Antithrombin, protein C or protein S deficiency (adjusted odds ratio [95%CI]: 15.60 [2.01-121]; p=0.009), hyperhomocysteinemia (HHCy; 3.22 [1.38-7.49]; p=0.007), high factor VIII (FVIII) levels (3.08 [1.20-7.89]; p=0.019), factor V Leiden (2.93 [0.97-8.86]; p=0.058) and the presence of at least one cardiovascular risk factor (1.79 [1.00-3.23]; p=0.050) were associated with an increased risk of branch RVO.
Frequencies of factor V Leiden and hyperhomocysteinaemia were not significantly different in patients and controls, nor were the other thrombophilic tests and some established cardiovascular risk factors, such as smoking, obesity or overweight and arterial hypertension.
Hyperinsulinemia, hyperandrogenemia, hypofibrinolysis, and hyperhomocysteinemia as well as APCR and factor V Leiden mutations are associated with RPL in patients with PCOS.
We evaluated 1,297 nonpregnant formerly preeclamptic women (6-12 months postpartum) for the presence of four risk profiles: circulatory risk profile (hypertension or latent hypertension [low plasma volume, increased vascular resistance, or both]; metabolic syndrome (World Health Organization criteria); thrombophilia (factor V Leiden, prothrombin mutation, or protein C or S deficiency); and hyperhomocysteinemia.
Some reports show a risk of thrombosis with the presence of factor V Leiden and hyperhomocysteinemia but these associations frequently disappear upon multivariate analysis.
The unadjusted odds ratio (OR) for sP-selectin >55.1 microg/L, representing the 95th percentile for controls, was 8.5 (95% CI, 3.7-23.3; P <0.001) and increased after adjustment for factor V Leiden, the prothrombin G20210A variant, increased factor VIII, and hyperhomocysteinemia (OR, 10.6; 95% CI, 4.1-31.2; P <0.001).
Both the meta-analyses of published studies and a large case-only study did not show evidence for interaction between factor V Leiden and hyperhomocysteinemia for risk of venous thrombosis.
The risk of ischemic stroke in oral contraceptive users was 13 times higher in women who were also carriers of factor V Leiden and 9 times higher in those who also had hyperhomocysteinemia.
We studied 65 patients with EHPVO, 500 with deep vein thrombosis (DVT) of the lower limbs, and 700 healthy controls referred for thrombophilia screening, including the search for gain-of-function mutations in genes encoding coagulation factor V (factor V Leiden) and prothrombin (prothrombin G20210A); antithrombin, protein C, and protein S deficiency; and hyperhomocysteinemia.
Although factor V Leiden is strongly associated with deep venous thrombosis, additional cofactors such as hyperhomocysteinemia may predispose to an increased risk of acute arterial thrombosis in areas of pre-existing peripheral arterial disease.
New, inherited - factor V Leiden (FVL) and prothrombin gene mutation (PTHRA20210) - and inherited/acquired - hyperhomocysteinemia (HHcy) - prothrombotic conditions have been detected recently.
Although case-control and perspective studies are available on hyperhomocysteinaemia and other gestational vascular complications the data are conflicting.Intervention studies have been carried out to prevent adverse obstetric outcomes in women with factor V Leiden or factor II A20210 mutations and previous adverse outcomes.
Cutaneous necrosis revealing the coexistence of an antiphospholipid syndrome with acquired protein S deficiency, factor V Leiden and hyperhomocysteinemia.
The results concerning the interaction between moderate hyperhomocysteinemia and inherited thrombophilic factors such as Factor V Leiden or the prothrombin G20210A mutation are contradictory.
Thrombophilic states such as factor V Leiden and hyperhomocysteinemia may also play a role in other gestational vascular complications, including intrauterine growth restriction, preeclampsia, and placental abruption.
An approximate estimate of 30-fold increased risk in carriers of both hyperhomocysteinaemia and factor V Leiden and 50-fold increased risk in carriers of both hyperhomocysteinaemia and prothrombin G20210A was calculated, suggesting a synergistic interaction between hyperhomocysteinaemia and such thrombophilic genotypes.
In addition, mild and moderate hyperhomocysteinaemia and Factor V Leiden (FVL; Arg506Gln) have recently been identified as thrombotic risk factors.FVL. which renders resistance to activated Protein C, is the most common inherited genetic risk factor for thrombosis with a high allelic frequency amongst Caucasians.
A recent report by Mandel et al (N Engl J Med 334:763, 1996) postulated factor V Leiden (FVL) to be an absolute prerequisite for the development of thromboembolism in patients with severe hyperhomocysteinemia.