• Postgraduate medicine · Nov 2024

    Giant cell arteritis (GCA) as a risk factor for seizures: a cohort study.

    • Paula David, Esther Houri Levi, Ariel Feifel, Yonatan Shneor Patt, Abdulla Watad, Omer Gendelman, Arnon D Cohen, Howard Amital, and Avishai M Tsur.
    • Department of Medicine 'B', Zabludowicz Center for Autoimmune Diseases, Sheba Medical Center, Tel-Hashomer, Israel; affiliated with Sackler Faculty of Medicine, Tel-Aviv University, Tel-Aviv, Israel.
    • Postgrad Med. 2024 Nov 1; 136 (8): 875882875-882.

    ObjectivesThe objective of this study was to assess the risk of seizures in Giant Cell Arteritis (GCA) patients in a large cohort of Israeli subjects, in comparison to matched controls.MethodsPatients diagnosed with GCA between 2002 and 2017 were included. Controls were matched based on sex, age, socioeconomic status, country of birth, diabetes mellitus, and hypertension in a 4:1 ratio. Patients with seizure records prior to the study period were excluded. Hazard ratios for seizures was obtained by cox regression models.ResultsThe study cohort was composed by 8,103 GCA patients and 32,412 matched controls. The GCA group included 5,535 women (68%), 2,644 patients born in Israel (33%), and 2,888 patients with low socioeconomic status (36%). The median age of this group was 71. During the followed cumulative person-years of 54,641 and 222,537 in the GCA and control group, respectively, 15.92 cases per 10,000 person-years was found in the GCA group, compared to 9.62 per 10,000 person-years in the controls. GCA was associated with seizures in the unadjusted (HR = 1.66, 95% CI [1.29 to 2.13]) and adjusted (HR = 1.67, 95% CI [1.3 to 2.14]) models. GCA was also associated with seizures after controlling for strokes (HR = 1.55, 95% CI [1.16 to 2.07]).ConclusionAccording to this study, individuals with GCA are at a higher risk of developing seizures when compared to the general population. This increased risk is independent of their predisposition for stroke. One proposed mechanism is that the GCA pro-inflammatory state may decrease the neuronal threshold for depolarization.

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