Khaled El-Sayed
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Khaled El-Sayed has a total of 3 co-authors. Here are the top co-authors by number of shared publications:
- Abdullah Alyazidi
King Khalid Hospital
1 shared publication - Ahood Mahjari
Department of Neurosurgery, King Khalid Hospital, Najran, Saudi Arabia
1 shared publication - Ehab Abdu
Sana'a University
1 shared publication
Latest Publications
- Open Access
- 24 December 2025
- Published by Cambridge University Press (CUP) in Cambridge Open Engage
Traumatic Brain Injury and Risk of Intracranial Meningioma: A Systematic Review and Meta-Analysis
Background: Meningiomas are the most common primary intracranial tumors, but the role of traumatic brain injury (TBI) as a risk factor remains unclear. This study aimed to systematically evaluate and quantify the association between TBI and meningioma risk. Methods: We conducted a systematic review and meta-analysis of observational studies and Mendelian randomization analyses following PRISMA guidelines. PubMed, Scopus, Web of Science, Embase, and Cochrane databases were searched through December 5, 2025. Studies comparing meningioma incidence in individuals with and without a history of TBI were included. Risk of bias was assessed using the Newcastle-Ottawa Scale and ROBINS-MR tool. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using random-effects models. Heterogeneity and sensitivity analyses were performed. Results: Eleven studies (seven case-control, three cohort, one Mendelian randomization) were included, with eight contributing to the quantitative synthesis. The pooled analysis demonstrated a statistically significant association between TBI and meningioma (OR = 1.96; 95% CI [1.31 to 2.95]; p = 0.0012) with moderate heterogeneity (I² = 65.6%). Sensitivity analyses confirmed the robustness of the findings, although funnel plot asymmetry suggested potential publication bias. Conclusion: While a statistical association exists between TBI and meningioma, current evidence suggests it is unlikely to be causal. The association is primarily driven by retrospective case-control studies prone to bias, whereas prospective and genetic studies do not support a direct etiological link. Further long-term prospective studies are warranted to fully elucidate this relationship.
- 24 December 2025
- Published by Cambridge University Press (CUP) in Cambridge Open Engage
Open AccessTraumatic Brain Injury and Risk of Intracranial Meningioma: A Systematic Review and Meta-Analysis
Background: Meningiomas are the most common primary intracranial tumors, but the role of traumatic brain injury (TBI) as a risk factor remains unclear. This study aimed to systematically evaluate and quantify the association between TBI and meningioma risk. Methods: We conducted a systematic review and meta-analysis of observational studies and Mendelian randomization analyses following PRISMA guidelines. PubMed, Scopus, Web of Science, Embase, and Cochrane databases were searched through December 5, 2025. Studies comparing meningioma incidence in individuals with and without a history of TBI were included. Risk of bias was assessed using the Newcastle-Ottawa Scale and ROBINS-MR tool. Pooled odds ratios (ORs) and 95% confidence intervals (CIs) were calculated using random-effects models. Heterogeneity and sensitivity analyses were performed. Results: Eleven studies (seven case-control, three cohort, one Mendelian randomization) were included, with eight contributing to the quantitative synthesis. The pooled analysis demonstrated a statistically significant association between TBI and meningioma (OR = 1.96; 95% CI [1.31 to 2.95]; p = 0.0012) with moderate heterogeneity (I² = 65.6%). Sensitivity analyses confirmed the robustness of the findings, although funnel plot asymmetry suggested potential publication bias. Conclusion: While a statistical association exists between TBI and meningioma, current evidence suggests it is unlikely to be causal. The association is primarily driven by retrospective case-control studies prone to bias, whereas prospective and genetic studies do not support a direct etiological link. Further long-term prospective studies are warranted to fully elucidate this relationship.