immune system. The intensified immune response causes T cells to mistakenly target healthy tissues, such as skin, increasing the likelihood of conditions like psoriasis. The mechanism mirrors how ICIs might trigger other immune-related events by enhancing T helper cell proinflammatory responses.

According to the findings, loss of T-cell tolerance contributes to the onset of psoriasis. It may underlie other immune-related adverse events associated with ICIs, ranging from mild to life-threatening across multiple organ systems.

This discovery adds a critical layer of understanding to how ICIs may contribute to the onset of psoriasis and other adverse effects. With previous studies linking elevated programmed cell death to psoriasis severity, the findings show the need for awareness among medical professionals regarding potential adverse effects. Balancing the advantages of ICIs with their risks is essential to ensure optimal care for patients with cancer.

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