Free Protein S Spectrum in Young Patients with Stroke

Nighoghossian, Norbert; Berruyer, Micheline; Getenet, Jean-Claude; Trouillas, P

doi:10.1159/000108499

Cited by 8 publications

(2 citation statements)

References 11 publications

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“…[1][2][3] These conditions, the thrombophilias, include deficiencies of the natural anticoagulants such as antithrombin III, 4,5 protein S, 6,7 and protein C; 8 -12 and single point mutations in coagulation molecules such as factor V Leiden (1691G/A) [13][14][15][16] ; or the 3Ј untranslated region of the prothrombin gene (factor II) (20210 G/A). 17,18 There is little doubt that inherited thrombophilias can cause venous thrombosis, but most individuals with a single genetic risk factor will not have a thrombotic event in the absence of circumstantial risk factors such as immobility or the oral contraceptive pill.…”

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confidence: 99%

Inherited Thrombophilia in Ischemic Stroke and Its Pathogenic Subtypes

Hankey

Eikelboom

Bockxmeer

et al. 2001

Stroke

136

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Background and Purpose-One or more of the inherited thrombophilias may be causal risk factor for a proportion of ischemic strokes, but few studies have addressed this association or the association between thrombophilia and pathogenic subtypes of stroke. Methods-We conducted a case-control study of 219 hospital cases with a first-ever ischemic stroke and 205 randomly selected community control subjects stratified by age, sex, and postal code. With the use of established criteria, cases of stroke were classified by pathogenic subtype in a blinded fashion. The prevalence of conventional vascular risk factors; fasting plasma levels of protein C, protein S, antithrombin III; and genetic tests for the factor V Leiden and the prothrombin 20210A mutation were determined in cases and control subjects. Results-The prevalence of any thrombophilia was 14.7% (95% CI, 9.9% to 19.5%) among cases and 11.7% (95% CI, 7.4% to 17.0%) among control subjects (OR, 1.3; 95% CI, 0.7% to 2.3%). The prevalence of individual thrombophilias among cases ranged from 0.9% (95% CI, 0.1% to 3.4%) for protein S deficiency to 5.2% (95% CI, 0.3% to 9.1%) for antithrombin III deficiency; among control subjects, the prevalence ranged from 1.0% (95% CI, 0.1% to 3.6%) for protein S deficiency to 4.1% (95% CI, 0.2% to 7.8%) for antithrombin III deficiency. There were no significant differences in the prevalence of thrombophilia between cases and control subjects or between pathogenic subtypes of ischemic stroke. Conclusions-One in 7 patients with first-ever acute ischemic stroke will test positive for one of the inherited thrombophilias, but the relation is likely to be coincidental rather than causal in almost all cases, irrespective of the pathogenic subtype of the ischemic stroke. These results suggest that routine testing for thrombophilia in most patients with acute ischemic stroke may be unnecessary. Whether the thrombophilias may still be important in younger patients with ischemic stroke or in predicting complications (eg, venous thrombosis) and stroke outcome remains uncertain.

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confidence: 99%

Inherited Thrombophilia in Ischemic Stroke and Its Pathogenic Subtypes

Hankey

Eikelboom

Bockxmeer

et al. 2001

Stroke

136

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“…These findings support the hypothesis that antiphospholipid an tibodies can appear transiently, and their proeoagulant effects contribute to the development of CL Regarding coagulation inhibitors, we observed 2 pa tients with acquired decrease of cither protein Sor AT-III. Nighoghossian et al [27] also found a patient with tran sient deficiency of protein S among 26 patients with Cl onset at a young age. Martinez ct al.…”

Section: Discussionmentioning

confidence: 94%

Expanded Spectrum of Coagulopathy in the Etiology of Cerebral Infarction in Younger Adults in Japan

Nagayama

Ohnuki

et al. 1996

Cerebrovasc Dis

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To clarify the role of coagulopathy in cerebral infarction (CI) in adults with onset before age 45, we performed comprehensive and repeated hemostatic analyses in 77 consecutive young adult patients with CI. Coagulopathy was found in 24% (9% in older adults, n = 241); inherited coagulopathy was observed in 14 patients, including protein-S deficiency in 6, abnormal plasminogen (genetically confirmed) in 5, and protein-C deficiency in 2. Acquired coagulopathy confined to the acute stage was observed in 6 patients, including siently present anticardiolipin antibody in 3, and transiently present lupus anticoagulant in 2. Of 20 patients who did not have any risk factor for atherosclerosis, acquired coagulopathy was observed in 6. We conclude that protein-S deficiency and abnormal plasminogen are frequent and might be critical causes of CI in younger adults; transient coagulopathy is also a possible cause.

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Les déficits congénitaux en protéineS ; difficultés diagnostiques

Guermazi

Conard

2009

Pathologie Biologie

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Free Protein S Spectrum in Young Patients with Stroke

Cited by 8 publications

References 11 publications

Inherited Thrombophilia in Ischemic Stroke and Its Pathogenic Subtypes

Inherited Thrombophilia in Ischemic Stroke and Its Pathogenic Subtypes

Expanded Spectrum of Coagulopathy in the Etiology of Cerebral Infarction in Younger Adults in Japan

Les déficits congénitaux en protéineS ; difficultés diagnostiques

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