Inhibitors of Coagulation, Atherosclerosis, and Arterial Thrombosis

Conard, J; Samama, M

doi:10.1055/s-2007-1003540

Cited by 15 publications

(7 citation statements)

References 14 publications

(17 reference statements)

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Our results show that AT III level was lower in women than in men before age 50; this gender difference was reversed after age 50. Others (10,12) have shown a similar low AT III value in women of reproductive age compared to men. A decrease in AT III with increasing age has been observed in men only by others ( 11,12).…”

Section: Pt(s)mentioning

confidence: 76%

“…Plasma levels of fibrinogen, factor VIle, and factor VIlle were associated with risk of cardiovascular diseases in several prospective studies (2,3). While it has been reported for a few Caucasian populations that values of plasma fibrinogen, factor VIle, and factor VIlle increase with age (4-9) and antithrombin III (AT III) value decreases with age (4,(10)(11)(12), the age ranges discussed in most of these studies are limited to middle ages. In addition, there is no such information available for Asian, to our knowledge.…”

Section: Introductionmentioning

confidence: 99%

See 1 more Smart Citation

Curvilinear Relations between Age and Hemostatic Parameters in Chinese

et al. 1994

View full text Add to dashboard Cite

SummaryThe role of hemostatic factors in the pathogenesis of cardiovascular disease has gained much attention recently. Information about hemostatic factors, and their age patterns is sparse for orientals. With the data collected in the Cardiovascular Disease Risk Factor Two-township Study in Taiwan, this study shows that, in general, the older the age, the stronger the tendency toward thrombosis. With advancing age, prothrombin time, activated partial thromboplastin time, and antithrom-bin-III level decreased steadily; but mean values of fibrinogen, factor VIIc, and factor VIIIc increased. Gender differences in the age patterns of the above factors are carefully described. Curvilinear relations between hemostatic factors and'age were demonstrated for adults aged 18 and above for all hemostatic factors studied. This curvilinearity should be taken into consideration when adjusting for the effect of age in data analysis to avoid residual confounding, particularly when the age range of the study subjects is wide.

show abstract

Section: Pt(s)mentioning

confidence: 76%

Section: Introductionmentioning

confidence: 99%

Curvilinear Relations between Age and Hemostatic Parameters in Chinese

et al. 1994

View full text Add to dashboard Cite

show abstract

“…Arterial thrombosis has not been found to be frequent in PC deficiency and is even less frequent in patients with AT or PS deficiency [57] (table 4). However, more recently, PS deficiency has been shown to increase the risk of arterial thrombosis, mainly in current smokers older than 50 years [58].…”

Section: Arterial Thrombosismentioning

confidence: 99%

Clinical Aspects and Laboratory Problems in Hereditary Thrombophilia

Samama

Gerotziafas²,

Conard³

et al. 1999

Pathophysiol Haemos Thromb

View full text Add to dashboard Cite

Hereditary thrombophilia is a multifactorial disease which is mono- or plurigenic and its clinical expression is associated with a heterogeneous expression. Factor V (FV) Leiden and FII gene mutations are more frequent than antithrombin, and protein C and S deficiencies. All thrombophilias are not the same. Heterozygous carriers of FV Leiden or FII gene mutation have a weaker risk of venous thrombosis. The mean age at the first episode is older in the former and higher rate of recurrences is observed in the latter. The cosegregation of mutations significantly increases the risk of thrombosis. Both mutations have a geographic and ethnic distribution in relation with a gene founder effect. Clinical expression consists of deep or superficial venous thrombosis with or without pulmonary embolism, thromboses at unusual sites (e.g. cerebral, portal, mesenteric) or with an increased incidence of fetal loss and abortion. A precipitating cause is present in more than 50% of patients. The risk pf arterial thromboses seems to be restricted to some protein S and FII gene mutations. Laboratory diagnosis strategy should be oriented by careful selection of patients and preanalytical variables should be considered. It is highly probable that other unindentified gene mutations are, at least partly, other causes of the heterogeneous expression of hereditary thrombophilia.

show abstract

“…In the first case (fibrinogen Poitiers), at least one functional abnormality of fibrinogen (a decreased binding to thrombin) may have contributed to an enhanced thrombotic tendency. It is more difficult to evaluate the responsibility of protein C deficiency, which is commonly associated with venous thrombosis (Griffin et al, 1981;Horellou et al, 1984: Broekmans, 1985: Marlar, 1985, but quite rarely with arterial thrombosis (Conard & Samama, 1986). However, in our patient, it is conceivable that a delay in the elimination of FV and FVIII activated during the clotting process, and a reduction of the enhancing effect of tPA (through the less efficient destruction of tPA inhibitor by protein C) may have increased the severity of thrombosis in diseased arteries.…”

Section: Discijssionmentioning

confidence: 99%

“…It has also been established that an interaction between protein C and tPA inhibitor is responsible for a profibrinolytic action (Sakata et al, 1985). Heterozygous hereditary protein C deficiency is associated with venous thrombosis (Broekmans, 1985) but only a few cases of arterial thrombosis have been reported (Conard & Samama, 1986).…”

mentioning

confidence: 99%

Association of inherited dysfibrinogenaemia and protein C deficiency in two unrelated families

et al. 1988

View full text Add to dashboard Cite

An inherited association of dysfibrinogenaemia and protein C deficiency was found in three members of the same family. The propositus was a 48-year-old man who suffered from severe and rapidly complicated atherosclerosis of the aorta and lower limbs arteries, which perhaps suggests that the association of these two molecular abnormalities may have enhanced the thrombotic process. The abnormal fibrinogen had a reduced ability to bind thrombin which may be thrombogenic. We found the same inherited association of dysfibrinogenaemia and protein C deficiency in a patient with venous thrombosis. The functional abnormality of the fibrinogen, which could have been responsible for thrombosis, was delayed proteolysis by plasmin. Not only fibrinogen, but also fibrin clots were resistant to plasmic degradation. These observations raise two questions: (1) Is the association of a protein C deficiency with a dysfibrinogenaemia fortuitous or the result of a common mechanism? (2) Is there a link between an increased thrombotic tendency and either both of the defects of haemostasis that we have found, or only one of them?

show abstract

Inhibitors of Coagulation, Atherosclerosis, and Arterial Thrombosis

Cited by 15 publications

References 14 publications

Curvilinear Relations between Age and Hemostatic Parameters in Chinese

Curvilinear Relations between Age and Hemostatic Parameters in Chinese

Clinical Aspects and Laboratory Problems in Hereditary Thrombophilia

Association of inherited dysfibrinogenaemia and protein C deficiency in two unrelated families

Contact Info

Product

Resources

About