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PubMed2004

Risk of venous thromboembolic disease associated with hormonal contraceptives and hormone replacement therapy: a clinical review.

Venous thromboembolic events (VTEs) represent a serious complication related to hormonal contraception and hormone replacement therapy (HRT). Evidence on hormonal contraceptive- and HRT-related VTEs is derived almost exclusively from observational studies and points to a 2- to 6-fold increased relative risk of VTEs with either therapy. Oral contraceptive pills that contain third-generation progestins (desogestrel or gestodene) seem to be associated with greater VTE risk than those that contain levonorgestrel. Oral contraceptive pill use and HRT are associated with exponentially higher VTE relative risks when used by women who carry an inherited hypercoagulable state. The indication of a lower or a lack of VTE risk associated with the use of progestin-only contraceptives and with transdermal HRT suggests that these therapies may be safer than combination oral contraceptive pills and oral HRT for women in whom oral estrogen therapy is considered contraindicated. Data that support such safety advantages are limited and should be interpreted with caution.

Contraceptives, Oral, Hormonal↗
PubMed2004

Patent foramen ovale in cryptogenic stroke: current understanding and management options.

There is increasing interest in the association between patent foramen ovale (PFO) and documented stroke of unknown cause, commonly referred to as cryptogenic stroke. We reviewed the literature and, on the basis of the available data, designed a diagnostic and treatment algorithm for patients with PFO and cryptogenic stroke. Patent foramen ovale is relatively common in the general population, but its prevalence is higher in patients with cryptogenic stroke. Importantly, paradoxical embolism through a PFO should be strongly considered in young patients with cryptogenic stroke. There is no consensus on the optimal management strategy, but treatment options include antiplatelet agents, warfarin sodium, percutaneous device closure, and surgical closure. High-risk features in the patient's history (ie, temporal association between Valsalva-inducing maneuvers and stroke, coexisting hypercoagulable state, recurrent strokes, and PFO with large opening, large right-to-left shunt, or right-to-left shunting at rest, and a coexisting atrial septal aneurysm) should prompt PFO closure.

Adult↗
PubMed1997

Stroke associated with cardiac surgery. Determinants, timing, and stroke subtypes.

OBJECTIVE: To determine the nature of strokes complicating cardiac surgery. DESIGN: A medical record review was undertaken of all patients who underwent cardiac surgery (either coronary bypass, valvular surgery, or both) between January 1990 and July 1995. Univariate and multivariate analyses were done using odds ratios (ORs) and logistic regression. RESULTS: A total of 2211 patients underwent cardiac surgery. A total of 44 patients (2%) had postoperative strokes. They were compared with 104 surgical controls. Univariate analysis revealed that the patients with stroke were significantly older and had significantly higher rates of transient ischemic attack, congestive heart failure, and peripheral vascular disease by history. A multivariate logistic regression revealed the significant variables associated with stroke were congestive heart failure (OR, 6.8) and transient ischemic attack (OR, 1.2). Analyses of surgical variables revealed that bypass pump time of more than 120 minutes (OR, 1.40) was the only significant predictor. The majority of strokes (61%) had occurred by postoperative day 2, but 39% occurred between postoperative days 3 to 9. Hemispheric syndromes occurred in 70%, brain stem and cerebellar syndromes in 14%, and lacunar syndromes in 16%. Computed tomographic scans revealed that 29 patients had new infarcts, of which 20 (69%) were territorial, 5 (17%) were small deep, and 4 (14%) were border zone. Hemorrhagic infarction was found in 2 cases (5%). One patient (2.5%) had a cardiorespiratory arrest while undergoing computed tomography. Discharge disposition was good in 88% of patients with stroke (12% with poor outcomes) vs 97% of controls with good outcomes (3% with poor outcomes) (P = .04). CONCLUSIONS: Strokes may be delayed following cardiac surgery perhaps because of ongoing risk of embolism or a hypercoagulable state. A surprisingly high proportion of patients have lacunar syndromes or small-deep infarcts shown on computed tomography. Early computed tomographic imaging may be useful to exclude hemorrhage if anticoagulation is considered, but is not without risk in these potentially unstable patients. Greater understanding of risk factors for stroke, timing, and subtypes may ultimately allow identification of patients at particularly high risk for perioperative stroke.

Aged↗
PubMed1999

Coagulation activation in patients with Binswanger disease.

BACKGROUND: A hypercoagulable state is often associated with an acute stroke in cerebrovascular disease (CVD). However, in Binswanger disease (BD), no information is available on the coagulation-fibrinolysis pathway except for the presence of high plasma fibrinogen levels. OBJECTIVE: To determine the association of BD and coagulation-fibrinolysis pathway activation. PATIENTS AND METHODS: We examined the levels of fibrinogen, thrombin-antithrombin complex, prothrombin fragment(1+2), and cross-linked D-dimer in 17 patients with BD, 24 neurologic patients without CVD, and 26 patients with lacunar infarction in either the acute or chronic stage. RESULTS: As compared with the non-CVD and lacunar infarction groups, the patients with BD had significantly elevated levels of thrombin-antithrombin complex (P<.001), prothrombin fragment(1+2) (P<.05), and cross-linked D-dimer (P<.01). There was also a significant increase in fibrinogen levels compared with the non-CVD group (P<.05). In the BD group, 8 patients in stable condition (ie, those without obvious neurologic deficits in the past 3 months) showed normal levels or a mild increase in their fibrinogen, thrombin-antithrombin complex, prothrombin fragment(1+2), or cross-linked D-dimer levels. In contrast, 9 patients with BD with a subacute aggravation of their focal or subcortical cerebral functions (deteriorating group) showed a significant increase in their thrombin-antithrombin complex levels compared with the stable patients (P<.01). Similarly, the fibrinogen, prothrombin fragment(1+2), and cross-linked D-dimer levels were elevated in the deteriorating patients, but this trend did not reach statistical significance. CONCLUSIONS: These results indicate that the coagulation-fibrinolysis pathway is activated in patients with BD with a subacute aggravation. Coagulation activation may result in the formation of microthrombi and microcirculatory disturbances in the brains of these patients, and thus promote further biological and neurologic insults.

Aged↗
PubMed1976

Platelet function, blood coagulability, and fibrinolysis in patients with low tension glaucoma.

Platelet function in vitro and in vivo and certain measurements of blood coagulability and fibrinolysis were examined in 12 patients with low tension glaucoma and the results were compared with those obtained in 12 normal subjects matched for age, race, and sex. The data obtained seem to indicate that patients with low tension glaucoma cannot be readily distinguished from individuals of similar age and sex not afflicted with this disorder by measuring these variables. Thus, a "hypercoagulable state," ie, a thrombotic tendency, does not appear to be of major importance in the pathogenesis of this disorder.

Aged↗
PubMed1976

Recurrent arterial thrombosis in nephrosis.

Recurrent arterial thrombosis without inciting trauma occurred in an 8-year-old boy with the nephrotic syndrome. Thrombosis of the left femoral artery was successfully managed by early thrombectomy and postoperative anticoagulation therapy, but the right leg finally had to be amputated. The development of hypovolemia in the nephrotic child receiving long-term steroid therapy apparently increases the tendency to a hypercoagulable state.

Adrenal Cortex Hormones↗
PubMed2000

Multiple arterial thromboembolisms in a patient with the 20210 A prothrombin gene mutation.

The most recently characterized genetic defect contributing to venous thrombophilia is the 20210 A prothrombin gene mutation. We describe a patient with this defect who had arterial thrombosis resulting in considerable mesenteric ischemia. Several environmental factors, which might otherwise be considered of low thrombotic risk, may also have contributed to her condition. The recognition of the potential for novel presentations of hypercoagulable states may contribute to a reduction in the morbidity associated with acute mesenteric ischemia.

Female↗
PubMed1987

Pylethrombosis. Serendipitous radiologic diagnosis.

Pylethrombosis is thrombosis of the portal vein or any of its branches. Five cases have been serendipitously detected, four by computed tomography and one by ultrasonography. Two patients had abdominal sepsis. A third patient had apparent acute cholecystitis with choledocholithiasis. The last two patients had a hypercoagulable state, mesenteric venous thrombosis, and enteric infarction that required resection. The newer diagnostic modalities of computed tomography and ultrasound may document unsuspected pylethrombosis. Surgery may be required because of signs of peritonitis, enteric ischemia, or unresolved sepsis. Anticoagulation is indicated for acute thrombosis of the portal or superior mesenteric veins to prevent further extension and enteric ischemia.

Adult↗
PubMed1988

Protein C deficiency. A cause of unusual or unexplained thrombosis.

Familial hypercoagulable states are a collection of syndromes characterized by an inherited deficiency of various proteins involved in the control of coagulation and include antithrombin III, plasminogen, protein C, and protein S. Affected patients usually develop venous thrombosis as adults. During a 15-month interval, we identified five patients with venous thrombosis accompanied by protein C deficiency. Four patients presented with deep venous thrombosis, which was recurrent in two, and one patient developed mesenteric venous thrombosis. The kindred of this last patient suggested an autosomal dominant genetic transmission of protein C deficiency. Patients' ages at the time of diagnosis of disease ranged from 28 to 41 years. All patients had low levels of protein C (range, 34 to 67 U/dL; normal, 70 to 130 U/dL). All patients were treated with heparin sodium immediately and then given long-term oral anticoagulation therapy with warfarin sodium. Protein C deficiency is a predisposing factor to the development of venous thrombosis that has only recently been recognized. Treatment of symptomatic protein C deficiency requires short-term heparin therapy followed by long-term oral anticoagulation therapy with warfarin. Oral anticoagulation treatment must be initiated slowly with no loading dose to avoid warfarin-associated skin necrosis. Patients with unexplained or unusual thrombosis, especially if it occurs at an early age, and patients with recurrent episodes of lower limb venous thrombosis should have their protein C levels measured. If a deficiency is documented, long-term warfarin anticoagulation therapy is recommended.

Adult↗
PubMed1996

Peroneal bypass is equivalent to inframalleolar bypass for ischemic pedal gangrene.

OBJECTIVE: To determine if peroneal bypass is a suitable alternative to inframalleolar bypass in patients with ischemic pedal gangrene. DESIGN: Review of a prospectively acquired vascular registry. SETTING: University practice limited to vascular surgery. PATIENTS: Patients with chronic lower-extremity ischemia and pedal gangrene evaluated between 1985 and 1995 in whom the only options for arterial reconstruction were bypass to the peroneal or an inframalleolar artery. INTERVENTIONS: Peroneal or inframalleolar reverse vein bypass. MAIN OUTCOME MEASURES: Time to healing and lifetable analyses of survival, primary patency, and limb salvage. RESULTS: Eighty-three peroneal and 46 pedal bypasses were performed for ischemic foot gangrene. The groups were equivalent for sex, diabetes mellitus, heart disease, hypertension, renal failure, hypercoagulable states, previous ipsilateral bypass, smoking, and preoperative ankle-brachial indices. Patients with inframalleolar bypass were younger than patients with peroneal bypass (63.9 vs 71.6 years, P = .005) and had higher postoperative ankle-brachial indices (1.02 vs 0.91, P = .004). However, 3-year survival rates (69.1% inframalleolar vs 60.0% peroneal, P = .35), limb salvage rates at 2 years (70.3% vs 85.8%, P = .10), and time to wound healing (19.7 vs 21.6 weeks, P = .66) were equivalent. CONCLUSION: Peroneal and inframalleolar bypass for ischemic pedal gangrene have equivalent intermediate-term survival, limb salvage, and wound healing. Surgeons should not feel obliged to perform inframalleolar bypass for pedal gangrene if peroneal bypass is possible.

Aged↗
PubMed1997

Factor V Leiden is not responsible for stroke in patients with sickling disorders and is uncommon in African Americans with sickle cell disease.

Cerebrovascular accidents in patients with sickle cell anemia are among the most devastating complications of the disease. It has recently been demonstrated that some patients have a hypercoagulable state on the basis of the presence of an abnormal factor V molecule, factor V Leiden. We undertook this study to evaluate the presence of factor V Leiden in sickle cell patients with stroke. Eighty-two patients with either Hgb SS, Hgb SC, or Hgb S(beta+)-thalassemia comprised the study population. Of the 82 patients in the study, 19 of them had a history of stroke. In our study population, none of the stroke patients possessed the factor V Leiden mutation. One of the non-stroke patients was a heterozygote for the mutation (P = 1.00). The overall frequency of the factor V Leiden allele in our population is 0.6%. The estimated prevalence for this mutation is reportedly between 3 and 7% in Caucasian populations. We conclude that the gene frequency for factor V Leiden is less common in Africa Americans with sickle cell disease. Furthermore, factor V Leiden does not appear to be responsible for the development of stroke in sickle cell patients.

Adolescent↗
PubMed1997

Fibrinolysis, inhibitors of blood coagulation, and monocyte derived coagulant activity in acute malaria.

Different parameters of fibrinolytic systems like t-PA, PAI, D-dimer, and inhibitors of blood coagulation, i.e., protein C (PC), protein S(PS), and antithrombin III (AT-III), have been studied in cases of acute malaria due to Plasmodium falciparum and plasmodium vivax infection, and these patients were followed up. It was observed that the plasma PAI-1 was very high in cases of P. falciparum malaria infection as compared to normal controls and P. vivax infection. The changes in complicated cases of P. falciparum were remarkable as compared to uncomplicated ones. The PC, PS, and AT-III levels were also low in P. falciparum, particularly so in complicated cases, and were normal in P. vivax infection. The factor VIII R:Ag levels were invariably high in acute malaria. On follow-up of some of these cases the values came back to normal after the antiparasite treatment. The monocyte procoagulant activity was found to be significantly higher in P. falciparum infection as compared to that of P. vivax infection. All these findings therefore contribute towards the production of a hypercoagulable state in P. falciparum infection and partly explain the complications of P. falciparum infection like cerebral malaria.

Antithrombin III↗
PubMed1997

Enhanced generation of monocyte tissue factor and increased plasma prothrombin fragment1+2 levels in patients with polycythemia vera: mechanism of activation of blood coagulation.

Polycythemia vera (PV) is associated with a high incidence of thrombosis. The association of apparent and secondary polycythemia with thrombosis is not clear. It was suggested that activation of the coagulation system contributes to thrombus formation in PV. However, the mechanism of activation is unknown. Monocytes generate a potent tissue factor (TF) upon stimulation with various substances, which is involved in thrombus formation in various disorders. Therefore, we studied the possibility that the factor is involved in the activation of coagulation and thrombus formation also in PV. Unstimulated peripheral blood mononuclear cells (PBMC) from each of the different types of polycythemia expressed weak TF activity (2 U) and antigen (41.4 to 52.9 pg/ml), which were similar to normal controls. Following stimulation with endotoxin, PBMC from normal controls and from apparent and secondary polycythemia showed a 3.9- to 4.5-fold increase in TF, while cells from PV showed a 21-fold increase (P<0.001). Similar levels were generated by PBMC after treatment of PV and at the spent phase. TF was generated by monocytes but not by lymphocytes. Plasma prothrombin fragment1+2 (F1+2) levels, assayed at the same time, were significantly higher in PV (2.46 nm) compared to normals and apparent and secondary polycythemia (0.22 to 0.32 nm), and were in a significant correlation with monocyte TF activity and antigen levels (r = 0.77, 0.87). The high levels of F1+2 confirm that the coagulation system is activated in PV. The increased capacity of monocytes to generate TF may be responsible for the activation of the coagulation system and thrombus formation. The hypercoagulability state that is induced by this mechanism suggests that long-life oral anticoagulation should be considered once thrombosis has been developed in PV.

Adult↗
PubMed1997

Thrombomodulin and induced tissue factor expression on monocytes as markers of diabetic microangiopathy: a prospective study on hemostasis and lipoproteins in insulin-dependent diabetes mellitus.

Vascular complications are the main cause of morbidity in diabetes mellitus. To evaluate lipoprotein and hemostatic parameters and their relationship with clinically detectable microangiopathy, we studied 58 insulin-dependent diabetes mellitus patients and 60 controls matched for age, sex, and body mass index. Thirteen patients presented clinically detectable microangiopathy (8 retinopathy and 5 both retinopathy and microalbuminuria). A cross-sectional study of lipid profile, coagulation parameters, and a flow-cytometric evaluation of tissue factor expression in normal monocytes induced by patient plasma were performed. Patients were re-evaluated for microangiopathy in a 3-year median follow-up. Patients showed triglyceride enrichment in low (P = 0.00002) and high density lipoproteins (P = 0.004) and increased levels of D-dimer (P < 0.00001), prothrombin fragment 1 + 2 (P < 0.00001), and thrombin-antithrombin III complex (P = 0.0001). Patients with clinically detectable microangiopathy had increased type 1 plasminogen activator inhibitor (P = 0.00001), thrombomodulin (P = 0.02), and induced monocyte tissue factor expression (P < 0.00001). Nine patients developed clinically detectable microangiopathy in the follow-up and the only predictive variable was increased induced tissue factor expression. In conclusion, in these patients elevated thrombin and fibrin generation reflects a hypercoagulable state but clinically detectable microangiopathy seems related to endothelial cell injury markers and to increased induced tissue factor expression on monocytes.

Adolescent↗
PubMed1998

Hereditary spherocytosis, thrombocytosis, and chronic pulmonary emboli: a case report and review of the literature.

Thrombocytosis in post-splenectomy patients with hereditary spherocytosis (HS) is usually not attended by an increased risk of thrombosis. Review of the literature revealed HS in association with pulmonary thrombosis, portal vein thrombosis, and cerebral infarction in two brothers, TTP in an asplenic patient and a patient with corpora cavernosum thrombosis causing segmental priapism. We report a case of a 30-year-old white male with HS who presented with hemoptysis 29 years after splenectomy. Work-up revealed a hypercoagulable state with thrombocytosis and recurrent pulmonary emboli resulting in severe pulmonary hypertension, cor pulmonale, atrial flutter, and syncope.

Adult↗
PubMed1998

Successful treatment of transient acquired factor X deficiency by plasmapheresis with concomitant intravenous immunoglobulin and steroid therapy.

Two patients with no history of previous bleeding diatheses presented with active bleeding from multiple body sites, declining hemoglobin levels, and markedly prolonged prothrombin times (PT) and activated partial thromboplastin times (aPTT) with incomplete correction on PT mix assays. Both patients demonstrated a severe deficiency of factor X (F.X) (<1%; reference range 60-150%). F.X levels and bleeding were refractory to multiple transfusions of fresh frozen plasma (FFP) in both patients. In contrast, daily therapeutic plasma exchange (PLEX) with concomitant administration of intravenous immunoglobulin (IV IgG) and steroids produced a rapid increase in F.X levels with cessation of bleeding, followed by stabilization and normalization of F.X levels and progressive correction of coagulation times. Neither patient has demonstrated a recurrence of the bleeding tendency following discontinuation of steroid therapy. These patients had transient acquired F.X deficiency, a rare coagulopathy, which can result in a lethal bleeding diathesis. An IgG inhibitor that selectively inhibited F.X activation in Russell's viper venom or tissue factor/F.VIIa assays was demonstrated in one patient's pretreatment plasma. Previous treatment of hemorrhage in transient acquired F.X deficiency has been prothrombin complex and/or activated clotting concentrates, which can be associated with transient hypercoagulable states. This is the first reported use of PLEX in transient acquired F.X deficiency. PLEX is safe, efficacious, and rapidly restores hemostasis in this rare acquired bleeding disorder.

Adult↗
PubMed1998

Factor V Leiden mutation does not account for central venous catheter-related thrombosis.

Indwelling central venous access devices are frequently associated with catheter-related thrombosis. The factor V Leiden gene mutation decreases the sensitivity of factor V to the anticoagulant activity of activated protein C, and has been shown to be the most common inherited defect associated with a hypercoagulable state. In this study, we sought to determine whether an increased prevalence of the factor V gene mutation could be identified in individuals with malignancies who had catheter-related thrombosis. Twenty-seven patients who had catheter-related thrombosis were identified and two (7%) tested positive for the heterozygous presence of the factor V gene mutation. Since the vast majority of patients with venous access devices who developed catheter-related thrombosis did not have the factor V gene mutation, pre-catheter placement testing for this mutation would have limited clinical utility.

Adult↗
PubMed1998

Inherited DNA mutations contributing to thrombotic complications in patients with sickle cell disease.

Thrombosis may play an important role in the pathophysiology of certain complications of sickle cell disease (SCD), including stroke and avascular necrosis (AVN). Currently there is no laboratory or clinical parameter that can identify patients who are at highest risk of developing these thrombotic complications. We hypothesized that some patients with SCD have an inherited hypercoagulable state that results in an increased risk of developing stroke or AVN. We examined the role of two common inherited thrombophilic mutations that, in other populations, have been associated with arterial and venous thrombosis and are amenable to screening with DNA restriction enzyme analysis. The C677T mutation in the methylenetetrahydrofolate reductase (MTHFR) gene and the C1565T mutation in the platelet glycoprotein IIIa (GPIIIa) gene were evaluated. We analyzed genomic DNA from 86 children and adults with SCD, including 16 patients with a history of a clinical stroke and 14 patients with AVN, for the presence of these mutations. The C677T MTHFR mutation was found in 19% of patients with stroke, 14% of patients with AVN, and 14% of patients with neither complication (P = NS). The C1565T GPIIIa mutation was found in 25% of patients with stroke, 14% of patients with AVN, and 18% of patients with neither complication (P = NS). Although each of these mutations is relatively common in patients with SCD, neither is independently associated with an increased risk of developing stroke or AVN.

Adolescent↗