AnxA1 administration regulated platelet function directly (eg, via reducing thromboxane B<sub>2</sub> and modulating phosphatidylserine expression) to promote cerebral protection post-I/RI and act as an effective preventative strategy for stroke by reducing platelet activation, aggregate formation, and cerebral thrombosis, a prerequisite for ischemic stroke.
Over-expression of A2 is seen in acute promyelocytic leukemia during the early hemorrhagic phase, while high titer antibodies to A2, as in antiphospholipid syndrome or cerebral venous thrombosis, are associated with thrombosis.
Our study suggested that both apoE epsilon3/epsilon4 genotype and epsilon4 carriers were risk factors for cerebral thrombosis in cortical artery region, whereas epsilon 2 carrier was a risk factor for hemorrhagic stroke in the elderly.
Therefore, the bright sinus appearance had higher sensitivities for identifying cerebral venous thrombosis than the susceptibility vessel sign, empty delta sign, and atypical distribution against arterial territory (with differences of 15%; P = .500, 46%; P = .031, and 50%; P = .031, respectively).Bright sinus appearance on ASL-PWI can provide important diagnostic clue for identifying cerebral venous thrombosis.
To our knowledge, malignant hyperthermia and cerebral venous thrombosis have not been reported in the literature in patients with COL4A1 mutations after surgery.
The study aimed at evaluating the contribution of genetic variations in the drug metabolizing enzyme, CYP2C9, and the influence of co-medication with the antiepileptic drug, phenytoin, to variability in acenocoumarol response, in patients with cerebral venous thrombosis (CVT).
Genetic thrombophilic conditions such as those associated with Factor V Leiden (FVL) and the prothrombin mutant (PT G20210A) have been identified as risk factors for cerebral venous thrombosis (CVT).
ProthrombinG20210A was found in 103/868 of the patients with cerebral venous thrombosis and 105/3999 of the healthy controls [random effects pooled OR 5.838, 95% CI 3.96 to 8.58; I217.9%].
However, the use of DOACs in unusual VTE, including cerebral venous thrombosis (CVT) and splanchnic venous thrombosis (SVT), and in patients with biological thrombophilia including minor thrombophilia (Factor V Leiden and prothrombinG20210A), major innate thrombophilia (protein C and S deficiency, and antithrombin) and major acquired thrombophilia (antiphospholipid syndrome [APS]), remains controversial due to the paucity of available data.
The 20210A allele of the prothrombin gene in association with other prothrombic factors may increase the risk of cerebral venous thrombosis, but case-control studies will be necessary to clarify these associations.
We screened 56 patients with cerebral vein thrombosis and 184 age- and sex-matched apparently healthy controls for prothrombin (factor II, FII) G20210A and factor V Leiden polymorphisms; protein S, protein C, and antithrombin deficiency; anticardiolipin antibodies; hyperhomocysteinaemia and other putative risk factors.