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Results for “hypercoagulable state”

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PubMed1990

A hypercoagulable state follows orthotopic liver transplantation.

Orthotopic liver transplantation may be associated during the postoperative period with hepatic artery thrombosis, a catastrophic occurrence generally necessitating emergency retransplantation. To assess the contribution of the coagulation mechanism to this complication, the levels of procoagulant and anticoagulant proteins were followed in 41 liver transplant patients during the first 10 postoperative days. The mean activities of all procoagulant factors reach normal values on day 1 except for factors V and VII, which achieve normal activity by day 3. Supernormal levels of factor VIII activity and antigen are noted (peak values on day 5 of 334% +/- 113% and 481% +/- 260%, respectively). The anticoagulant proteins show delayed recovery, with deficient antithrombin III levels seen in 81% of patients on day 3 and 57% on day 5. Similarly, proteins C and S are subnormal in 24% and 21%, respectively on day 3, and 20% and 10%, respectively, on day 5. During this period, elevated levels of thrombin/antithrombin complexes are encountered, reflecting in vivo activation of the coagulation mechanism. Activated thrombin is, therefore, being generated at a time when a decrease in the major regulatory anticoagulant proteins exists. These data suggest an imbalance between the hemostatic and thrombotic mechanisms and indicate a sustained prothrombotic state that may contribute to the risk for hepatic artery thrombosis. Using a regimen of low-dose heparin and fresh frozen plasma infusion, no thromboses have been seen in 65 consecutive liver transplants.

Blood Coagulation Disorders↗
PubMed1995

Recurrent venous thrombosis as the presenting manifestation of acute lymphocytic leukemia: leukemic cell procoagulant activity is not responsible for the hypercoagulable state.

The association of cancer with clinical abnormalities of blood coagulation, including superficial thrombophlebitis, deep vein thrombosis (DVT), and disseminated intravascular coagulation (DIC) is well-known, particularly in patients with solid tumors and acute promyelocytic leukemia (APL). Less commonly appreciated is the potential for the development of venous thromboembolic disease (TED) in patients with acute lymphocytic leukemia (ALL). Multiple mechanisms have been implicated for the activation of coagulation in these patients, with an emphasis on the contribution made by the procoagulant properties of the tumor cells themselves. We present two cases of patients with pre-B cell ALL, both of whom developed recurrent TED as the presenting manifestation of their leukemia and/or heralding relapse. The blast cells from one of the patients were studied for the presence of procoagulant activity (PCA) and by Northern blot analysis for tissue factor (TF) messenger RNA (mRNA). Neither PCA nor TF mRNA could be identified in highly purified populations of the lymphoblast cells. We conclude that recurrent TED can be a manifestation of ALL and that mechanisms other than the release of tumor cell procoagulants should be sought to explain the pathogenesis of thrombosis in some patients.

Adult↗
PubMed1996

The possible risk of lower-limb sclerotherapy causing an extended hypercoagulable state.

The risk of thrombosis after lower-extremity sclerotherapy is still an unresolved issue. This study was conducted to investigate the influence of sclerotherapy on coagulation and fibrinolysis by examining 20 patients who underwent surgical procedures, 10 of whom were treated by surgery alone (control group), while the other 10 were given sclerotherapy using 1% hydroxypolyaetoxydodecan as polidocanol (sclerotherapy group). Sex, age, and severity of disease was comparable between the two groups. No significant difference was found in the transient elevation of acute phase proteins, C-reactive protein (CRP), or fibrinogen. Thrombin antithrombin III complex (TAT), a marker of coagulation, transiently increased following treatment. In the control group, TAT peaked 3 days after treatment, whereas in the sclerotherapy group the elevation was prolonged, peaking 7 days after treatment. Elevation of the markers of fibrinolysis, plasmin plasmin inhibitor complex (PIC) and fibrin degradation products (FDP), was slower than that of TAT, peaking 7 days after treatment in both groups, the plasma PIC being significantly enhanced 7 days after treatment in the sclerotherapy group. A significant decrease in the platelet count was observed 3 days after treatment in the sclerotherapy group. These results suggest that sclerotherapy may enhance coagulation or fibrinolysis after surgical procedures.

Adult↗
PubMed1998

Study on the hypercoagulable state in patients with angina and myocardial infarction.

The molecular markers of platelet activation, coagulation and fibrinolysis were detected in 60 cases of coronary heart disease (CHD), including 15 cases of stable angina (SA), 21 cases of unstable angina (UA) and 24 cases of acute myocardial infarction (AMI). The results showed that the platelet granule membrane protein 140 (GMP-140) level increased obviously in CHD groups compared with normal control, suggesting that platelet activation existed in CHD. Prothrombin fragment F1 + 2 and fibrinopeptide A (FPA) were examined to observe the activation of coagulation. No difference was found between SA group and normal controls, while their levels in both UA group and AMI group were significantly higher than in normal control and SA group (both P < 0.05). D-D dimer and alpha 2-plasma inhibitor (alpha 2-PI) were detected to observe fibrinolytic state. The results showed that no difference existed between SA group and normal controls, while both D-D dimer and alpha 2-PI in UA group and AMI group were significantly elevated than those in SA group and normal controls (P < 0.05).

Angina Pectoris↗
PubMed1999

Hypercoagulable state mutation analysis in white patients with early first-trimester recurrent pregnancy loss.

OBJECTIVE: Antiphospholipid antibodies (APA) and other coagulation abnormalities have been associated with an increased risk of venous, arterial, and placental thrombosis and recurrent pregnancy loss (RPL). Factor V Leiden (a point mutation [1691G-->A] in the factor V gene), the prothrombin 20210G-->A mutation, and homozygosity for a common polymorphism in the methylene tetrahydrofolate reductase (MTHFR) gene (677C-->T) have been associated with arterial and venous thrombosis and arterial occlusive disease. We explored an association between these markers of thrombophilic states and RPL. DESIGN: Prospective case-control evaluation. SETTING: University-associated private practice. PATIENT(S): Fifty nonpregnant women with three or more pregnancy losses and 50 healthy, nonpregnant controls. INTERVENTION(S): None. MAIN OUTCOME MEASURE(S): Anticardiolipin and antiphosphatidylserine antibodies were detected in serum by ELISA. Polymerase chain reaction was performed to identify the factor V Leiden (1691G-->A) mutation, the thermobile MTHFR (677C-->T) mutation, and the prothrombin 20210G-->A mutation. RESULT(S): The following were identified by restriction fragment-linked polymorphism analyses: 1 (2%) factor V Leiden heterozygosity; 1 (2%) prothrombin 20210G-->A heterozygosity; and 4 (8%) thermolabile MTHFR homozygosity. None of these mutation frequencies in women with RPL were statistically significantly different from controls. CONCLUSION(S): These data suggest that factor V Leiden, thermolabile MTHFR (677C-->T), and prothrombin 20210G-->A are not found at an increased frequency in women with a history of early RPL.

Abortion, Habitual↗