scholarly journals Association between blood coagulability and migraine

2022 ◽  
Vol 58 (1) ◽  
Author(s):  
Ebtesam Mohamed Fahmy ◽  
Mona Salah Eldin Hamdy ◽  
Reem Medhat Mahmoud ◽  
Haidy Elshebawy
Keyword(s):  
Serum Protein ◽  
Protein C ◽  
Brain Mri ◽  
Management Strategies ◽  
Protein S ◽  
Conclusive Evidence ◽  
Mri Findings ◽  
Protein C Deficiency ◽  
Increased Risk ◽  
Blood Coagulability

Abstract Background An association between migraine and stroke has been suggested for a long period, although conclusive evidence has not been reported. Several theories about hypercoagulability have been proposed for the association of ischemic stroke and migraine especially migraine with aura. This study aimed to assess blood coagulability in patients with migraine. Results Mean serum levels of protein S and anti-thrombin III were significantly lower in migraine patients compared to control subjects. Migraine patients showed abnormal MRI findings in the form of white matter hyper-intense lesions and ischemic foci compared to healthy controls. A significant negative correlation was detected between serum protein C level and intensity of migraine headache. Also, a significant correlation was found between deficient serum protein S and abnormal findings in brain MRI. Serum protein C deficiency is an independent predictor for migraine intensity grade. Conclusions There is an association between migraine and hypercoagulability, which may indicate increased risk of cerebral ischemic events in migraine patients and suggest adding prophylactic therapy to the management strategies of such patients.

Severe Arterial Cerebral Thrombosis in a Patient with Protein S Deficiency (Moderately Reduced Total and Markedly Reduced Free Protein S): A Family Study

1989 ◽  
Vol 61 (01) ◽  
pp. 144-147 ◽  
Author(s):  
A Girolami ◽  
P Simioni ◽  
A R Lazzaro ◽  
I Cordiano
Keyword(s):  
Arterial Thrombosis ◽  
Protein C ◽  
Protein S ◽  
Protein S Deficiency ◽  
Protein C Deficiency ◽  
Free Protein ◽  
Her Family ◽  
S Deficiency ◽  
Increased Risk ◽  
Patient Reported

SummaryDeficiency of protein S has been associated with an increased risk of thrombotic disease as already shown for protein C deficiency. Deficiencies of any of these two proteins predispose to venous thrombosis but have been only rarely associated with arterial thrombosis.In this study we describe a case of severe cerebral arterial thrombosis in a 44-year old woman with protein S deficiency. The defect was characterized by moderately reduced levels of total and markedly reduced levels of free protein S. C4b-bp level was normal. Protein C, AT III and routine coagulation tests were within the normal limits.In her family two other members showed the same defect. All the affected members had venous thrombotic manifestations, two of them at a relatively young age. No other risk factors for thrombotic episodes were present in the family members. The patient reported was treated with ASA and dipyridamole and so far there were no relapses.

scholarly journals Deficiency of the natural anticoagulant proteins in women with pregnancy related venous thromboembolism

2009 ◽  
Vol 62 (1-2) ◽  
pp. 53-62 ◽  
Author(s):  
Gorana Mitic ◽  
Ljubica Povazan ◽  
Radmila Lazic ◽  
Dragan Spasic ◽  
Milana Maticki-Sekulic
Keyword(s):  
Venous Thromboembolism ◽  
Protein C ◽  
Protein S ◽  
Single Woman ◽  
Control Group ◽  
Protein S Deficiency ◽  
Clotting Factors ◽  
Protein C Deficiency ◽  
S Deficiency ◽  
Increased Risk

Inherited thrombophilia can be defined as a predisposition to thrombosis caused by heritable defects, such as mutations in genes encoding the natural anticoagulants or clotting factors. Pregnancy related risk of VTE is sixfold increased comparing to non pregnant age matched women. Pregnancy is an independent risk factor for the development of venous thromboembolism and this risk is further increased by the presence of thrombophilia. Aim of the study: The aim of the study was to evaluate the association between deficiency of natural anticoagulants: antithrombin, protein C and protein S and pregnancy related thromboembolism. We have determined the activities of antithrombin, proten C and protein S in 74 women with pregnancy related thrombosis and in 45 healthy women who had at least two uncomplicated pregnancies. Among the women with the history of venous thromboembolism antithrombin deficiency was found in 4 (5.4%), protein C deficiency in 2 (2.7%) and protein S deficiency in 5 (6.76%). The total of 11 (14.6%) women was found to be deficient. Not a single woman in the control group was found to be deficient in natural anticoagulants. Deficiencies of coagulation inhibitors are associated with an increased risk of venous thrombosis during pregnancy and puerperium (p= 0.006). Antithrombin, protein C and protein S deficient women are at higher risk of developing venous thromboembolism during antepartal period (p= 0.0097). Prophylactic treatment with heparin should be recommended from the very beginning of the following pregnancy in women with antithrombin, protein C or protein S deficiency.

Co-inheritance of the 20210A Allele of the Prothrombin Gene Increases the Risk of Thrombosis in Subjects with Familial Thrombophilia

1997 ◽  
Vol 78 (06) ◽  
pp. 1426-1429 ◽  
Author(s):  
M Makris ◽  
F E Preston ◽  
N J Beauchamp ◽  
P C Cooper ◽  
M E Daly ◽  
...  
Keyword(s):  
Venous Thromboembolism ◽  
Protein C ◽  
Factor V Leiden ◽  
Protein S ◽  
Factor V ◽  
Protein C Deficiency ◽  
Antithrombin Deficiency ◽  
Control Subjects ◽  
Increased Risk ◽  
Venous Thromboembolic

SummaryThe presence of the 20210A allele of the prothrombin (PT) gene has recently been shown to be a risk factor for venous thromboembolism. This is probably mediated through increased plasma prothrombin levels. The aim of this study was to compare the prevalence of the prothrombin 20210A allele in control subjects and in subjects with recognised thrombophilia and to establish whether the additional inheritance of the PT 20210A allele is associated with an increased risk of venous thromboembolism. 101 subjects with a history of venous thromboembolism and diagnosed as having either factor V Leiden (R506Q) or heritable deficiencies of protein C, protein S or antithrombin were studied. The prevalence of the PT 20210A allele in this group was compared with the results obtained for 150 control subjects. In addition, the relationships were examined between genetic status and the number of documented thromboembolic episodes, and between plasma prothrombin levels and possession of the PT 20210A allele. 8 (7.9%) of the 101 patients were also heterozygous for the PT 20210A allele. This compares with 0.7% in the control subjects (p = 0.005). After exclusion of patients on warfarin, the mean plasma prothrombin of 113 subjects without 20210A was 1.09 U/ml, as compared with 1.32 U/ml in 8 with the allele (p = 0.0002). Among the 101 patients with either factor V Leiden, protein S deficiency, protein C deficiency or antithrombin deficiency, the age adjusted mean (SD) number of venous thromboembolic episodes at diagnosis was 3.7 (1.5) in those with the PT 20210A allele, as compared with 1.9 (1.1) in those without (p = 0.0001). We have demonstrated that the prevalence of the PT 20210A allele is significantly greater in subjects with venous thrombosis and characterised heritable thrombophilia than in normal control subjects and that the additional inheritance of PT 20210A is associated with an increased risk of venous thromboembolism. We have also confirmed that plasma prothrombin levels are significantly greater in subjects possessing the PT 20210A compared with those who do not.

The Frequency of Type I Heterozygous Protein S and Protein C Deficiency in 141 Unrelated Young Patients with Venous Thrombosis

1988 ◽  
Vol 59 (01) ◽  
pp. 018-022 ◽  
Author(s):  
C L Gladson ◽  
I Scharrer ◽  
V Hach ◽  
K H Beck ◽  
J H Griffin
Keyword(s):  
Venous Thrombosis ◽  
Protein C ◽  
Antithrombin Iii ◽  
Young Patients ◽  
Protein S ◽  
Type I ◽  
Protein S Deficiency ◽  
Protein C Deficiency ◽  
Low Protein ◽  
S Deficiency

SummaryThe frequency of heterozygous protein C and protein S deficiency, detected by measuring total plasma antigen, in a group (n = 141) of young unrelated patients (<45 years old) with venous thrombotic disease was studied and compared to that of antithrombin III, fibrinogen, and plasminogen deficiencies. Among 91 patients not receiving oral anticoagulants, six had low protein S antigen levels and one had a low protein C antigen level. Among 50 patients receiving oral anticoagulant therapy, abnormally low ratios of protein S or C to other vitamin K-dependent factors were presented by one patient for protein S and five for protein C. Thus, heterozygous Type I protein S deficiency appeared in seven of 141 patients (5%) and heterozygous Type I protein C deficiency in six of 141 patients (4%). Eleven of thirteen deficient patients had recurrent venous thrombosis. In this group of 141 patients, 1% had an identifiable fibrinogen abnormality, 2% a plasminogen abnormality, and 3% an antithrombin III deficiency. Thus, among the known plasma protein deficiencies associated with venous thrombosis, protein S and protein C. deficiencies (9%) emerge as the leading identifiable associated abnormalities.

Elevated Levels of Prothrombin Activation Fragment 1+2 in Plasma from Patients with Heterozygous Arg506 to Gin Mutation in the Factor V Gene (APC-Resistance) and/or Inherited Protein S Deficiency

1996 ◽  
Vol 75 (02) ◽  
pp. 270-274 ◽  
Author(s):  
Benget Zöller ◽  
Johan Holm ◽  
Peter Svensson ◽  
Björn Dahlbäck
Keyword(s):  
Plasma Concentration ◽  
Protein C ◽  
Protein S ◽  
Factor V ◽  
Protein S Deficiency ◽  
Apc Resistance ◽  
S Deficiency ◽  
Increased Risk ◽  
Factor V Gene ◽  
V Gene

SummaryInherited resistance to activated protein C (APC-resistance), caused by a point mutation in the factor V gene leading to replacement of Arg(R)506 with a Gin (Q), and inherited protein S deficiency are associated with functional impairment of the protein C anticoagulant system, yielding lifelong hypercoagulability and increased risk of thrombosis. APC-resistance is often an additional genetic risk factor in thrombosis-prone protein S deficient families. The plasma concentration of prothrombin fragment 1+2 (F1+2), which is a marker of hyper-coagulable states, was measured in 205 members of 34 thrombosis-prone families harbouring the Arg506 to Gin mutation (APC-resistance) and/or inherited protein S deficiency. The plasma concentration of F1+2 was significantly higher both in 38 individuals carrying the FV:Q506 mutation in heterozygous state (1.7 ± 0.7 nM; mean ± SD) and in 48 protein S deficient cases (1.9 ± 0.9 nM), than in 100 unaffected relatives (1.3 ±0.5 nM). Warfarin therapy decreased the F1+2 levels, even in those four patients who had combined defects (0.5 ± 0.3 nM). Our results agree with the hypothesis that individuals with APC-resistance or protein S deficiency have an imbalance between pro- and anti-coagulant forces leading to increased thrombin generation and a hypercoagulable state.

scholarly journals Probable Dysfunctional Protein S in a Patient with Congenital Heterozygous Protein C Deficiency

1991 ◽  
Vol 2 (6) ◽  
pp. 518-523 ◽  
Author(s):  
Toshiyuki SAKATA ◽  
Nobuko TSUSHIMA ◽  
Kaoru HATANAKA ◽  
Takashi MORISHITA ◽  
Hiroyuki HATSUYAMA ◽  
...  
Keyword(s):  
Protein C ◽  
Protein S ◽  
Protein C Deficiency ◽  
Heterozygous Protein C Deficiency

PROTEIN C, PROTEIN S AND THE FIBRINOLYTIC SYSTEM IN PATIENTS WITH A HISTORY OF THROMBOSIS

1987 ◽  
Author(s):  
J Malm ◽  
M Laurell ◽  
I M Nilsson ◽  
B Dahlbäck
Keyword(s):  
Plasminogen Activator ◽  
Fibrinolytic Activity ◽  
Protein C ◽  
Protein S ◽  
Protein S Deficiency ◽  
Functional Protein ◽  
Protein C Deficiency ◽  
S Deficiency ◽  
Tissue Plasminogen ◽  
History Of

Consecutive patients with a history of thrombo-embolic disease (n = 241, 109 males, 132 females, mean age 46 y), referred to the Coagulation Laboratory during an 18 month period, were analysed for defects in their coagulation and fibrinolytic systems. The diagnosis of thrombosis had been verified with phlebography and that of pulmonary embolus with scintigraphy or angiography. Retinal venous thrombosis was found in 15 of the patients. In 15 cases the thrombotic episodes occurred postoperatively, in 15 during pregnancy, in 12 during the postpartum period and in 20 during use of oral contraceptives. In the remaining cases no clinical riskfactors were identified.The concentration of protein C zymogen was measured with an immunoradiometric assay. Functional protein C was determined with a clotting inhibition assay. Protein C deficiency was found in 8 cases. Two of these had a functional protein C deficiency with normal zymogen levels. The concentration of total, as well as free (not in complex with C4b-binding protein), protein S was determined with a radioimmunoassay. Two cases of protein S deficiency were detected. Three patients with antithrombin III deficiency and two with plasminogen deficiency were found.The fibrinolytic activity after venous occlusion was analysed in 216 patients. Decreased levels were found in 32 %. The concentration of tissue plasminogen activator inhibitor (PAI) was measured in 110 patients and found to be increased in 65 % of the cases. In 99 patients both the fibrinolytic activity and the PAI concentration were measured. A combination of decreased fibrinolytic activity and increased levels of PAI was found in 44 cases. The concentration of tissue plasminogen activator antigen was decreased in 22 % of 105 cases analysed.Thus, in this material of patients with thrombo-embolic disease, abnormalities were found in 47 %. Defects in the fibrinolytic system were the most common findings. Protein C or protein S deficiency was diagnosed in less than 5 % of the cases.

THROMBOPHILIA:ITS CAUSES AND A ROUGH ESTIMATE OF ITS PREVALENCE

1987 ◽  
Author(s):  
E Briët ◽  
L Engesser ◽  
E J P Brommer ◽  
A W Broekmans ◽  
R M Bertina
Keyword(s):  
Plasminogen Activator ◽  
Protein C ◽  
Antithrombin Iii ◽  
Plasminogen Activator Inhibitor ◽  
Protein S ◽  
Factor Vii ◽  
Type I ◽  
Factor V ◽  
Protein C Deficiency ◽  
Familial Cases

Idiopathic venous thrombosis and embolism have gained widespread interest since the discovery that, deficiencies of antithrombin III, protein C, and protein S are associated with familial venous thrombophilia. The purpose of our study was to obtain an estimate of the prevalence of this syndrome and to establish the etiology in as many cases as possible.We collaborated with specialists from 37 Dutch hospitals, covering about 10% of the Dutch population. A history as well as blood samples were obtained from 113 unrelated cases with familial thrombophilia and from 90 isolated cases. Assuming that each proband in a family with thrombophilia has an average of four affected relatives, a rough estimate of the prevalence of familial thrombophilia in The Netherlands is 40 cases per 100.000. The prevalence of non-familial thrombophilia is probably lower.In 35 out of the 113 familial cases we established a diagnosis of hereditary antithrombin III deficiency (n=5), protein C deficiency (type I: n=9; type II: n=4), protein S deficiency (n=15) and dysfibrinogenemia (n=2). In 36 cases we found no abnormality at all and in the remaining 42 cases abnormalities were found in one or more of the following: heparin cofactor II, factor V, factor VII, factor VIII, von Willebrand factor, plasminogen, tissue plasminogen activator, plasminogen activator inhibitor, alpha 2 antiplasmin and histidine rich glycoprotein. In most of these cases, however, the hereditary nature of the abnormalities could not be demonstrated and the causal relationships remain to be established.In the 90 isolated cases, we diagnosed hereditary deficiencies of anti thrombin III, protein C and protein S each in one case and a lupus anticoagulant in two cases. In 54 cases no abnormality was found and in the remaining 31 cases various abnormalities were found in one or more of the proteins mentioned above.We conclude that the syndrome of thrombophilia is not rare but its true prevalence needs to be established by more rigorous means. An etiological diagnosis can be made with confidence in only one third of the familial cases and in less than 10 percent of the isolated cases.

Risk of venous thromboembolism in relatives of symptomatic probands with thrombophilia: a systematic review

2003 ◽  
Vol 90 (07) ◽  
pp. 17-26 ◽  
Author(s):  
Nicole Langlois ◽  
Philip Wells
Keyword(s):  
Venous Thromboembolism ◽  
Relative Risk ◽  
Observational Studies ◽  
Protein C ◽  
Retrospective Studies ◽  
Factor V Leiden ◽  
Protein S ◽  
Clinical Equipoise ◽  
Factor V ◽  
Protein C Deficiency

SummaryClinical equipoise exists regarding whether relatives of individuals with venous thromboembolism (VTE) and thrombophilia should be screened for thrombophilia. There have been no systematic attempts to summarize studies that have assessed the incidence of VTE in relatives. The purpose of this review was to systematically identify and review observational studies with thrombophilic relatives and to summarize their findings with respect to their risk of VTE.We conducted a systematic literature review and included nine observational studies meeting a priori inclusion criteria. Potentially eligible studies evaluated VTE incidence in relatives of index patients (probands) with symptomatic thrombophilia. In the four prospective studies, the incidence of VTE for asymptomatic family members with factor V Leiden ranged from 0.58-0.67% per year, 1.0-2.5% for protein C deficiency, 0.7-2.2% for protein S deficiency, and 4% for antithrombin deficiency. About half of all VTEs occurred during well-known risk periods but incidence rates were decreased by use of prophylaxis. No deaths from pulmonary embolism or fatal hemorrhages from anticoagulants were reported. The incidence of VTE was generally lower in the retrospective studies. The pooled relative risk from four retrospective studies for factor V Leiden carriers was 3.69 (CI 2.27, 6.00) and from two studies the pooled relative risk for deficiencies of protein C, protein S, and antithrombin was 10.58 (CI 5.38, 20.81).In conclusion, the risk of VTE events in asymptomatic relatives is low, but this may be an underestimate. Anticoagulant prophylaxis during risk periods appears to be of benefit but further research in this area is required.

scholarly journals Protein C deficiency in a controlled series of unselected outpatients: an infrequent but clear risk factor for venous thrombosis (Leiden Thrombophilia Study) [see comments]

Blood ◽  
1995 ◽  
Vol 85 (10) ◽  
pp. 2756-2761 ◽  
Author(s):  
T Koster ◽  
FR Rosendaal ◽  
E Briet ◽  
FJ van der Meer ◽  
LP Colly ◽  
...  
Keyword(s):  
Relative Risk ◽  
Venous Thrombosis ◽  
Protein C ◽  
Protein S ◽  
Population Based ◽  
Repeated Measurements ◽  
Protein C Deficiency ◽  
Antithrombin Deficiency ◽  
Vein Thrombosis ◽  
Thrombosis Risk

A deficiency of protein C (PC), antithrombin, or protein S is strongly associated with deep-vein thrombosis in selected patients and their families. However, the strength of the association with venous thrombosis in the general population is unknown. This study was a population-based, patient-control study of 474 consecutive outpatients, aged less than 70 years, with a first, objectively diagnosed, episode of venous thrombosis and without an underlying malignant disease, and 474 healthy controls who matched for age and sex. Relative risks were estimated as matched odds ratios. Based on a single measurement, there were 22 (4.6%) patients with a PC deficiency (PC activity, less than 0.67 U/mL or PC antigen, less than 0.33 U/mL when using coumarins). Among the controls, the frequency was 1.5% (seven subjects). Thus, there is a threefold increase in risk of thrombosis in subjects with PC levels below 0.67 or 0.33 U/mL [matched odds ratio, 3.1; 95% confidence interval (CI), 1.4 to 7.0]. When a PC deficiency was based on two repeated measurements, the relative risk for thrombosis increased to 3.8 (95% CI, 1.3 to 10); when it was based on DNA-confirmation, the relative risk increased further to 6.5 (95% CI, 1.8 to 24). In addition, there was a gradient in thrombosis risk, according to PC levels. The results for antithrombin are similar to those for PC, although less pronounced (relative risk, 2.2; 95% CI, 1.0 to 4.7). We could not find an association between reduced total protein S (relative risk, 0.7; 95% CI, 0.3 to 1.8) or free protein S levels (relative risk, 1.6; 95% CI, 0.6 to 4.0) and thrombosis risk. Although not very frequent, PC and antithrombin deficiency are clearly associated with an increase in thrombosis risk.

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