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PubMed1998

Coexistence of primary antiphospholipid syndrome and protein S deficiency in a Hispanic man with ischemic stroke.

The primary antiphospholipid syndrome and protein S deficiency are known hypercoagulable states predisposing to ischemic strokes. The pathogenesis of those hypercoagulable states has been independently studied and, recently, interaction between them has been proposed. A 48-year-old Hispanic man had generalized seizures 5 months after the acute onset of a left middle cerebral artery infarct. He had a strong family history of strokes. After evaluation for cardiologic, rheumatologic, hematologic and metabolic etiologies for stroke, anticardiolipin antibodies and protein S deficiency were detected. Cerebral angiography was normal. First degree relatives were evaluated and screened for these conditions. Lupus anticoagulant was detected in a sister who reported a transient hemisensory deficit. None of the relatives studied had clinical or laboratory criteria for collagen vascular diseases. Coexistence of the primary antiphospholipid syndrome and protein S deficiency, two known prothrombotic states, has rarely been reported in Hispanic adults in association with ischemic stroke.

Antiphospholipid Syndrome↗
PubMed2003

Etiology of pulmonary thromboembolism in the absence of commonly recognized risk factors.

Pulmonary thromboembolism is an often fatal complication of venous thrombosis. Any component or combination of the components composing Virchow's triad (venostasis, hypercoagulability, and endothelial damage) increases the propensity for a thrombophilic state. Hypercoagulable states may be inherited or acquired. While the etiology in many cases may be evident either on physical examination or on evaluation of the decedent's medical history, this is often not the case. We conducted a retrospective study of cases presenting to the Jefferson County Coroner/Medical Examiner's Office in Birmingham, Alabama, who were given a diagnosis of pulmonary embolism. A search of cases within the past 23 years yielded 81 cases. An underlying cause was determined in 70 cases (86%). The remaining 11 (14%) cases had no identifiable cause. We believe that a number of these cases may represent an underlying thrombophilic disorder. Since these disorders may be of an inherited or acquired nature, the determination of an etiology may be relevant to the decedent's family. Postmortem blood analyses may in selected cases be useful and appropriate for the detection of some of these disorders. However, such analyses are not practical in all cases, with each case having to be evaluated on its own merits.

Adolescent↗
PubMed2003

Blood coagulation and fibrinolytic activity in hypothyroidism.

The influence of hypothyroidism on haemostasis is controversial; both hypocoagulable and hypercoagulable states have been reported. Hypothyroidism has been associated with atherosclerosis; a hypercoagulable state in addition might represent a risk factor for thromboembolic disease. The aim of the present study was to investigate the markers of endogenous coagulation and vascular endothelial cell function and to evaluate the relationship between serum lipid profile, thyroid hormones and haemostatic parameters in hypothyroid patients. We investigated various haemostatic parameters in 20 patients with hypothyroidism and compared them with 20 euthyroid controls. The relationship between serum thyroid hormones and the haemostatic parameters was examined. The plasma levels of fibrinogen, AT III and PAI-1 were significantly increased in hypothyroid patients compared with the control group, whereas factors VIII and X activity was decreased. We showed that free T3 levels correlated with factor IX activity. Free T4, FT3 and TSH did not correlate with fibrinogen, vWF, AT III, t-PA, or PAI-1. aPTT correlated inversely with t-PA activity and positively with protein C activity. Anti-Tg correlated inversely with FV. There was a positive correlation between triglycerides and protein C. Protein S correlated inversely with high density lipoprotein cholesterol. We found a hypofibrinolytic state in patients with hypothyroidism. Our results suggest that the risk of developing thrombosis and ultimately myocardial infarction via high PAI-1 levels may be increased in patients with hypothyroidism, a result in line with recent epidemiological data. However, thyroid hormones may play a role at different levels of the complex haemostatic system.

Adult↗
PubMed1996

Hypercoagulability following multiple trauma.

We sought evidence of hypercoagulability in 59 seriously injured trauma patients. An extended coagulation profile (consisting of tissue plasminogen activator antigen concentration, plasminogen activator inhibitor, serum antithrombin III, protein C antigen, functional protein C, protein S antigen, D-dimer, and prothrombin fragment 1.2) was compared to control values. Laboratory evidence of hypercoagulability was seen in 85% (n = 50) of the patients. Patients with an Injury Severity Score (ISS) > or = 16 (n = 36) had significantly elevated levels of D-dimer and decreased levels of functional protein C compared to patients with an ISS < or = 15 (n = 23). Functional protein C had a negative correlation (r = -0.44; p < 0.001) with the ISS. A hypercoagulable state exists immediately following severe trauma. Greater injury severity may increase this hypercoagulable state. Decreased levels of functional protein C best correlated with increased injury severity.

Adult↗
PubMed1993

Hypercoagulability in patients undergoing autologous or allogeneic BMT for hematological malignancies.

Severe thrombotic alterations, such as veno-occlusive disease of the liver, may occur in the early phase following high-dose chemoradiotherapy and BMT. In this study, performed in patients with hematological malignancies subjected to allogeneic (10 cases) and autologous (20 cases) BMT, we have monitored laboratory hemostatic parameters to better understand the pathogenetic mechanism of thrombosis and particularly of veno-occlusive disease. Prothrombin time, activated partial thromboplastin time, plasma fibrinogen, markers of hypercoagulability (thrombin-antithrombin complex and prothrombin fragment F1+2); natural anticoagulants (protein C, protein S and antithrombin) together with fibrinolytic parameters (plasminogen, alpha 2-antiplasmin, tissue-plasminogen activator, plasminogen activator inhibitor and D-dimer) were assessed before transplant, on day 0 and weekly for 1 month thereafter. A hypercoagulability state, not related to an impairment of the anticoagulant and fibrinolytic systems, was documented before and after autologous and allogeneic transplant. Two patients developed veno-occlusive disease: they did not show any difference from the other patients before transplant while they presented a decrease of the natural anticoagulants along with altered fibrinolytic parameters only at the clinical onset of veno-occlusive disease. In conclusion, in this study a state of marked hypercoagulability was documented in BMT patients and the hemostatic laboratory parameters evaluated were not able to predict the occurrence of the thrombotic complications.

Antithrombin III↗
PubMed1991

[Retinal vascular occlusion in a young patient with hemostatic abnormalities].

Retinal vascular occlusion (RVO) in the young patient without vascular parietal disease have been encountered in different pathologic states, coagulopathy being frequent. We started a prospective study in Geneva to find out the hypercoagulable states responsible for RVO. We give suggestions to the paraclinical investigations to perform. We discuss the primary and secondary hypercoagulable states in the light of two patients who had coagulation abnormalities.

Adult↗
PubMed1987

The pathophysiology of the prethrombotic state in humans: insights gained from studies using markers of hemostatic system activation.

Numerous investigators have postulated that a hypercoagulable state exists in humans for a period of time before the development of thrombotic episodes. A clear biochemical definition of the prethrombotic state, however, has proved elusive due in part to the lack of reliable techniques for monitoring pertinent changes in blood coagulability. Based on recent advances in our knowledge of the biochemistry of the coagulation system, a series of highly sensitive and specific immunochemical tools has been developed that can quantitate the activities of various steps of the hemostatic mechanism in vivo at the subnanomolar level. We have established assays for F1+2 and the protein C activation peptide, which measure the cleavage of the prothrombin molecule by factor Xa and the scission of protein C by the thrombin-thrombomodulin complex, respectively. Nossel and coworkers had previously constructed similar assays for fibrinopeptide A (FPA) and fragment B beta 1-42, which monitor the cleavage of fibrinogen by thrombin and the proteolysis of fibrin I by plasmin, respectively. Substantial elevations in the levels of these markers have been found in patients with disseminated intravascular coagulation and many subjects with acute deep venous thrombosis. The F1+2 and FPA assays have been used to demonstrate that significant increments in factor Xa activity but not thrombin activity regularly occur in the blood of nonanticoagulated individuals with congenital deficiencies of antithrombin or protein C. These two disorders are known to be correlated with the subsequent development of thrombosis. Patients with protein C deficiency have also been noted to have significantly reduced plasma levels of protein C activation peptide. By using the immunoassays for FPA and B beta 1-42 in studies of postoperative patients, it has been shown that an imbalance between the procoagulant action of thrombin and the anticoagulant effect of plasmin on fibrin I polymer may induce an acquired thrombotic diathesis. Finally, we have recently demonstrated that prothrombin activation as measured by the F1+2 assay is suppressed by oral anticoagulants in the blood of patients with thrombotic diatheses. These investigations suggest that these assay techniques can be used to improve our understanding of the hypercoagulable state as well as to develop more effective treatment strategies for the prevention of thromboembolic events.

Administration, Oral↗
PubMed1992

Acute aortic thrombosis associated with spinal cord infarction in nephrotic syndrome.

Acute aortic thrombosis associated with spinal cord infarction in a 47-year-old man with nephrotic syndrome is described. He was admitted to our hospital presenting with the nephrotic syndrome. Renal biopsy revealed mild mesangial proliferative glomerulonephritis. The urinary protein excretion rate transiently decreased after the start of treatment with prednisolone, but it increased again and was followed by the development of the signs and symptoms of spinal cord infarction, which was diagnosed by magnetic resonance signal abnormalities, and then symptoms of ischemia in the lower limbs. Digital subtraction angiography revealed an obstruction at the bifurcation of the abdominal aorta. Emergency thrombectomy was performed, and the arterial blood flow was reestablished. Laboratory data on the fibrinocoagulation system showed a hypercoagulable state. In this case, fibrinocoagulation abnormalities due to the nephrotic syndrome led to the hypercoagulable state, and dehydration might have triggered the thrombotic complication.

Acute Disease↗
PubMed1983

Peripheral arterial thrombosis due to the nephrotic syndrome: the clinical spectrum.

We reviewed the literature concerning arterial thromboses associated with the nephrotic syndrome and the hypercoagulable state. An illustrative case of peripheral arterial thrombosis and pulmonary emboli attributed to the hypercoagulable state of the nephrotic syndrome is included. In our patient, serum levels of antithrombin III, plasminogen, factor VII activity, factor VIII activity, and factor VIII antigen were abnormal. Arterial thromboses in patients with the nephrotic syndrome are often associated with steroid and diuretic use. In pediatric patients, a predisposing factor may be femoral venipuncture.

Adolescent↗
PubMed1994

[Markers of coagulation/fibrinolysis in angitis].

Endothelial cells exhibit antithrombogenic properties, including PGI2 and NO production which inhibit platelet functions and induce blood vessel dilatation. Endothelium also produces thrombomodulin which converts thrombin from a procoagulant protease to an anticoagulant. These antithrombogenic properties are altered by several factors, which include inflammatory cytokines (IL-1, TNF) resulting hypercoagulable state in inflammation. Thus increased markers of coagulation/fibrinolysis were observed in angitis syndrome. The hypercoagulable state showing the activity of angitis may cause thrombosis and may act as a progressive factor for angitis.

Blood Coagulation↗
PubMedDate not supplied

Fibrinolysis in patients with diabetic nephropathy determined by plasmin-alpha 2 plasmin inhibitor complexes in plasma.

Activation of fibrinolysis in patients with diabetic nephropathy was determined by the plasma levels of plasmin-alpha 2 plasmin inhibitor complexes (alpha 2PIC) using a one-step sandwich enzyme immunoassay (EIA). Plasma levels of alpha 2PIC in diabetic patients with persistent proteinuria were significantly higher than those in diabetic patients without proteinuria, patients with chronic glomerulonephritis, and healthy adults. Plasma levels of alpha 2PIC in diabetic patients with intermittent proteinuria were also significantly higher than those of diabetic patients without proteinuria, patients with chronic glomerulonephritis, and healthy adults. Diabetic patients have been suggested to have a hypercoagulable state. The findings obtained from this study indicated that activation of fibrinolysis might counteract the hypercoagulable state in patients with diabetic nephropathy.

Adult↗
PubMed2001

Is blood homocysteine elevated in migraine?

OBJECTIVE: To determine total serum homocysteine levels in a large group of patients with migraine with and without aura. BACKGROUND: Hypercoagulable state is a known risk factor for stroke in the young. The existence of a hypercoagulable state has been postulated in migraine and homocysteinemia with young-onset stroke. To the best of our knowledge, blood homocysteine has not been studied in a significant number of patients with various forms of migraine. METHODS: Total serum homocysteine was measured with high-performance liquid chromatography in 78 patients with migraine and in 126 age- and sex-matched healthy volunteers. RESULTS: Seventy-eight patients aged 18 to 65 years were studied: 22 with migraine with aura and 56 with migraine without aura. Only 1 man had significantly elevated blood homocysteine (38.6 micromol/L), while another had a borderline elevation (15.8 micromol/L) (reference value for both sexes in our laboratory is 4 to 14 micromol/L). Both patients suffered from migraine without aura. CONCLUSIONS: Blood homocysteine is not elevated in migraine.

Adult↗
PubMed1998

Annual review of systemic diseases: 1995-1996. Part I.

Systemic illnesses, such as vasculitides and systemic lupus erythematosus, may have ocular symptoms, or they may present with ocular signs and undiagnosed or occult systemic signs. The recently described ophthalmic and neurologic presentations and new diagnostic modalities for Wegener's granulomatosis, giant cell arteritis, and systemic lupus erythematosus are reviewed. Hypercoagulable states and their role in visual diseases are assessed, and strategies for evaluating patients with hypercoagulable states are described.

Blood Coagulation Disorders↗
PubMed2003

[Vascular complications associated with inflammatory bowel disease].

Thromboembolic episode is a well known extraintestinal manifestation of inflammatory bowel disease, but it is a clinical rare complication. Histological and hematological studies suggest that a hypercoagulable state is involved in the pathogenesis of inflammatory bowel disease. However, the exact mechanism of hypercoagulability is still unknown. During the acute recurrences there is an increase of factor VIII, fibrinogen, platelet, factor V and decrease of antithrombin III. Hematologic disorders seem markedly correlated with the activity of the disease. We report on two patients with Inflammatory bowel disease and hypercoagulable state. We review the literature and discuss about the pathogenic mechanisms of such complication.

Adult↗
PubMedDate not supplied

Pro-thrombotic states and their diagnosis.

The authors define pro-thrombotic states as conditions associated with a high frequency of thrombosis; this association is based on pathogenetic or simply clinical and epidemiological relationships. Thrombophilic states have well-defined, specific causes: antithrombin III, protein C and S and similar deficiencies for inherited thrombophilias, and lupus anticoagulant, antiphospholipid antibodies for the acquired forms. Another identifiable group is made up of several conditions predisposing to thrombosis (CPT) characterized by less specific and multiple mechanisms (e.g. malignancy, inflammatory bowel disease, nephrotic syndrome, diabetes, obesity, etc.). These conditions may induce thrombosis by themselves or contribute to its clinical onset in patients with true thrombophilic states. This is especially the case for patients who are taking contraceptive drugs, are pregnant, have undergone surgery or trauma. The term hypercoagulability states is by no means equivalent to either thrombophilia or CPT. In fact, hypercoagulability may be defined as "activation of blood coagulation" in the presence of specific markers such as fibrinopeptide A and prothrombin fragment F1 + 2. Hypercoagulability is therefore a laboratory rather than a clinical condition and can be a transient feature appearing during certain phases of thrombophilia or CPT. Lastly, conditions involving the presence of hemostatic risk factors for atherothrombosis are simply terms used to describe a statistical-epidemiological relationship between certain hemostatic variables (fibrinogen, factor VII, PAI, etc.) involving the risk of cardiovascular morbidity and mortality but not necessarily indicating a hypercoagulability state.

Arteriosclerosis↗
PubMed1993

Coagulation abnormalities associated with the use of anabolic steroids.

According to a number of recent reports, persons using anabolic steroids may be subject to an increased risk of thromboembolism. We evaluated the effect of anabolic steroid use on the coagulation and fibrinolytic systems of 16 male bodybuilders to determine whether alterations occurred that would predispose them to a hypercoagulable state. No attempt was made to regulate or guide steroid use. Paired blood samples, both with and without steroid use, were obtained from six individuals, and the remaining subjects provided single samples obtained either during steroid use or nonuse. No differences were noted in most parameters, but we did find a significant increase in protein C antigen (p = 0.008) and free protein S antigen (p = 0.015), with a decreased euglobulin lysis time (p = 0.021) during steroid use. We also found a reduction in total cholesterol levels (p = 0.035) during steroid use. At least some of these findings suggest an activated fibrinolytic state, a known effect of anabolic steroids. The results do not support the presence of a hypercoagulable state. If anabolic steroids do produce a thrombotic tendency, they may do so through alterations in other hemostatic mechanisms or changes in lipid fractions, or more sensitive coagulation assays may be required for detection.

Adult↗
PubMed2000

Aortic-origin reconstruction of the great vessels: risk factors of early and late complications.

OBJECTIVE: Great vessel reconstruction for arterial occlusive disease has been shown to be a durable procedure. The purpose of this report is the examination of the influence of cause and risk factors on outcomes for the identification of patients who may be better treated with endovascular techniques or other surgical approaches. METHODS: Data for patients who underwent aortic-origin great vessel reconstruction between 1988 and 1998 were reviewed. The data were analyzed with Fisher exact test, life-table analysis, and log-rank test. RESULTS: Ninety-two vessels underwent revascularization in 58 patients (15 men, 43 women; mean age, 54 years; age range, 20 to 82 years). Etiology was atherosclerosis obliterans (n = 40; 69%), Takayasu's arteritis (n = 13; 22%), radiation arteritis (RA; n = 4; 7%), and mediastinal fibrosis (n = 1; 2%). The symptoms were cerebrovascular (n = 25), upper extremity (n = 8), or both (n = 23), and two patients were asymptomatic. The bypass grafting was performed with single-limb synthetic grafts (n = 23) or grafts plus side arms (n = 28). Seven patients underwent innominate endarterectomy. The mean follow-up period was 45 months (range, 0 to 126 months). The perioperative stroke (n = 4; 7%) and death (n = 2; 3%) rates were not related to the cause of disease. The patients with creatinine levels of 2 or more (n = 4) had a combined perioperative stroke/death rate of 50% (vs 7% for patients with healthy creatinine levels; P <.05). The patients with hypercoagulable states (ie, thrombophilia; n = 6) had an increased perioperative stroke rate (33% vs 4% for patients without hypercoagulable states; P <.05) and an increased late thrombosis rate. The primary and secondary graft patency rates at 5 years were 80% +/- 7% and 91% +/- 5%, respectively. Patients with RA had a greater risk of stroke or death at 3 years (33% free of stroke or death vs 79% for patients with atherosclerosis obliterans and 92% for patients with Takayasu's arteritis; P =.02) and an increased major late infection rate (50% vs 2% for all others; P =.01). CONCLUSION: Patients with thrombophilia and renal insufficiency have increased perioperative stroke and stroke/death rates, respectively. Patients with RA have an increased incidence rate of late major infection, which directly contributes to an increased rate of stroke or death. Patients with thrombophilia have an increased rate of late graft thrombosis. These patient conditions should be approached cautiously, and some patients may benefit from endovascular therapy.

Adult↗
PubMed2005

Upper body venous thrombosis associated with ovarian stimulation: case report and review of the literature.

Thromboembolic events are a serious complication of assisted conception treatment. Thrombosis may be either arterial or venous but the latter is far more common. This phenomenon is more frequent in the lower limb, but several cases of upper extremity thrombosis have been described in the literature. Although the aetiology of these thromboembolic disorders is not fully understood, the mechanism is thought to be due to a hypercoagulable state associated with haemostasis and thrombophilia. Predisposing factors seem to be hyperoestrogenism, ovarian hyperstimulation syndrome, a hereditary hypercoagulable state and multifoetal pregnancy. We report a case of superior sagittal sinus thrombosis that developed in a patient following successful assisted conception in the absence of evident risk factors. In the current literature, the site of thrombosis, possible predisposing factors, oestrogen levels, number of foetuses, maternal and foetal outcomes, and management of thrombosis were analysed.

Adult↗