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At least 595 records · Page 33Linked to original sources
PubMed2001

Plasma von Willebrand factor, fibrinogen and soluble P-selectin levels in paroxysmal, persistent and permanent atrial fibrillation. Effects of cardioversion and return of left atrial function.

BACKGROUND: Atrial fibrillation is associated with increased risk of stroke and thromboembolism, possibly by conferring a prothrombotic or hypercoagulable state. However, it is unclear whether or not this differs in the clinical subgroups of chronic atrial fibrillation patients, that is, in those with paroxysmal, persistent or permanent atrial fibrillation. We therefore hypothesized that: (i) there are differences in the prothrombotic state between these patients; and (ii) reduction in indices of hypercoagulability would follow elective electrical cardioversion of persistent atrial fibrillation and the return of left atrial function. PATIENTS AND METHODS: We studied 69 patients with chronic atrial fibrillation: 23 with paroxysmal atrial fibrillation (16 males; mean age 65 years+/-SD 13); 23 with persistent atrial fibrillation (16 males; 65 years+/-13), with a mean duration of atrial fibrillation of 3 months (range 2 to 6 months); and 23 with permanent atrial fibrillation (16 males; 67 years+/-10). Blood results were compared to 20 age- and sex-matched healthy controls. The patients with persistent atrial fibrillation then underwent elective DC cardioversion, with Doppler echocardiographic examinations and bloods tests performed prior to cardioversion, and at 3 and 12 weeks afterwards. The prothrombotic state was quantified by measurement of plasma levels of fibrinogen, soluble P-selectin (an index of platelet activation) and von Willebrand factor (a marker of endothelial dysfunction). RESULTS: Permanent atrial fibrillation was associated with significantly raised levels of von Willebrand factor, soluble P-selectin and fibrinogen (all P<0.001); paroxysmal atrial fibrillation with significantly elevated levels of plasma von Willebrand factor (P=0.0067) and fibrinogen (P=0.0001) but not soluble P-selectin (P=0.472); and persistent atrial fibrillation with normal levels of fibrinogen, von Willebrand factor and soluble P-selectin when compared to healthy controls (all P=ns). Stepwise multiple regression analyses demonstrated that the presence of atrial fibrillation was an independent predictor of abnormal von Willebrand factor, fibrinogen and soluble P-selectin levels. Electrical cardioversion of the patients with persistent atrial fibrillation did not significantly alter levels of von Willebrand factor (P=0.766), soluble P-selectin (P=0.726) or fibrinogen (P=0.50) despite maintenance of sinus rhythm and a significant return of left atrial systolic function (as quantified by the presence of A wave on Doppler echocardiography) at 3 months. CONCLUSION: There were significant differences in the prothrombotic state when patients with paroxysmal and permanent atrial fibrillation are compared to matched patients with persistent atrial fibrillation or controls in sinus rhythm. Cardioversion of persistent atrial fibrillation did not significantly alter indices of hypercoagulability even after 3 months maintenance of sinus rhythm, despite the return of atrial systole.

Adult↗
PubMed1999

Coagulation and fibrinolysis in viable mid-trimester pregnancies of normal, intrauterine growth retardation, chromosomal anomalies and hydrops fetalis and their eventual obstetric outcome.

A total of 71 pregnant women diagnosed by ultrasound to have viable fetus in late mid- trimester pregnancies of normal, IUGR, hydrops fetalis and chromosomal anomalies were studied for their coagulation, fibrinolytic and inhibitor levels with association on eventual obstetrics outcome. A hypercoagulable state was observed in all the pregnancies studied. However, higher hypercoagulation evidenced by significantly raised prothrombin formation and clot elasticity together with higher levels of D-dimer, uPA antigen and PAI-1 than observed in normal pregnancy suggests a hyperfibrinolytic/inhibitor state in hydrops fetalis pregnancy associated with bad obstetric outcome. In IUGR pregnancy associated with good outcome further enhanced clot elasticity was seen whilst no significant differences were observed in pregnancy with chromosomal anomalies when compared to uncomplicated normal pregnancy. Our study suggests that in hydrops fetalis pregnancy, further enhanced prothrombin formation and hyperfibrinolysis/inhibitor at late mid-trimester is associated with a poor obstetric outcome.

Adult↗
PubMed1990

Massive hepatic infarction in systemic lupus erythematosus.

Liver disease in systemic lupus erythematosus, as demonstrated by abnormal histopathology, is rare and usually mild; typically, this hepatic disease is of chronic nature and not related to a hypercoagulable state. A patient is described in whom life-threatening hypercoagulability in association with systemic lupus erythematosus resulted in extensive liver infarction. Follow-up radionuclide liver scintigraphy suggested that regenerative recovery in the infarcted areas of the liver may be delayed or absent, but there was no evident functional hepatic impairment.

Adult↗
PubMed1996

Platelet-associated bleeding disorders.

OBJECTIVE: To provide a review of platelet disorders, treatment, and nursing care. DATA SOURCES: Review articles and book chapters pertaining to quantitative and qualitative platelet disorders. CONCLUSIONS: Platelet-associated bleeding disorders are classified as quantitative (abnormal number), qualitative (abnormal function), or hypercoagulable states (errors in hemostasis). The resulting complications include thrombocytosis, thrombocytopenia, hypercoagulation, or bleeding dyscrasias. The administration of drugs, plasma, or platelet therapy may be beneficial to these patients. IMPLICATIONS FOR NURSING PRACTICE: Patients with platelet disorders are at great risk of life-threatening hemorrhage and require close monitoring to prevent unnecessary sequelae. Patient instruction to prevent trauma is required.

Blood Platelet Disorders↗
PubMed1999

The thrombophilic state induced by therapeutic agents in the cancer patient.

Multiple risk factors contribute to the hypercoagulable state in cancer patients. Antineoplastic therapy, including single- or multiagent chemotherapy, hormonal therapy, and hematopoietic growth factors, is an unavoidable and a significant precipitant of venous and arterial thromboses. The risk of thrombosis following cancer treatment also depends on the interaction between treatment agents, type and stage of cancer, and the presence of other risk factors for thrombosis such as advanced age, surgery, immobilization, and the use of central venous catheters. Therefore, although a causal role of cancer treatment in thrombosis is widely accepted, the pathogenic mechanisms are poorly understood and are difficult to investigate because of the multiple confounding factors that are involved. Alterations in coagulation factors, anticoagulant proteins, and endothelial damage have all been shown to occur following cytotoxic agents. The best-studied drugs with definite hypercoagulable effects are L-asparaginase and tamoxifen.

Antineoplastic Agents↗
PubMedDate not supplied

Acquired and congenital clotting syndromes.

Although Virchow postulated 100 years ago that hypercoagulability states exist, it has only been in recent years that methods of documenting hypercoagulability have been developed. These clotting tendencies can be acquired or congenital. The common causes of acquired clotting tendencies include conditions which result in tissue and cellular damage, shock, transfusion reactions, and tissue necrosis. Certain drugs and drug reactions, and certain disease states which include blood dyscrasias and cancer are also associated with clotting problems. In certain diseases such as homocystinuria, hyperlipidemia, and lupus erythematosus, abnormal clotting tendencies may also develop. Important advances in the recognition of hypercoagulability have come with the documentation that congenital clotting abnormalities exist. Moreover, these abnormalities are proving to be more common than are congenital bleeding syndromes. Patients who appear to have spontaneous clotting manifestations and are under 40 years of age should be screened for one of these abnormalities. These congenital clotting tendencies can be classified as defects in thrombosis inhibitors, dysfibrinogenemias, or defects in fibrinolysis. The first thrombotic inhibitor defect recognized was antithrombin III deficiency which was reported in 1965. Subsequently, Protein C, Protein S, and Heparin cofactor II deficiencies have been recognized as contributing to thrombotic tendencies. Dysfibrinogenemias are relatively rare and most are associated with bleeding problems; however, 11% of the abnormal fibrinogens are associated with a clotting tendency. The reason appears to be that these fibrins are resistant to fibrinolysis. The most common defects which are associated with thrombotic tendencies appear, at the present time, to be due to defects in fibrinolysis. These include hypoplasminogenemia, decreases in plasminogen activator, increases in plasminogen activator inhibitor, and Factor XII deficiency.

Blood Coagulation Disorders↗
PubMed2004

Factor XIII Val34Leu polymorphism modulates the prothrombotic and inflammatory state associated with atrial fibrillation.

UNLABELLED: Atrial fibrillation (AF) has been shown to confer a prothrombotic or hypercoagulable state, which could be related to inflammation. Factor XIII (FXIII) catalyses the cross-linking of fibrin monomers, increasing clot resistance; specifically, a common polymorphism, Val34Leu, in the FXIII-A subunit gene has been associated with more rapid FXIII activation. We hypothesised a role for this polymorphism in the prothrombotic state and inflammation in AF, and tested this hypothesis by measurement of indices of coagulation (tissue factor (TF) and fibrinogen), inflammation (interleukin-6 (IL6)) and platelet activation (soluble P selectin (sPsel)). METHODS: We studied 90 stable outpatients (73 +/- 8 years) with persistent AF. The FXIII Val34Leu polymorphism was determined by polymerase chain reaction-allelic specific restriction assay (PCR-ASRA). Prevalence of Val34Leu polymorphism of patients was compared to 585 unrelated subjects from the same geographical area. Plasma fibrinogen (Clauss), TF, IL6 and sPsel (all ELISA) were quantified in patient group. Research indices were compared to 74 controls in sinus rhythm with similar clinical characteristics. RESULTS: There were no statistical differences in FXIII polymorphism prevalence between AF patients and controls. Patients carrying the Leu34 allele had higher plasma levels of TF, IL6 and sPsel (all P < 0.05) compared to controls. Plasma IL6 and TF levels were significantly correlated (Spearman coefficient, r = 0.33, P < 0.01). On multivariate analysis, the Leu34 allele was independently associated with IL6 levels (P < 0.01), whereas TF levels were only associated with IL6 concentrations. However, sPsel and fibrinogen levels were not related to Leu34 allele. CONCLUSION: FXIII Val34Leu polymorphism was independently associated with IL6 levels in AF. The Leu34 allele may potentially influence the prothrombotic state in these patients by modulating the inflammatory state.

Aged↗
PubMed2005

Relationship of serum interleukin-7 concentration and the coagulation state in children with nephrotic syndrome.

BACKGROUND: Enhanced platelet reactivity may play a significant role in the hypercoagulable state of nephrotic syndrome (NS). Thrombocytosis with platelet aggregation cause the release of some cytokines, among them interleukin-7 (IL-7). The aim of the study was to evaluate serum IL-7 levels in children with the symptoms of NS and to determine a correlation between its concentration and platelet count, other hemostatic factors, and NS intensity. METHODS: The study was performed in two groups. I--the examined group of 26 children with NS (12 boys, 14 girls) aged 6.8 +/- 2.1 years, subjected to two examinations: A--before treatment, B--during treatment with prednisone (60 mg/kg 24 h after albuminuria regression); and II--the control group (C) of 20 healthy children. Serum IL-7 level was assayed by enzyme-linked immunosorbent assay method using a R & D Quantikine set. RESULTS: In group I, IL-7 level in examination A (33.33 +/- 33.24 pg/mL) was higher than in the control subjects (P < 0.01). In examination B, IL-7 concentration was reduced to the level of 10.86 +/- 5.22 pg/mL and did not differ from the controls (P > 0.05). A positive correlation was observed between IL-7 and platelet count and serum fibrinogen level. A negative correlation was noted with antithrombin III concentration. No correlation was found with serum levels of albumin and cholesterol or urine protein. CONCLUSION: In children with NS, serum IL-7 level increases proportionally to the elevated platelet count and other hemostatic components, but shows no correlation with serum albumin or urine protein.

Child↗
PubMed2002

Treatment of venous thromboembolism.

The combination of unfractionated heparin or low molecular weight heparin and oral anticoagulants is currently the treatment of choice for most patients with venous thromboembolism. Oral anticoagulants are started at the same time and heparin is discontinued after at least 5 days when the levels of the International Normalized Ratio reach the therapeutic range between 2.0 and 3.0. Low molecular weight heparin has potential advantages over heparin and is administered in subcutaneous weight-adjusted fixed doses without need for monitoring. This has made the home treatment of a large proportion of patients possible. Randomized clinical trials and several subsequent reports from clinical practice have demonstrated the efficacy and safety of this approach. The results of currently ongoing trials aimed to assess the efficacy and safety of newer compounds for the initial treatment of venous thromboembolism are expected. Oral direct thrombin inhibitors or selective factor-Xa inhibitors have the potential to become the treatment of choice in the next decade. The optimal duration of the secondary prophylaxis with oral anticoagulants is still a matter of debate. The rate of recurrence has been shown to be elevated, particularly in patients with idiopathic venous thromboembolism. A 3-month therapy is therefore currently recommended when a transient risk factor is identified, life-long treatment is recommended for patients with a second episode of venous thromboembolism. The presence of active cancer or a thrombophilic state may require long-term anticoagulation, although not all the congenital hypercoagulable states seem to carry the same level of risk. In all other cases, 6 months are recommended, but a long-term monitoring of the patients is advisable. The use of more aggressive strategies such as thrombolysis is limited to patients presenting with massive pulmonary embolism or signs of right ventricular dysfunction.

Anticoagulants↗
PubMed2000

Treatment of venous thromboembolism.

The combination of heparin and oral anticoagulants has been the treatment of choice for most patients with venous thromboembolism in the last two decades. Heparin has been proven to be effective when administered by intravenous continuous infusion or by subcutaneous injection. Oral anticoagulants should be started at the same time and heparin should be discontinued when the levels of the International Normalized Ratio reach the therapeutic range, between 2.0 and 3.0. Low molecular weight heparin has potential advantages over heparin and can be administered in subcutaneous weight-adjusted fixed doses without need for monitoring. This has made home treatment of a large proportion of patients possible. Randomized clinical trials have demonstrated the efficacy and safety of this approach. The optimal duration of the secondary prophylaxis with oral anticoagulants is still a matter of debate. The rate of recurrence has been shown to be elevated, particularly in those patients with idiopathic venous thromboembolism. The presence of an active cancer or a thrombophilic state may require long-term anticoagulation, although not all the congenital hypercoagulable states seem to carry the same level of risk. A 3-month therapy is recommended when a transient risk factor is identified; lifelong treatment is recommended for patients with a second episode of venous thromboembolism. In all other cases, 6 months are currently recommended, but thereafter close monitoring of the patients is advisable. The use of different treatment strategies such as vena caval filter placement, thrombolysis, and surgical thrombectomy should be restricted to a limited number of situations.

Administration, Oral↗
PubMed1975

[Thrombosis of the Björk-Shiley valve as an early fatal complication of the prothetic aortic valve replacement (author's transl)].

From a series of 28 patients subjected to aortic valve replacement with the Björk-Shiley tilting disc valve prosthesis 3 cases are reported in which massive thrombosis with valve dysfunction and fatal outcome occurred in the very early postoperative period. The autopsy findings and the examination of the blood coagulation state during the first 24 hours postoperatively disclosed in all 3 cases a hypercoagulability being responsible for the massive clot formation. The early recognition and establishment of the diagnosis of a hypercoagulability state and an immediate anticoagulant therapy with heparin are necessary for preventing such early fatal complications in patients with cardiac valve replacement.

Adult↗
PubMed2004

Relationship of interleukin-6 and C-reactive protein to the prothrombotic state in chronic atrial fibrillation.

OBJECTIVES: We sought to test the hypothesis that there is a relationship between inflammation and the prothrombotic state in atrial fibrillation (AF). BACKGROUND: Atrial fibrillation is associated with a prothrombotic or hypercoagulable state, which may contribute to an increased risk of stroke and thromboembolism. Inflammation may be involved in the pathogenesis of AF, but the role of inflammation in the pathophysiology of the prothrombotic state of AF has not been studied in detail, despite evidence of a link between inflammation and arterial atherothrombotic disorders. METHODS: We measured plasma indexes of inflammation (C-reactive protein [CRP] and interleukin-6 [IL-6]) and the prothrombotic state, including markers of platelet activation (soluble P-selectin), endothelial damage/dysfunction (von Willebrand factor), the coagulation cascade (tissue factor [TF], fibrinogen), and indexes of blood rheology (plasma viscosity, plasma fibrinogen, and hematocrit) in 106 patients with chronic AF and 41 healthy control subjects included in a cross-sectional analysis. RESULTS: Compared with controls, AF patients had higher levels of IL-6 (p = 0.034), CRP (p = 0.003), TF (p = 0.019), and plasma viscosity (p = 0.045). Plasma IL-6 levels were higher among AF patients at "high" risk of stroke (p = 0.003). After adjusting for potential confounding clinical variables (e.g., vascular disease), AF remained significantly associated with a raised logarithmic transformation (log) of TF (p = 0.04), but the relationships between AF and log IL-6, log CRP, and plasma viscosity became nonsignificant. Among AF patients, log TF (p < 0.001) and high stroke risk (p = 0.003) were independent associates of log IL-6 (adjusted r(2) = 0.443), whereas log fibrinogen (p < 0.001) and plasma viscosity (p = 0.04) were independent associates of log CRP (adjusted r(2) = 0.259). CONCLUSIONS: Increased plasma IL-6, CRP, and plasma viscosity support the case for the existence of an inflammatory state among "typical" populations with chronic AF. These indexes of inflammation are related to indexes of the prothrombotic state and may be related to the clinical variables of the patients (underlying vascular disease and co-morbidities), rather than simply to the presence of AF itself.

Aged↗
PubMed2002

Independent contribution of psychological factors to fibrin turnover in subjects with sleep apnoea and/or systemic hypertension.

By promoting atherosclerosis and thrombosis, a blood-clotting diathesis could contribute to excess cardiovascular morbidity and mortality in patients with systemic hypertension and/or obstructive sleep apnoea. Since psychological states affect haemostatic activity, we wondered about the contribution of behavioural factors to a hypercoagulable state in subjects with increased risk of cardiovascular disease. To tease apart the potential additive nature of cardiovascular disease risk, we examined four patient groups - hypertensives and normotensives, with and without sleep apnoea. The procoagulant molecules thrombin-antithrombin III complex, fibrin D-dimer and von Willebrand factor antigen were measured in 88 subjects (mean age 47 years; range 32-64 years) who underwent full polysomnography. Subjects completed the Center for Epidemiological Studies - Depression (CES-D) Scale, the Cook-Medley (CM) Hostility Scale, and the Profile of Mood States (POMS). Sleep apnoea, hypertension status, age, body mass index and psychological variables (CES-D, CM Stress, and POMS Vigour-Activity) together explained 29% of the variance in D-dimer, a marker of fibrin turnover ( r (2)=0.29, P =0.001). CES-D, CM Stress and POMS Vigour-Activity explained 17% of this variance even after controlling for sleep apnoea, hypertension status, age and body mass index (Delta r (2)=0.17, P =0.001). Thrombin-antithrombin III complex and von Willebrand factor were not significantly related to psychological variables, but this may reflect limited statistical power. Thus psychological factors are independently associated with D-dimer and explain as much of its variance as do traditional correlates (hypertension, sleep apnoea, age and body mass index). These results may provide a rationale for linking behavioural aspects with cardiovascular events.

Adult↗
PubMed1998

The effect of very-low-dose warfarin on markers of hypercoagulation in metastatic breast cancer: results from a randomized trial.

Malignancy is a risk factor for thromboembolism and anti-cancer chemotherapy can increase this risk. Prophylaxis of thrombosis with very-low-dose warfarin given concurrently with chemotherapy has a significantly reduced rate of thromboembolism in a randomized trial in women with stage IV breast cancer. In a group of 32 patients randomized in one center (16 subjects on warfarin and 16 on placebo), we have prospectively studied the plasma levels of: 1. Markers of 'in vivo' clotting activation (thrombin-antithrombin complex [TAT], prothrombin fragment 1+2 [F1+2] and D-dimer), 2. Factor VII (FVII), and 3. Natural anticoagulants (protein C [PC] and antithrombin [AT]). The aims of this study were: 1. to examine whether laboratory tests predicted those patients who developed thrombosis, and 2. to evaluate the effect of very-low-dose warfarin on hemostatic variables. The patients' hemostatic parameters were evaluated before entry into the study and after starting chemotherapy +/- prophylaxis, before each course for nine courses. Before-treatment results were compared to those of a sex and age-matched non-cancer control group. There was a significant elevation of plasma levels of TAT (p <0.001), F1+2 (p <0.001), D-dimer (p <0.0001) and FVIIa (p <0.05), as well as an increase of FVII proteolysis (p <0.05), whereas plasma PC and AT concentrations were not different from controls. After starting chemotherapy, markers of clotting activation were progressively lower in the group receiving warfarin prophylaxis compared to the group on placebo. Differences between the groups became statistically significant (p <0.01) after the 4th course of chemotherapy. Deep vein thrombosis occurred in two patients in the placebo arm. The results of this study indicate that before therapy, an hypercoagulable state is present in stage IV breast cancer, and after starting chemotherapy, abnormalities of hypercoagulation markers persist, however they are reduced by very-low-dose-warfarin. None of the laboratory variables could predict thrombosis in the single patient.

Adult↗
PubMed1993

Ischemic stroke in the young: evaluation and age comparison of patients six months to thirty-nine years.

Ischemic stroke in the young is uncommon, but we currently evaluate at least one young stroke patient at our institutions each week. We undertook this chart review of strokes in patients between the ages of 6 months and 39 years to review all conditions associated with, and thus possibly contributory to, the stroke. We also compare younger and older age groups to observe if age-dependent factors exist. Of 100 total ischemic strokes, 22 were in persons 6 months to 18 years and 78 were in persons 19 to 39 years. Seventy-five percent of strokes were associated with a condition known or postulated to increase stroke risk. Some of these conditions are well accepted as causes for stroke, such as some forms of heart disease, whereas others are only postulated, such as the hypercoagulable states. Taken as a whole, associated conditions were approximately equally divided between infectious/inflammatory, structural, and presumed hypercoagulable conditions. Strokes in the first two decades of life were more commonly associated with infectious/inflammatory conditions, whereas strokes in the next two decades more commonly had structural or presumed hypercoagulable associated conditions. Since many strokes remain unexplained, it would be valuable to determine the significance, if any, of conditions less well known as risk factors for stroke.

Adolescent↗
PubMed1993

Hypercoagulability in the left atrium: Part II: Coagulation factors.

The relationship between a hypercoagulable state and intracardiac thrombus formation is reviewed, with reference to the pathophysiology of intracardiac thrombus in patients with acute cardioembolic stroke, and those with mitral stenosis. When the development or enlargement of intracardiac thrombus is followed serially by echocardiography, the diameter of the inferior vena cava is seen to decrease as the hematocrit increases, particularly in patients with negative water balance taking diuretics. These findings strongly suggest that dehydration could play an important role in the formation of thrombus. A hypercoagulable and secondarily enhanced fibrinolytic state exists in the cardiac chamber of patients with acute cardioembolic stroke or with intracardiac thrombus. This can be evaluated by plasma levels of fibrinopeptide A, fibrinopeptide B beta 15-42, thrombin-antithrombin III complex and D-dimer. Anticoagulant treatment suppresses thrombin activity in the cardiac chamber, allowing plasma fibrinolytic activity to predominate and reduce the size of the intracardiac thrombus.

Atrial Fibrillation↗
PubMed1997

Antithrombin and its inherited deficiency states.

Antithrombin is the primary inhibitor of thrombin that also inhibits many of the other activated serine proteinases involved in blood coagulation. A hypercoagulable state occurs when a deficiency of antithrombin exists in plasma; the deficiency may be either inherited or acquired. This failure to regulate adequately the activity of coagulation proteinases can, with additional provocation, result in clot formation and in the clinical presentation of thromboembolic disease. The structure and function of antithrombin, nature and heterogeneity of the molecular defects in the antithrombin gene associated with inherited antithrombin deficiency, prevalence and the natural history of inherited antithrombin deficiency are all reviewed here.

Antithrombin III↗
PubMed2004

Oxidative status of platelets in normal and thalassemic blood.

Chronic platelet activation may be involved in thromboembolic complications, a leading cause of morbidity and mortality in beta-thalassemia. Oxidative stress, with the generation of reactive oxygen species (ROS), is suspected to play a role in the patho-physiology of thalassemia and cardiovascular disorders. In the present study, we adapted flow cytometric techniques to measure oxidative state markers, ROS generation and reduced glutathione (GSH) content in platelets. Our results show that platelets obtained from beta-thalassemic patients contain higher ROS and lower GSH levels than do platelets from normal donors, indicating a state of oxidative stress. In the absence of any known inherent abnormality in thalassemia platelets, this may be attributed to continuous exposure to oxidative insults from extra-platelet sources. We found that exposure of platelets to oxidants such as hydrogen peroxide and tertbutylhydroperoxide or to the platelet activators thrombin, calcium ionophore or phorbol myristate acetate stimulated the platelets' oxidative stress. This was also increased by plasma of thalassemia patients, and decreased following treatment of the plasma with the iron-chelator Desferoxamin. Iron and hemin, the levels of which are augmented in plasma of thalassemia patients, stimulated the platelets' oxidative stress. The oxidative status of the platelets was also affected by red blood cells (RBC); it was higher in normal platelets incubated with thalassemic RBC than with normal RBC. Normal RBC stimulated with hydrogen peroxide had a greater effect on platelets than did unstimulated RBC. The platelets' oxidative stress was ameliorated by antioxidants such as N-acetyl-L-cysteine and vitamin C. Our findings indicate that in thalassemia, platelets undergo a state of oxidative stress, leading to their activation and potentially to thromboembolic consequences, and suggest that this hypercoagulable state might be treated with antioxidants.

Antioxidants↗