Department of Anatomical Pathology, Faculty of Medicine Universitas Trisakti - Indonesia
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https://fktrisakti.ac.id
Department of Anatomical Pathology
Faculty of medicine
Universitas Trisakti
Introduction: Ruptured intracranial aneurysms (IAs) are a devastating cause of subarachnoid hemorrhage (SAH), often driven by complex inflammatory mechanisms. Pro-inflammatory cytokines such as IL-6, IL-1β, and TNF-α have been implicated in vascular wall degeneration leading to rupture.
Methods: A cross-sectional study was conducted on 30 patients with radiologically confirmed ruptured IAs in Satya Negara Hospital and Mitra Keluarga Hospital. Blood samples were collected within 72 hours post-ictus. Expression of IL-6, IL-1β, and TNF-α mRNA was quantified using real-time PCR at Hopkins Clinic and Lab, with GAPDH and β-actin as reference genes. CT values were analyzed and correlated with clinical severity based on Hunt & Hess grading.
Results: Mean CT values were IL-6: 32.56 ± 1.15, IL-1β: 31.47 ± 1.23, and TNF-α: 30.69 ± 1.15. Strong inverse correlations were observed between CT values and Hunt & Hess scores: IL-6 (r = -0.891), IL-1β (r = -0.930), and TNF-α (r = -0.919), all with p < 0.0001.
Conclusion: Expression of IL-6, IL-1β, and TNF-α is significantly elevated in ruptured IAs, correlating with clinical severity. These cytokines may serve as biomarkers and therapeutic targets in aneurysmal SAH.
Keywords: Intracranial Aneurysm; IL-6;IL-1β; TNF-α; Subarachnoid Hemorrhage; Inflammation
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