Cerebral infarction and familial protein S deficiency.

Davous, P.; Horellou, M.H.; Conard, J; Samama, M

doi:10.1161/01.str.21.12.1760

Cited by 22 publications

(6 citation statements)

References 15 publications

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“…At the 6-month follow-up, one more patient (protein C, 31% at 2 months) had died because of recurrent stroke, raising the overall mortality to 50%. Among the three survivors, two had returned to normal protein C, The patients with normal protein C on admission had a mean score of 75±32 on the Barthel scale, 8.7±3 on the CaNeSc scale, and a mean lesion size of 8±22 mL. The prevalence of emboligenic cardiac disease was 8.1% (3 of 37) (two atrial fibrillation and one recent myocardial infarction).…”

Section: Resultsmentioning

confidence: 95%

Early prognostic factors in ischemic stroke. The role of protein C and protein S.

Anzola

Magoni

Ascari

et al. 1993

Stroke

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Background and Purpose: Protein C and protein S have been found reduced in some patients with ischemic cerebrovascular diseases, but the relevance of this finding for prognosis is unsettled.Methods: In 43 consecutive patients admitted over 6 months for acute ischemic stroke, protein C and free protein S were evaluated on admission, and at 2 and 6 months after stroke. Excluded were all patients with known causes liable to reduce the levels of protein C, free protein S, or both.Results: In 14% of patients, abnormally low levels of protein C were found at entry. In comparison to the remaining sample, this group had a significantly lower initial score on the Barthel and Canadian neurological scales, a higher prevalence of emboligenic cardiac diseases, and had a higher mortality at 6 months. No statistical difference was found for the other vascular risk factors. Eight patients (18.4%) had abnormally low levels of free protein S at entry. In comparison to the remaining sample, there was no statistical difference in the severity scores, prevalence of emboligenic cardiac diseases, mortality, or

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Section: Resultsmentioning

confidence: 95%

Early prognostic factors in ischemic stroke. The role of protein C and protein S.

Anzola

Magoni

Ascari

et al. 1993

Stroke

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“…40 Among them, inherited protein S deficiency has been related to arterial thrombotic complications. [41][42][43][44][45][46] However, this abnormality as a prothrombotic disorder is still a controversial issue. 40,47 It has been reported that the levels of protein S are influenced by sex, age, pregnancy, and hormonal state.…”

Section: Discussionmentioning

confidence: 99%

Prothrombotic Disorders in Children With Moyamoya Syndrome

Bonduel¹,

Hepner

Sciuccati

et al. 2001

Stroke

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Background and Purpose — Moyamoya syndrome is an uncommon chronic occlusive cerebrovascular disease in children. The origin of moyamoya syndrome remains undetermined. The role of the prothrombotic disorders contributing to its pathogenesis has not been completely elucidated. The purpose of this study was to determine the frequency of prothrombotic disorders in a pediatric population with moyamoya syndrome. Methods — From May 1992 to April 2000, a prospective study of 10 consecutive children with moyamoya syndrome was carried out at a single center. Evaluation included the following assays: protein C, protein S, antithrombin, plasminogen, activated protein C resistance, factor V Leiden, and prothrombin gene mutations. Lupus anticoagulant, anticardiolipin antibodies, and anti–β 2 -glycoprotein I antibodies assays were also performed. The clinical characteristics, underlying diseases, family history of thrombosis, radiological findings, treatment, and outcome were also recorded. Results — In our series, prothrombotic disorders were detected in 4 patients (40%). Inherited protein S deficiency was found in 1 patient; lupus anticoagulant and anticardiolipin antibodies were detected in the remaining 3 patients. One presented persistent lupus anticoagulant for 2.7 years until his death. In the case of the other 2 patients, 1 has maintained lupus anticoagulant for 9 months, whereas the other has kept anticardiolipin/anti–β 2 -glycoprotein I antibodies for 10 months. Conclusions — We report the hemostatic data of the largest prospective pediatric study carried out at a single center in the western hemisphere. In 4 patients (40%), a prothrombotic disorder was detected. It is tempting to speculate that these hemostatic abnormalities may contribute to the pathogenesis of moyamoya syndrome in some of our patients.

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“…Of the 17 studies that reported on protein S deficiency (8,9,(99)(100)(101)(102)(103)(104)(105)(106)(107)(108)(109)(110)(111)(112)(113), 5 were not eligible (9,(99)(100)(101)(102). The analysis of the remaining 12 studies showed that the prevalence of a history of venous thrombotic disease was statistically significantly higher (p < 0.001) in deficient family members (56%; 40/71) than in nondeficient family members (4%; 3/69) (estimated common odds ratio, 10.0; 95% confidence interval, 4.5-22.2).…”

Section: Protein S and Venous Thrombosismentioning

confidence: 99%

Familial Thrombophilia: A Review Analysis

Belt¹,

Prins²,

Huisman

et al. 1996

Clin Appl Thromb Hemost

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The correct approach to the management of the asymptomatic carrier with a recognized inherited thrombophilic disorder is uncertain because reliable in formation of the risk of spontaneous (unprovoked) throm bosis in these disorders is not available. To determine the best available estimate of the annual incidence of spon taneous thrombosis in asymptomatic carriers of disorders that have been linked to familial thrombophilia, we per formed a literature review. Using Medline search from 1965 to 1992, supplemented by manual searches, we re trieved all articles that presented data on antithrombin III, protein C, protein S, dysfibrinogenemia, plasmino gen, histidine-rich glycoprotein, heparin cofactor II, and fibrinolysis in relation to thrombosis. Publications were included in the analysis if they (1) reported one or more probands with thrombotic disease and a heterozygous biochemical abnormality of the hemostatic system, (2) assessed the presence of this abnormality in family mem bers independent of the presence or absence of a history of thrombotic disease, and (3) assessed the presence of a history of thrombotic disease in all available family mem bers. The biochemical status and clinical details of all family members reported were extracted from each eligi ble article. For each abnormality the odds ratio for throm bosis was compared in family members with and without the biochemical abnormality. If applicable, thrombosis- free survival and age-specific incidences of thrombosis were calculated. The thrombotic episodes were classified as spontaneous or secondary to a recognized risk factor, and the proportion of spontaneous episodes was calcu lated. The influence of diagnostic suspicion bias in symp tomatic patients with a family history of thrombosis was reduced by recalculating the absolute incidence of throm bosis from the odds ratio after adjusting the incidence of venous thrombosis in nonaffected family members to that observed in the general population. Statistically signifi cant associations between the presence of a biochemical abnormality and a history of venous thrombosis were found for antithrombin III deficiency types 1 and 2a and 2b, protein C deficiency type 1, and protein S deficiency type I. Dysfibronogenemia was statistically significantly associated with venous as well as arterial thrombosis. Thirty-five to 67% of the events were classified as being provoked, as they occurred following exposure to a rec ognized risk factor for thrombosis. The recalculated an nual incidence of spontaneous thrombosis was 0.6 to 1.6%/year. It is concluded that this relatively low inci dence does not warrant life-long continuous use of anti coagulant prophylaxis since the reported risk of major and fatal bleeding associated with the use of oral antico agulants is 2-3 and 0.4%/year, respectively.

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Cerebral infarction and familial protein S deficiency.

Cited by 22 publications

References 15 publications

Early prognostic factors in ischemic stroke. The role of protein C and protein S.

Early prognostic factors in ischemic stroke. The role of protein C and protein S.

Prothrombotic Disorders in Children With Moyamoya Syndrome

Familial Thrombophilia: A Review Analysis

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