Psoriasis may be associated with a 50% increased risk of developing Sjögren’s syndrome, shedding new light on the potential immunologic overlap between the two autoimmune diseases.
In a recent cohort study, published in BMC Medicine, investigators analyzed data from nearly 294,000 patients with psoriasis and an equal number of matched controls without psoriasis, drawn from the TriNetX global health research network. During the follow-up period, 3,339 patients with psoriasis developed Sjögren’s syndrome (SS) compared with 1,937 in the control group.
Psoriasis is a chronic autoimmune disease that triggers a rapid buildup of skin cells, resulting in red or discolored, scaly, and itchy patches. Meanwhile, SS primarily targets the salivary and tear glands, causing dry eyes and mouth. Its hallmark features include lymphocytic infiltration, glandular epithelial damage, and heightened B-cell activity producing autoantibodies
"Psoriasis significantly impacts the quality of life of patients, mainly when skin lesions are extensive or in sensitive areas, leading to psychological distress and an increased risk of depression," explained lead study author Zijian Kang, of the Department of Rheumatology and Immunology at Shanghai Sixth People’s Hospital Affiliated to Shanghai Jiao Tong University School of Medicine in Shanghai, China, and colleagues.
After adjusting for multiple confounding factors, patients with psoriasis showed a hazard ratio (HR) of 1.50 (95% confidence interval [CI] = 1.42–1.58) for developing SS. This suggested a 50% higher risk of SS compared with patients who didn't have psoriasis.
The Kaplan-Meier curves further demonstrated a statistically significant difference in SS development between the two groups.
Subgroup analyses revealed that patients with psoriatic arthritis and those receiving biologic treatments had an even higher likelihood of developing SS. The investigators emphasized the potential role of overlapping immunologic mechanisms, including cellular proliferation, immune cell recruitment, cytokine secretion, and interferon responses to viral infections.
To explore the potential shared pathogenesis, the investigators conducted transcriptomic analyses that identified several differentially expressed genes and pathways common to both psoriasis and SS. These findings underscored the possibility that immune dysregulation could be a critical factor in the co-occurrence of these conditions.
The study showed that autoimmune diseases often share common pathologic mechanisms and may not occur in isolation. Further research is needed to better understand the clinical implications of these findings and explore targeted therapeutic strategies for patients at risk.
