Researchers have discovered a strong association among patients with cancer between the use of immune checkpoint inhibitors (ICIs) and an increased risk of new onset psoriasis, according to findings from research published in JAMA Dermatology.
Findings from a nationwide cohort study used data from the Taiwan National Health Insurance database and the Taiwan Cancer Registry, utilizing information from patients who received antineoplastic medications for stage 3 and 4 cancers between Jan. 1, 2019 and June 30, 2021, investigators explained.
Glossary:
Antineoplastic: Drugs that block the formation of neoplasms, or growths that may become cancer, according to the National Cancer Institute.
Person-years: A way of measuring the time patients are observed in a study which multiplies the number of people participating by the amount of time they participated.
PD-1, PD-L1 and CTLA-4: PD-1 and CTLA-4 are proteins found on T cells, a type of immune cell, that help keep the body’s immune responses in check, according to the National Cancer Institute. PD-L1 is a protein that acts as a “brake” to keep immune responses under control and may be found on some normal cells and in high amounts on some cancer cells, according to the National Cancer Institute.
“This nationwide cohort study demonstrated that patients with cancer receiving ICIs had a higher risk of developing psoriasis compared to those receiving chemotherapy or targeted therapy,” lead study author, Dr. Sheng-Yin To, of the Department of Pharmacy Practice, Tri-Service General Hospital, in Taipei, Taiwan, and colleagues wrote in their research. “Although this adverse effect is relatively uncommon, it is important for medical professionals, clinicians and caregivers to be aware of this potential risk to improve skin health and ensure optimal cancer care.”
In the study, 3,188 patients were eligible for and treated with immune checkpoint inhibitors, and 132,042 patients were eligible for and treated with chemotherapies or targeted therapies. With an overall mean follow-up period of 1.46 years, during 197,107 person-years of follow-up, 295 patients, or 0.2%, received a diagnosis of psoriasis: 16, or 0.5%, of patients treated with immune checkpoint inhibitors and 279, or 0.2%, of patients not treated with immune checkpoint inhibitors.
Incidence rates of psoriasis were 5.76 cases per 1,000 person-years among patients treated with immune checkpoint inhibitors and 1.44 cases per 1,000 person-years among patients who did not receive treatment with immune checkpoint inhibitors.
Researchers noted that it was within the first 180 days of follow-up that patients treated with immune checkpoint inhibitors exhibited the highest risk increase.
Incidence of psoriasis was also less frequent across subgroups of non-immune checkpoint inhibitor treatment types, with researchers finding that psoriasis events occurred at rates of 0.2% (158 events) among chemotherapy users, 0.1% (34 events) among monoclonal antibody users and 0.3% (87 events) among protease inhibitor users.
Immune checkpoint inhibitors, as defined by the National Cancer Institute, are drugs that block proteins known as immune checkpoints made by some immune cells and some cancer cells and prevent immune responses from being too strong. By blocking immune checkpoints, immune cells known as T cells can better kill cancer cells.
Psoriasis, as researchers explained in JAMA Dermatology, is a chronic inflammatory skin disease that can impact patients’ physical, psychological and emotional health, and commonly requires lifelong treatment. Previous research has found that immune checkpoint inhibitors may contribute to the risk of psoriasis.
“Although the mechanism remains unclear, ICIs block inhibitory pathways, such as PD-1/PD-L1 and CTLA-4, which cancer cells use to evade the immune system, thereby leading to the reactivation of T cells,” To and colleagues concluded. “This may enhance immune activity and can quickly lead to inflammation and autoimmunity, manifesting as psoriasis.”
Reference: “Psoriasis Risk With Immune Checkpoint Inhibitors” by Sheng-Yin To et al., JAMA Dermatology.
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