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Psoriasis Linked to Risk of Sjögren’s Syndrome, Study Finds

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Key Takeaways

  • Patients with psoriasis show a 50% increased risk of developing Sjögren’s syndrome (SS), with higher risk in those with psoriatic arthritis or on biological treatments.
  • Shared pathogenic mechanisms between psoriasis and SS include cellular proliferation, immune recruitment, cytokine secretion, and interferon responses.
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These findings may offer more personalized treatment and prevention recommendations for patients with psoriasis.

Psoriasis may increase the risk of developing Sjögren’s syndrome (SS) due to overlapping immunological mechanisms that may lead to the co-occurrence of both diseases, according to a retrospective study published in BMC Medicine.1

Sjögren's syndrome | Image credit: MQ-Illustrations - stock.adobe.com

Psoriasis may increase the risk of developing Sjögren’s syndrome. | Image credit: MQ-Illustrations - stock.adobe.com

“In our study, leveraging the expansive TriNetX network data, we discovered a significantly elevated risk of SS in patients with psoriasis after PSM [propensity score matching] for confounders,” wrote the researchers of the study. “We also found that patients with PsA [psoriatic arthritis] and those treated with biological agents had an even higher risk of developing SS. Moreover, transcriptomic analysis suggests that shared pathological mechanisms between these diseases may include cellular proliferation, immune recruitment, cytokine release, and IFN [interferon] response to viral infections.”

SS is a chronic autoimmune disorder that predominately affects women.2 It occurs when the immune system attacks the glands that make moisture in the eyes, mouth, and other parts of the body. While the main symptoms are dry eyes and mouth, individuals with SS have reported fatigue and joint and muscle pain. Moreover, SS can impact the lungs, kidneys, and nervous system. There is currently no cure for SS.

The study utilized de-identified electronic health records from the TriNetX database, a large collaborative network in the US, encompassing data from approximately 118 million patients.1 Adults aged 20 years or older with records from 2004 to 2022 were included. The case group consisted of patients diagnosed with psoriasis, defined by at least 2 instances of the International Classification of Diseases, Tenth Revision, Clinical Modification (ICD-10-CM) code L40, while the control group included patients without psoriasis, identified using ICD-10-CM code Z00.

To mitigate potential confounding factors, a set of baseline covariates were included, encompassing demographic characteristics, socioeconomic status, and lifestyle factors. Additionally, a wide range of comorbidities was considered, including hypertensive diseases, disorders of lipoprotein metabolism and other lipidemias, diabetes mellitus, depressive episodes, ischemic heart diseases, liver diseases, cerebrovascular diseases, and other connective tissue diseases (CTD).

The primary outcome was an initial diagnosis of SS identified by ICD-10-CM code M35.

A total of 293,905 patients with psoriasis and an equal number of patients without psoriasis were included in the cohort. After propensity score matching, baseline characteristics were balanced between the groups.

During the follow-up period, 3339 patients with psoriasis and 1937 individuals without psoriasis developed SS. The analysis demonstrated a significantly higher risk of developing SS in the psoriasis group compared with the nonpsoriasis group (P < .05). Multivariable analysis further confirmed this association, showing a 50% increased risk of SS in the psoriasis group (HR, 1.50; 95% CI, 1.42–1.58) after adjusting for confounding factors.

Subgroup analyses supported these findings, revealing an even greater risk of SS among patients with psoriatic arthritis (PsA) and those receiving biological treatments.

Furthermore, transcriptomic analysis suggested shared pathogenic mechanisms between psoriasis and SS, including cellular proliferation, immune cell recruitment, cytokine secretion, and interferon (IFN) responses to viral infections.

However, the researchers acknowledged several limitations. Because the TriNetX platform does not provide data on psoriasis severity or duration, the researchers could not evaluate the impact of disease progression over time. Additionally, the study was observational and could not confirm causality. Finally, the relatively low rate of SS in patients with psoriasis may reduce the immediate clinical applicability of the study.

Despite these limitations, the researchers believe the study finds a link between psoriasis and SS, in which future studies should explore the molecular links between these diseases to identify biomarkers and therapeutic targets.

“Our study suggests that psoriasis is a risk factor for SS and that the risk may vary slightly according to age, sex, race, lifestyle habits, and comorbidities,” wrote the researchers. “PsA may augment the risk of developing SS. The overlapping immunological mechanisms may underlie the co-occurrence of psoriasis and SS.”

References

1. Kang Z, Du Y, Cui R, et al. Psoriasis increases the risk of Sjögren's syndrome: evidence from a propensity score-matched cohort study and transcriptomic analysis. BMC Med. 2025;23(1):26. doi:10.1186/s12916-025-03856-y

2. Overview of Sjögren’s disease. NIH. Last reviewed June 2024. Accessed January 22, 2025. https://www.niams.nih.gov/health-topics/sjogrens-disease#:~:text=Sj%C3%B6gren's%20disease%2C%20also%20known%20as,other%20parts%20of%20the%20body

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