Peripheral blood-derived expression of IL-6, IL-1β, and TNF-α inpatients with ruptured intracranial aneurysms
Abstract
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. 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. 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. Expression of
IL-6, IL-1β, and TNF-α is associated with greater severity within ruptured IA cases, correlating with
clinical severity. These cytokines may serve as biomarkers and therapeutic targets in aneurysmal SAH.
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