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T M Metso,
T Tatlisumak,
S Debette,
J Dallongeville,
S T Engelter,
P A Lyrer,
V Thijs,
A Bersano,
S Abboud,
D Leys, C Grond-Ginsbach,
M Kloss,
E Touzé,
A Pezzini,
A J Metso
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ABSTRACT: Several small to medium-sized studies indicated a link between cervical artery dissection (CeAD) and migraine. Migrainous CeAD patients were suggested to have different clinical characteristics compared to nonmigraine CeAD patients. We tested these hypotheses in the large Cervical Artery Dissection and Ischemic Stroke Patients (CADISP) population.
A total of 968 CeAD patients and 653 patients with an ischemic stroke of a cause other than CeAD (non-CeAD IS) were recruited. CeAD patients with stroke (CeAD(stroke), n = 635) were compared with non-CeAD IS patients regarding migraine, clinical characteristics, and outcome. CeAD patients with and without migraine were compared in terms of clinical characteristics and outcome.
Migraine was more common among CeAD(stroke) patients compared to non-CeAD IS patients (35.7 vs 27.4%, p = 0.003). The difference was mainly due to migraine without aura (20.2 vs 11.2%, p < 0.001). There were no differences in prevalence of strokes, arterial distribution, or other clinical or prognostic features between migrainous and nonmigrainous CeAD patients.
Migraine without aura is more common among CeAD(stroke) patients compared to non-CeAD IS patients. The mechanisms and possible causative link remain to be proved. Although CeAD is often complicated by stroke, our data do not support increased risk of stroke in migrainous CeAD patients.
Neurology 04/2012; 78(16):1221-8. · 8.31 Impact Factor
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S T Engelter,
J Dallongeville,
M Kloss,
T M Metso,
D Leys,
T Brandt,
Y Samson,
V Caso,
A Pezzini,
M Sessa, [......], C Grond-Ginsbach,
A J Metso,
V Thijs,
C Lamy,
E Medeiros,
J J Martin,
A Bersano,
T Tatlisumak,
E Touzé,
P A Lyrer
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ABSTRACT: To examine whether thrombolysis for stroke attributable to cervical artery dissection (CeAD(Stroke) ) affects outcome and major haemorrhage rates.
We used a multicentre CeAD(Stroke) database to compare CeAD(Stroke) patients treated with and without thrombolysis. Main outcome measures were favourable 3-month outcome (modified Rankin Scale 0-2) and 'major haemorrhage' [any intracranial haemorrhage (ICH) and major extracranial haemorrhage]. Adjusted odds ratios [OR (95% confidence intervals)] were calculated on the whole database and on propensity-matched groups.
Among 616 CeAD(Stroke) patients, 68 (11.0%) received thrombolysis; which was used in 55 (81%) intravenously. Thrombolyzed patients had more severe strokes (median NIHSS score 16 vs. 3; P < 0.001) and more often occlusion of the dissected artery (66.2% vs. 39.4%; P < 0.001). After adjustment for stroke severity and vessel occlusion, the likelihood for favourable outcome did not differ between the treatment groups [OR(adjusted) 0.95 (95% CI 0.45-2.00)]. The propensity matching score model showed that the odds to recover favourably were virtually identical for 64 thrombolyzed and 64 non-thrombolyzed-matched CeAD(Stroke) patients [OR 1.00 (0.49-2.00)]. Haemorrhages occurred in 4 (5.9%) thrombolyzed patients, all being asymptomatic ICHs. In the non-thrombolysis group, 3 (0.6%) patients had major haemorrhages [asymptomatic ICH (n = 2) and major extracranial haemorrhage (n = 1)].
As thrombolysis was neither independently associated with unfavourable outcome nor with an excess of symptomatic bleedings, our findings suggest thrombolysis should not be withheld in CeAD(Stroke) patients. However, the lack of any trend towards a benefit of thrombolysis may indicate the legitimacy to search for more efficient treatment options including mechanical revascularization strategies.
European Journal of Neurology 03/2012; 19(9):1199-206. · 3.69 Impact Factor
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ABSTRACT: Hypothermia is one of the most robust experimental neuroprotective interventions against cerebral ischemia. Identification of molecular pathways and gene networks together with single genes or gene families that are significantly associated with neuroprotection might help unravel the mechanisms of therapeutic hypothermia.
We performed a microarray analysis of ischemic rat brains that underwent 90 min of middle cerebral artery occlusion (MCAO) and 48 h of reperfusion. Hypothermia was induced for 4 h, starting 1 h after MCAO in male Wistar rats. At 48 h, magnetic resonance imaging (MRI) was performed for infarct volumetry, and functional outcome was determined by a neuroscore. The brain gene expression profile of sham (S), ischemia (I), and ischemia plus hypothermia (HI) treatment were compared by analyzing changes of individual genes, pathways, and networks. Real-time reverse-transcribed polymerase chain reaction (RT-PCR) was performed on selected genes to validate the data.
Rats treated with HI had significantly reduced infarct volumes and improved neuroscores at 48 h compared with I. Of 4067 genes present on the array chip, HI compared with I upregulated 50 (1.23%) genes and downregulated 103 (3.20%) genes equal or greater than twofold. New genes potentially mediating neuroprotection by hypothermia were HNRNPAB, HIG-1, and JAK3. On the pathway level, HI globally suppressed the ischemia-driven gene response. Twelve gene networks were identified to be significantly altered by HI compared with I. The most significantly altered network contained genes participating in apoptosis suppression.
Our data suggest that although hypothermia at the pathway level restored gene expression to sham levels, it selectively regulated the expression of several genes implicated in protein synthesis and folding, calcium homeostasis, cellular and synaptic integrity, inflammation, cell death, and apoptosis.
Neuroscience 02/2012; 208:109-22. · 3.38 Impact Factor
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A J Metso,
T M Metso,
S Debette,
J Dallongeville,
P A Lyrer,
A Pezzini,
C Lichy,
M Kloss,
T Brandt,
E Touzé,
A M Southerland,
B B Worrall,
S Abboud,
E del Zotto,
D Leys,
S Engelter, C Grond-Ginsbach,
T Tatlisumak
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ABSTRACT: To analyze previously established gender differences in cervical artery dissection (CeAD).
This case-control study is based on the CADISP (Cervical Artery Dissection and Ischemic Stroke Patients) population comprising 983 consecutive CeAD patients (mean age: 44.1 ± 9.9 years) and 658 control patients with a non-CeAD ischemic stroke (IS) (44.5 ± 10.5 years).
Cervical artery dissection was more common in men (56.7% vs. 43.3%, P < 0.001) and men were older (46.4 vs. 41.0 years, P < 0.001). We assessed putative risk factors for CeAD including vascular risk factors, recent cervical trauma, pregnancies, and infections. All gender differences in the putative risk factors and outcome were similar in the CeAD and the non-CeAD IS groups.
Our analysis of the largest collection of CeAD patients to date confirms male predominance and differences in age at dissection between men and women. Gender differences in putative risk factors may explain the higher frequency of CeAD in men and their older age, but the putative risk factors are probably not specific for CeAD.
European Journal of Neurology 12/2011; 19(4):594-602. · 3.69 Impact Factor
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S Debette, C Grond-Ginsbach,
M Bodenant,
M Kloss,
S Engelter,
T Metso,
A Pezzini,
T Brandt,
V Caso,
E Touzé, [......],
S Abboud,
G Giacalone,
P Lyrer,
E Del Zotto,
M Giroud,
Y Samson,
J Dallongeville,
T Tatlisumak,
D Leys,
J J Martin
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ABSTRACT: To examine whether risk factor profile, baseline features, and outcome of cervical artery dissection (CEAD) differ according to the dissection site.
We analyzed 982 consecutive patients with CEAD included in the Cervical Artery Dissection and Ischemic Stroke Patients observational study (n = 619 with internal carotid artery dissection [ICAD], n = 327 with vertebral artery dissection [VAD], n = 36 with ICAD and VAD).
Patients with ICAD were older (p < 0.0001), more often men (p = 0.006), more frequently had a recent infection (odds ratio [OR] = 1.59 [95% confidence interval (CI) 1.09-2.31]), and tended to report less often a minor neck trauma in the previous month (OR = 0.75 [0.56-1.007]) compared to patients with VAD. Clinically, patients with ICAD more often presented with headache at admission (OR = 1.36 [1.01-1.84]) but less frequently complained of cervical pain (OR = 0.36 [0.27-0.48]) or had cerebral ischemia (OR = 0.32 [0.21-0.49]) than patients with VAD. Among patients with CEAD who sustained an ischemic stroke, the NIH Stroke Scale (NIHSS) score at admission was higher in patients with ICAD than patients with VAD (OR = 1.17 [1.12-1.22]). Aneurysmal dilatation was more common (OR = 1.80 [1.13-2.87]) and bilateral dissection less frequent (OR = 0.63 [0.42-0.95]) in patients with ICAD. Multiple concomitant dissections tended to cluster on the same artery type rather than involving both a vertebral and carotid artery. Patients with ICAD had a less favorable 3-month functional outcome (modified Rankin Scale score >2, OR = 3.99 [2.32-6.88]), but this was no longer significant after adjusting for baseline NIHSS score.
In the largest published series of patients with CEAD, we observed significant differences between VAD and ICAD in terms of risk factors, baseline features, and functional outcome.
Neurology 09/2011; 77(12):1174-81. · 8.31 Impact Factor
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M. DE GAETANO,
G. QUACQUARUCCIO,
A. PEZZINI,
M. C. LATELLA,
A. DI CASTELNUOVO,
E. DEL ZOTTO,
A. PADOVANI,
C. LICHY, C. GROND-GINSBACH,
M. GATTONE,
P. GIANNUZZI,
N. NOVAK,
J. DORN,
M. TREVISAN,
M. B. DONATI,
L. IACOVIELLO
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ABSTRACT: Summary Objective: The exposure of tissue factor (TF) to blood flow is the initial step in the coagulation process and plays an important role in thrombogenesis. We investigated the role of genetic polymorphisms and haplotypes of the TF gene in the risk of ischemic vascular disease. Methods: Four hundred and twenty-two Italian patients with juvenile myocardial infarction (MI) and 434 controls, 808 US cases with MI and 1005 controls, 267 Italian cases with juvenile ischemic stroke and 209 controls and 148 German cases with juvenile ischemic stroke and 191 controls were studied. rs1361600, rs3917629 (rs3354 in the US population), rs1324214 and rs3917639 Tag single nucleotide polymorphisms were genotyped. Additionally, a meta-analysis of all previous studies on TF loci and the risk of ischemic coronary disease (ICD) was performed. Results: After multivariable analysis none of the SNPs, major SNP haplotypes or haplotype-pairs showed any consistent association with MI. Pooled meta-analysis of six studies also suggested that TF polymorphisms are not associated with CHD. A significant, independent association between SNP rs1324214 (C/T) and juvenile stroke was found in Italian and German populations (OR for TT homozygotes = 0.47, 95% CI 0.24–0.92, in combined analysis). Pooled analysis also showed a significant association for haplotype H3 (OR = 0.76, 95% CI 0.57–1.00) and haplotype-pair H3–H3 (OR = 0.43, 95% CI 0.20–0.92). Conclusions: TF genetic variations were associated with the risk of ischemic stroke at young age, but did not affect ischemic coronary disease.
Journal of Thrombosis and Haemostasis 07/2009; 7(9):1465 - 1471. · 5.73 Impact Factor
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S Debette,
T M Metso,
A Pezzini,
S T Engelter,
D Leys,
P Lyrer,
A J Metso,
T Brandt,
M Kloss,
C Lichy, [......],
H S Markus,
S Abboud,
V Caso,
A Bersano,
A Grau,
A Altintas,
P Amouyel,
T Tatlisumak,
J Dallongeville, C Grond-Ginsbach
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ABSTRACT: Cervical artery dissection (CAD) is a frequent cause of ischemic stroke, and occasionally death, in young adults. Several lines of evidence suggest a genetic predisposition to CAD. However, previous genetic studies have been inconclusive mainly due to insufficient numbers of patients. Our hypothesis is that CAD is a multifactorial disease caused by yet largely unidentified genetic variants and environmental factors, which may interact. Our aim is to identify genetic variants associated with an increased risk of CAD and possibly gene-environment interactions.
We organized a multinational European network, Cervical Artery Dissection and Ischemic Stroke Patients (CADISP), which aims at increasing our knowledge of the pathophysiological mechanisms of this disease in a large group of patients. Within this network, we are aiming to perform a de novo genetic association analysis using both a genome-wide and a candidate gene approach. For this purpose, DNA from approximately 1100 patients with CAD, and 2000 healthy controls is being collected. In addition, detailed clinical, laboratory, diagnostic, therapeutic, and outcome data are being collected from all participants applying predefined criteria and definitions in a standardized way. We are expecting to reach the above numbers of subjects by early 2009.
We present the strategy of a collaborative project searching for the genetic risk factors of CAD. The CADISP network will provide detailed and novel data on environmental risk factors and genetic susceptibility to CAD.
International Journal of Stroke 07/2009; 4(3):224-30. · 2.38 Impact Factor
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Journal of Neurology 07/2008; 255(9):1421-2. · 3.47 Impact Factor
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ABSTRACT: Ischemic stroke provokes a systemic inflammatory response. The purpose of this study was to characterize this response on the gene expression level in circulating mononuclear leukocytes from acute ischemic stroke (AIS) patients.
RNA from peripheral blood mononuclear cells (PBMCs) of AIS patients (24 + 2 hours after onset of symptoms) was analyzed with Affymetrix U133A GeneChips using a pooled design. We compared the gene expression signature from AIS patients (n = 20), stroke survivors (n = 15), patients with acute traumatic brain injury (ATBI, n = 15) and healthy control subjects without vascular risk factors (n = 15).
Expression levels of 9682 probe sets with present calls on each GeneChip were compared. Between AIS patients and stroke survivors or between AIS patients and ATBI patients there were no significant differences in expression values of single genes after correction for multiple testing. However, comparison of the PBMC expression profiles from AIS patients and healthy subjects revealed significantly different expression (p = 0.012) of a single probe set, specific for phosphodiesterase 4 D (PDE4D). In order to detect modest expression differences in multiple genes with a presumed cumulative effect we studied the gene expression of functional groups of genes by global statistical tests. Analysis of 11 gene groups revealed differential expression between AIS patients and healthy subjects for genes involved in the inflammatory response (GeneOntology GO:0006954). Genes encoding the N-formyl peptide receptor-like 1 (FPRL1), interleukin-1 receptor antagonist (IL1RN) and complement component 3a receptor 1 (C3AR1) contributed most to the observed difference.
This transcriptome analysis did not identify significant changes between circulating mononuclear cells from AIS patients 24 hours after stroke and closely matched stroke survivors. However, comparing AIS patients with healthy control subjects revealed measurable differences in PDE4D and in inflammatory response genes when considered as a set.
Journal of Neurology 06/2008; 255(5):723-31. · 3.47 Impact Factor
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ABSTRACT: Die seltene Erkrankung okulodentodigitale Dysplasie (ODDD), die in der Regel autosomal-dominant vererbt wird, ist charakterisiert
durch Veränderungen der Augen, Zähne und der Finger und geht auf eine Mutation des GJA1-Gens zurück. Im Hinblick auf die Zahnveränderungen ist ein früher Zeitpunkt für Beurteilung und Behandlung von entscheidender
Bedeutung. Im vorliegenden Fallbericht wird dargestellt, dass an verschiedenen Zähnen unterschiedlich stark ausgeprägte Veränderungen
erkennbar werden können. Dies könnte erklären, dass in der Literatur die Zahnveränderungen bei ODDD so unterschiedlich beschrieben
werden.
Oculodentodigital dysplasia (ODDD), a rare inherited autosomal dominant disorder, characterized by developmental abnormalities
of the eyes, teeth and digits, has been linked to mutations in the GJA1 gene. Regarding tooth abnormalities an early evaluation and treatment of the enamel is of crucial importance. It is unclear
whether different descriptions of enamel defects in ODDD are due to actual different dental symptoms or just correlate of
different stages of secondary damage.
Medizinische Genetik 11/2007; 19(4):427-431. · 0.06 Impact Factor
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ABSTRACT: A common pro-inflammatory promoter variant of the selenoprotein S encoding gene (SEPS1) was studied in young stroke patients from Italy and Germany and in healthy control subjects. The -105A-allele was found in 56 of 205 (27.3%) patients with ischemic stroke IS because of a spontaneous cervical artery dissection (CAD), and in 69 of 295 (23.4%) patients <50 years with IS of non-CAD origin. The SEPS -105A promoter variant was detected in 87 of 393 healthy control subjects (22.1%) and in 11 of 55 CAD patients without IS (20%). The non-significant differences of SEPS1 allele frequencies between disease groups and healthy controls suggest that the SEPS1 -105A allele is not a major-risk factor for stroke.
European Journal of Neurology 10/2007; 14(10):1173-5. · 3.69 Impact Factor
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ABSTRACT: The methylene tetrahydrofolate reductase (MTHFR) C677T polymorphism was studied in 174 German patients with cervical artery dissection (CAD). The results were compared with published data on 927 healthy German controls. In the series of patients, the frequency of T alleles and of TT carriers was slightly higher (13.8%) than among the healthy controls (10.6%). In patients with multiple dissections (n = 50), the proportion of TT carriers (18%) was found to be even higher and correlated with the number of events. The MTHFR C677T polymorphism was suggested to modify the risk for CAD.
Journal of neurology, neurosurgery, and psychiatry 09/2006; 77(8):951-2. · 4.87 Impact Factor
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Clinical Genetics 08/2006; 70(1):71-2. · 3.13 Impact Factor
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ABSTRACT: In a primary study on proinflammatory genetic profiles in stroke, the authors found the E469K polymorphism of the intercellular adhesion molecule 1 (ICAM-1) highly represented in the subgroup with spontaneous cervical artery dissection (sCAD). They further investigated the same genetic variant in a second group of 65 patients with sCAD. An association between sCAD and EE genotype was confirmed (odds ratio 3.16; p < 0.01), indicating that a proinflammatory predisposition is a risk factor for sCAD.
Neurology 04/2006; 66(8):1273-5. · 8.31 Impact Factor
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ABSTRACT: Microbial agents may play a role in the pathogenesis of multiple sclerosis (MS). C. pneumoniae has been recently associated with MS; however, study results are at variance. We tested the hypothesis that Chlamydia pneumoniae-specific DNA and RNA are more often detected in cerebrospinal fluid (CSF) of patients with multiple sclerosis than patients with other neurological diseases (OND). We investigated CSF samples from 84 patients with definite MS and 89 OND patients (n = 62 with normal CSF; n = 27 with pathological CSF) using a nested polymerase chain reaction (PCR) to detect ompA gene sequences of C. pneumoniae. In subjects with positive PCR, we probed for chlamydial heat shock protein 60-mRNA and 16S-rRNA by reverse transcriptase (rt)-PCR. C. pneumoniae-specific DNA was more often detected in MS patients (50 %) than in all OND patients combined (28.1%, p = 0.003) and in OND patients with normal CSF (24.2%, p = 0.003) but not than in OND patients with pathological CSF (37%, p = 0.24). In relapsing-remitting MS (n = 55), the prevalence of C. pneumoniae DNA was higher (66.7 %) than in both OND subgroups (p <or= 0.05). In MS patients (n = 20), chlamydial heat shock protein 60-mRNA (75%) and 16S-rRNA (70%) were more often detected than in OND patients (n = 16; 18.8%; p < 0.005). Although more often detected in remitting-relapsing MS, C. pneumoniae DNA in CSF is not specific for MS owing to its high prevalence in OND controls. However, the higher rate of gene transcription suggests a more active metabolism of C. pneumoniae in MS patients.
Journal of Neurology 05/2004; 251(5):542-7. · 3.47 Impact Factor
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ABSTRACT: The authors searched for the presence of alpha-1-antitrypsin (AAT) deficiency alleles PiZ and PiS in 74 patients with spontaneous cervical artery dissections (sCADs) and in 74 healthy control subjects. In both groups, the authors found four carriers of deficiency alleles. The connective tissue morphology of one additional patient with sCAD with PiZM genotype and her relatives was studied in skin biopsies. The PiZ allele did not segregate with morphologic alterations of the dermal connective tissue in the family. Therefore, AAT deficiency alleles may not play a role in the etiology of sCAD.
Neurology 05/2004; 62(7):1190-2. · 8.31 Impact Factor
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ABSTRACT: Microbial agents may play a role in the pathogenesis of multiple sclerosis (MS). C. pneumoniae has been recently associated with MS; however, study results are at variance. We tested the hypothesis that Chlamydia pneumoniae-specific DNA and RNA are more often detected in cerebrospinal fluid (CSF) of patients with multiple sclerosis than patients with other neurological diseases (OND). We investigated CSF samples from 84 patients with definite MS and 89 OND patients (n = 62 with normal CSF; n = 27 with pathological CSF) using a nested polymerase chain reaction (PCR) to detect ompA gene sequences of C. pneumoniae. In subjects with positive PCR, we probed for chlamydial heat shock protein 60-mRNA and 16S-rRNA by reverse transcriptase (rt)-PCR.C. pneumoniae-specific DNA was more often detected in MS patients (50 %) than in all OND patients combined (28.1%, p = 0.003) and in OND patients with normal CSF (24.2%, p = 0.003) but not than in OND patients with pathological CSF (37%, p = 0.24). In relapsing-remitting MS (n = 55), the prevalence of C. pneumoniae DNA was higher (66.7 %) than in both OND subgroups (p 0.05). In MS patients (n = 20), chlamydial heat shock protein 60-mRNA (75%) and 16S-rRNA (70%) were more often detected than in OND patients (n = 16; 18.8%; p < 0.005).Although more often detected in remitting-relapsing MS, C. pneumoniae DNA in CSF is not specific for MS owing to its high prevalence in OND controls. However, the higher rate of gene transcription suggests a more active metabolism of C. pneumoniae in MS patients.
Journal of Neurology 04/2004; 251(5):542-547. · 3.47 Impact Factor
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ABSTRACT: The vitamin K-dependent protein Z (PZ) has been shown to possess anticoagulant as well as procoagulant properties. Plasma levels of PZ show a broad interindividual variation, but it is unknown to which extent this variation is under genetic control. Recent clinical studies revealed contradictory results on the association of PZ plasma levels and the risk of ischemic stroke.
We performed a case-control study including 200 patients with cerebral ischemia aged < or =50 years and 199 control subjects from the same South German region. We investigated a possible association of 2 common single nucleotide mutations in the PZ gene with the risk of cerebral ischemia. Furthermore, enzyme-linked immunosorbent assay measurements were done in control subjects without vascular disease to detect a potential association of different genotypes with PZ plasma (antigen) levels.
In patients, the frequency of the A allele of the intron F polymorphism G79A was significantly lower than in controls (15.7% versus 24.4%; odds ratio, 0.58; 95% CI, 0.39 to 0.86; P=0.007; adjusted for age, sex, and conventional risk factors). The G allele of the promoter polymorphism A-13G tended to be less common in patients (4.2% versus 7.0%; adjusted odds ratio, 0.56; 95% CI, 0.28 to 1.13; P=0.105). In 42 control subjects, the A allele of the intron F polymorphism was associated with lower PZ antigen levels (P=0.0032; Spearman correlation coefficient rs=-0.48).
The A allele of an intron F polymorphism of the PZ gene appears to be a novel protective genetic marker for the risk of cerebral ischemia in young adults. In the context of juvenile stroke, high PZ plasma levels may represent a prothrombotic condition.
Stroke 02/2004; 35(1):40-5. · 5.73 Impact Factor
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Journal of Neurology 07/2003; 250(8):1004-1005. · 3.47 Impact Factor
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ABSTRACT: The monocyte receptor for bacterial lipopolysaccharide CD14 is an important mediator of the inflammatory response. Recently, a polymorphism in the promotor of the CD14 gene, C (-260) T, was detected as a risk factor for coronary heart disease.
We tested the hypotheses that this polymorphism is a risk factor 1. for cerebral ischemia in general and 2. for cerebral ischemia due to large artery atherosclerosis or microangiopathy in particular.
We performed a case control study including 151 consecutive patients with acute cerebral ischemia treated at our university hospital and 149 control subjects. All control subjects were randomly selected from the general population of the same region in South-West Germany. Genotype frequencies of the C(-260) T polymorphism in the promotor of the CD14 gene were examined by restriction length analysis.
The TT-genotype was not associated with cerebral ischemia in general either in univariate or in multivariate analysis together with classical vascular risk factors (odds ratio in multivariate analysis: 1.11; 95 %CI, 0.63 to 1.95). In 70 patients with cerebral ischemia due to atherosclerosis of large arteries or microangiopathy, there was a significantly higher prevalence of the TT-genotype than into control subjects (38.6 % vs. 23.5 %; odds ratio in multivariate analysis 2.26; 95 %CI, 1.13 to 4.54).
We demonstrated that the TT-genotype of the CD14 C(-260) T polymorphism in a South-German population is not associated with an increased risk of cerebral ischemia in general. However, we found that the TT-genotype is associated with a risk of atherosclerotic or microangiopathic stroke. This finding requires confirmation by future studies in larger populations.
Journal of Neurology 08/2002; 249(7):821-3. · 3.47 Impact Factor
