1. Interleukin 1 -511 C/T polymorphism and risk of aneurysmal subarachnoid haemorrhage
- Author
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Joanna Pera, T Dziedzic, R Czepko, M Betlej, W Turaj, A Szczudlik, T Krzyszkowski, A Borratynska, A Slowik, and Dorota Wloch
- Subjects
medicine.medical_specialty ,Pathology ,Letter ,Subarachnoid hemorrhage ,Neurology ,medicine.medical_treatment ,Inflammation ,Gastroenterology ,Proinflammatory cytokine ,Pathogenesis ,Risk Factors ,Internal medicine ,medicine ,Humans ,cardiovascular diseases ,Allele ,Promoter Regions, Genetic ,Polymorphism, Genetic ,business.industry ,Interleukin ,Intracranial Aneurysm ,Subarachnoid Hemorrhage ,medicine.disease ,nervous system diseases ,Psychiatry and Mental health ,Cytokine ,Chromosomes, Human, Pair 2 ,Surgery ,Neurology (clinical) ,medicine.symptom ,business ,Interleukin-1 - Abstract
Production of the proinflammatory cytokine interleukin 1β (IL1β) increases in several acute or chronic diseases.1 The IL1β gene is a member of the IL1 gene family clustered on chromosome 2.1 A C/T polymorphism in the promoter region of the IL1β gene at position −511 influences the protein production, with the highest levels in T allele carriers.2 Data suggest that inflammation plays a role in the pathogenesis of subarachnoid haemorrhage (SAH) from ruptured aneurysm.3 We hypothesise that individuals genetically predisposed to an exaggerated cytokine production may be at risk of aneurysmal SAH. We studied the significance of IL1β –511 C/T polymorphism in patients with aneurysmal SAH and in healthy controls. We included 231 unrelated patients with aneurysmal SAH, of a total of 401 patients with SAH admitted to the Institute of Neurology, Krakow, Poland between 2003 and 2005. Patients with dissecting and fusiform aneurysms (n = 10), arteriovenous malformations (n = 30), SAH of unknown origin (n = 39), those who were comatose …
- Published
- 2006
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