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PubMed1979

Babesia bovis (argentina): analysis of fibrinogen-like proteins during infection.

Fibrinogen and fibrinogen-like proteins (FLP) were isolated from plasma and serum of cattle acutely infected with Babesia bovis. The sizes and chain structures of these proteins were examined and clotting assays performed. The results indicated that the blood was in a hypercoagulable state due mainly to enhanced production of hydrogen bonded fibrin and offset partly by slight inhibition of chain cross-linking. The latter appeared due to a Factor XIII inhibitor. Reduction of A alpha chains of plasma FLP was not evident, nor could lower molecular weight remnants be regularly detected strongly suggesting that fibrin(ogen) lysis rarely occurred. Similarly the size and chain structure of the majority of noncoagulable FLP of serum was consistent with their being the product of coagulation and not fibrinolysis. Only in heavily infected splenectomized cattle were products from lysed cross-linked fibrin detected and these constituted only about 3% of total serum FLP.

Animals↗
PubMed1994

Thromboembolic complications associated with brain tumors.

Thromboembolic complications are the second most common cause of death in hospitalized cancer patients; they are caused by alterations of hemostasis and include hypercoagulable states, acute and chronic disseminated intravascular coagulation, and primary fibrinolysis. The fibrinolytic system is comprised of several serine protease enzymes and their inhibitors and is associated in various biological systems with physiological and pathological events such as tissue development, remodeling, invasiveness, and migratory potentials of both normal and malignant cells. It also plays a key role in the dissolution of fibrin strands. Defective fibrinolysis, which is often associated with the pathogenesis of venous thrombosis and other thromboembolic complications, occurs when the balance is disrupted, resulting in either inhibition or enhancement of fibrinolysis. The association between thromboembolic complications and neoplastic disease has been well-established since Trousseau in 1865 first reported a high incidence of venous thrombosis in a series of patients with gastric carcinoma. In this article, we discuss the factors that have been shown to be associated with thromboembolic complications in patients who harbor brain tumors, namely, hemostatic alterations caused by the tumors themselves or through interactions with neural tissue around the tumors, pre-operative hemostatic alterations in certain patients, and defective fibrinolysis associated with specific tumor types and/or tumor locations.

Brain Neoplasms↗
PubMed1994

Pathogenetical consideration of spontaneous dural arteriovenous fistulas (DAVFs).

Sinus thrombosis has been regarded as an aetiological factor in DAVFs. However, this claim has been disputed in the literature; because it is not possible to prove that DAVFs arise as a result of sinus thrombosis in all cases, and there is evidence that venous thrombosis can be acquired from a DAVF. The purpose of this study is to examine the hypothesis that the different angiomorphologies of DAVFs depend on the location of their venous outflow, and that a territorial classification of spontaneous DAVFs can be created which is based on their acquired development as a consequence of the breakdown of autoregulation of dural microvascularisation after venous thrombosis. The clinical and radiographic findings of 96 patients with DAVFs were reviewed. The angiomorphology of these lesions was examined using extensive prospective and retrospective angiographic studies, especially with regard to their venous characteristics. The associated phlebothrombosis of the venous outflow was determined in all cases by angiography, and in 8 cases by CT or MRI. We also applied the Venturi effect, a well-confirmed engineering principle, to propose a new hypothesis concerning the development of acquired DAVFs: namely, that there is an acceleration of the shunt volume of the physiological dural AVshunts afer a breakdown of their autoregulation occurs. This acceleration seems to be proportional to the flow volume of the venous outflow. The imaging examination showed venous thrombosis in 51 cases. In 98% (44) of the non-thrombotic cases, predisposing histories for phlebothrombosis were documented-for example, hypercoagulable states (venous embolism, phlebothrombosis of the leg, cardiac disease), diabetes mellitus, chronic otitis media, or various low-grade infections. In addition, in 78% of the non-thrombotic cases (excluding the DAVFs of the venous plexus at the base of the skull) there were also angiographically documented deformations of the sinus wall, including hypoplasia of the sigmoid or transverse sinus (20 cases), segmental narrowing of the sinus (8 cases), septation of the sinus lumen (2 cases), and cavernous nodules projecting into the lumen of the transverse (6 cases), sigmoid (4 cases), or sagittal (3 cases) sinuses. The clinical presentation suggested that DAVFs probably develop after a breakdown of the autoregulation of the physiological AV shunts resulting from a venous thrombosis, when there are suitable arteriovenous pressure gradients in the venous recipient. This development would depend on the haemodynamic action of the Venturi effect.(ABSTRACT TRUNCATED AT 400 WORDS)

Adolescent↗
PubMed1978

[Peripheral microthrombotic purpura associated with acute promyelocytic leukemia in pregnancy. A light and electron microscopic study].

A case is presented of a pregnant patient in the 28th week of gestation with promyelocytic leukemia and an unusual thrombohemorrhagic skin lesion. Ultrastructural examination revealed a microthrombotic purpura. Reduced coagulation factors increased during heparin treatment. The exacerbation of disseminated intravascular coagulation is explained by a hypercoagulable state in pregnancy in association with the as yet unknown etiology of "promyelocytic fibrinopathic leukemia".

Adult↗
PubMed1980

Studies of intravascular components in cerebral vasospasm following subarachnoid hemorrhage.

Cerebral vasospasm with subsequent infarction gives important influence to the prognosis of patients with ruptured intracranial aneurysms. Many factors should be considered in the pathogenesis of cerebral infraction. Clinical and experimental studies of intravascular components with particular reference to platelet and coagulation factors were performed. Both studies revealed systemic platelet hyperactivity and a hypercoagulable state; in further experimental studies, crenated red blood cells were recognized in the course of cerebral vasospasm. These systemic changes of intravascular components are thought to accelerate cerebral ischemia through formation of microthrombosis, increased blood viscosity and reduced deformability of the red blood cells.

Animals↗
PubMed1993

Persistent activation of thrombocytes in neurosurgical patients operated for primary brain tumours.

A prospective study was designed to investigate whether platelet hyperactivity exists following neurosurgical removal of primary brain tumours. The level of beta-thromboglobulin (beta TG), a protein released by platelets during the activation process, was measured in the plasma of 13 consecutive patients prior to surgery (T 1) and on the first (T 2) and seventh (T 3) post-operative days. A significant and sustained increase in beta TG levels from a baseline of 20.7 +/- 1.7 ng/ml (mean +/- sem) at T 1 to 37.0 +/- 5.2 ng/ml (p < 0.005) at T 2 and 35.9 +/- 3.7 at T 3 (p < 0.005) occurred. When patients were grouped according to tumour malignancy, significantly higher beta TG levels were found in the malignant group at T 2 (51.8 +/- 6.3 ng/ml) when compared to the benign group (30.6 +/- 6.0 ng/ml) (p = 0.025). Postoperative T 3 levels were linearly correlated to T 1 levels (r = 0.58, p = 0.04). This significant and sustained platelet activation that occurs following brain surgery may be part of the biochemical sequel leading to a hypercoagulable state and thrombo-embolic phenomena (TEP) in these patients.

Adolescent↗
PubMed1992

Value of CT and sonography in the conservative management of acute splenoportal and superior mesenteric venous thrombosis.

Acute splenoportal and superior mesenteric venous thrombosis were diagnosed on sonography and computed tomography (CT) in six patients. Sonography demonstrated the presence of echoic material filling the involved vessels in all patients. Precontrast CT scans demonstrated an increased, intra luminal density of the clots in four patients with splenoportal thrombosis. However, in two cases of superior mesenteric venous thrombosis, no hyperdensity was observed within the lumens. Nevertheless, the clots were always visualized as low-density regions in the vessel lumens after bolus injection. Intravenous anticoagulant therapy was started immediately after the diagnosis. All patients were evaluated twice a week with sonography and/or CT until recanalization occurred. The patency of the previously involved vessels was assessed from 6 days to 4 weeks after the acute episode (average time of recanalization: 17 days) without development of collateral pathways. It is concluded that, in the absence of clinical signs of a life-threatening process, a conservative management of acute splanchnic thrombosis can be successfully achieved by (1) early diagnosis, (2) efficacious intravenous anticoagulant therapy, (3) careful imaging follow-up of these patients by sonography and/or CT during the acute phase and, finally, (4) by an extensive search for a hypercoagulable state.

Acenocoumarol↗
PubMed1993

Coagulation effects of cyclosporine in liver transplantation.

Thromboembolic complications have been described in graft recipients receiving cyclosporine (CS). Whether these individuals have a hypercoagulable state when compared to healthy controls was evaluated. Recalcification times (RT) of saline-incubated citrated whole blood and endotoxin-incubated whole blood of both control and transplant patients were determined. There was no difference between the RT saline or RT endotoxin groups in both patient groups. These data suggest that CS alone has no procoagulant effects, but that additional factors such as endotoxin and/or graft-induced antigen production may provoke the thrombotic complications.

Blood Coagulation↗
PubMed1995

Clinical and CT evaluation of a new stretch polytetrafluoroethylene aortic graft.

A new stretch polytetrafluoroethylene (PTFE) aortic graft became available for clinical use in early 1991. We prospectively evaluated our first 107 stretch aortic PTFE grafts by means of serial CT imaging and compared them with a cohort of concurrently placed Dacron grafts. Stretch PTFE requires no preclotting and is claimed to resist long-term dilation and conform well to anastomoses. Consecutive patients undergoing placement of stretch PTFE grafts were seen at least yearly. Within the first 2 years after implantation, contrast-enhanced CT scans of the abdomen and pelvis were obtained. Caliper measurements were made of the native arteries and the body and any limbs of the aortic grafts. Graft elongation was assessed by noting distortions from the normally circular or minimally ovoid configuration of the grafts on transverse CT images. Indications for grafting were elective repair of abdominal aortic aneurysm in 60 patients, aortoiliac occlusive disease in 31, both aneurysm and occlusive disease in eight, and ruptured abdominal aortic aneurysm in eight. The overall operative mortality rate was 6.5%. There were two early postoperative graft limb thromboses resulting from hypercoagulable states, and there was one graft infection. Mean follow-up was 14.1 months (range 1 to 34 months). CT scans were obtained from 61 patients with stretch PTFE grafts and 10 with concomitantly placed Dacron grafts. Ten patients had two or more postoperative CT scans. Primary stretch PTFE patency was 98% and secondary patency, 100%. There was significantly less dilation of both the graft body and limbs in the stretch PTFE group (body mean 16.5%, range 6.3% to 28.1%; limb mean 19.3%, range 10% to 43%) compared to the Dacron group (body mean 33%, range 22% to 78%; limb mean 62%, range 12.5% to 88.9%) (p < 0.01, unpaired t test).(ABSTRACT TRUNCATED AT 250 WORDS)

Adolescent↗
PubMed1999

Systemic coagulation activation and anastomotic leakage after colorectal cancer surgery.

PURPOSE: The aim of the present study was to study whether patients developing anastomotic leakage after colorectal resections for colorectal cancer have laboratory signs of an altered hemostatic balance in the systemic circulation, preoperatively and postoperatively, causing an impaired healing process. METHODS: Patients operated on for colorectal cancer were studied. Seventeen consecutive patients with anastomotic leakage and 17 patients without anastomotic leakage were matched according to age, gender, tumor stage, and localization of tumor. Hemostatic balance was estimated preoperatively and at one, two, and seven days and at three months after surgery by plasma levels of sensitive markers of coagulation activation and fibrinolysis, i.e., prothrombin fragment 1 + 2, thrombin-antithrombin complexes, soluble fibrin, tissue-type plasminogen activator activity, and plasminogen activator inhibitor Type 1. RESULTS: Preoperatively, the hemostatic balance was comparable in patients with and without anastomotic leakage. In the early postoperative period, patients developing anastomotic leakage exhibited signs of systemic coagulation activation, i.e., elevated plasma levels of prothrombin fragment 1 + 2, thrombin-antithrombin complexes, soluble fibrin, and plasminogen activator inhibitor Type 1. The observed coagulation activation appeared before the anastomotic leakage became clinically evident. More patients with anastomotic leakage received perioperative blood transfusions than patients without leakage, despite the fact that duration of surgery and intraoperative blood loss were comparable in the two groups. CONCLUSIONS: Enhanced coagulation activity was observed postoperatively in patients developing anastomotic leakage after colorectal resections for colorectal cancer. Such a hypercoagulable state may contribute to the development of anastomotic leakage by facilitating formation of microthromboses in the perianastomotic area.

Age Factors↗
PubMed1999

Budd-Chiari syndrome complicating restorative proctocolectomy for ulcerative colitis: report of a case.

PURPOSE: This is a case of hepatic vein thrombosis presenting in a delayed fashion after proctocolectomy with ileal pouch-anal anastomosis for ulcerative colitis. Search for a causative thrombotic condition resulted in the diagnosis of polycythemia vera, a myeloproliferative disorder associated with hypercoagulability. The polycythemia was masked by an iron deficiency associated with the ulcerative colitis. METHODS: The history, physical, diagnostic modalities, and treatment for this patient are described, and the literature of Budd-Chiari syndrome associated with ulcerative colitis is reviewed. RESULTS: Six cases of Budd-Chiari syndrome in the setting of ulcerative colitis are reported in the literature from 1945 to 1997. CONCLUSIONS: Hepatic vein thrombosis is a rare complication of ulcerative colitis. The diagnosis of Budd-Chiari syndrome demands a thorough search for a hematologic condition predisposing to thrombosis. Our patient had a myeloproliferative disorder, polycythemia vera, that is associated with a hypercoagulable state. The disorder was masked by an iron deficiency associated with the ulcerative colitis. Recognition of the entity will permit successful treatment.

Adult↗
PubMed1994

Deep cerebral venous thrombosis and hereditary tissue plasminogen activator (t-PA) deficiency.

We describe a patient with defective tissue plasminogen activator (t-PA) release who developed internal cerebral vein thrombosis. She recovered completely and, as shown by MRI, favourable outcome was probably related to vascular recanalisation. Other members of the pedigree had a similar fibrinolytic deficiency without clinical manifestations. The use of oral contraceptives may have contributed to the patient's hypercoagulable state.

Adult↗
PubMed1985

Hemostatic defects in experimental obstructive jaundice.

To elucidate the etiology of hemostatic abnormalities in cases of obstructive jaundice, we occluded the bile duct of rats for one week and found that the moderately jaundiced rats exhibited a marked reduction in the value of Hepaplastin test and Thrombotest with minimum histological changes in liver. All other coagulation and fibrinolysis profiles were within normal limits. These findings exclude the occurrence of a hypercoagulable state or hypofibrinolytic state in the jaundiced rats due to bile duct occlusion. Similar results were obtained in rats with tube choledochostomy. The abnormalities were almost completely prevented by the daily parenteral administration of vitamin K. These observations suggest that malabsorption of vitamin K may be the sole etiologic factor producing hemostatic defects in case of uncomplicated obstructive jaundice.

Animals↗
PubMed1989

Postoperative changes in hemostasis analyzed by the serial determination of fibrinopeptides and D-dimer.

In order to elucidate the postoperative changes in hemostasis, three molecular markers; fibrinopeptide A (FPA), fibrinopeptide B beta 15-42 (B beta 15-42) and D-dimer, were serially determined in 27 gastric resections (group A), 27 hepatic resections (group B) and 4 probe laparotomies (group C). Unexpectedly, a postoperative hypercoagulable state was transient and of a low magnitude, as determined by the obtained value of FPA. On the other hand, a significant fibrinolysis (an elevation of B beta 15-42) was observed immediately after surgery which continued for over 10 days. The early phase of fibrinolysis, up until the 3rd postoperative day, is likely to be primary fibrinolysis, as it was not accompanied by the formation of D-dimer, which results from the digestion of fibrin by plasmin. The late phase, however, is considered to be secondary fibrinolysis, as D-dimer was elevated during this phase. Despite the different surgical procedures, these changes were basically similar between the patients who underwent gastric resections and those who underwent liver resections. The postoperative changes in hemostasis as presented herein may therefore be the general physiological response, at least against abdominal surgery.

Abdomen↗
PubMed2003

Neonatal thrombosis.

Neonatal thrombosis is a serious event that can cause mortality or result in severe morbidity and disability. The most important risk factor for the development of thrombosis during the neonatal period is the presence of an indwelling central line and consequently the vessels involved tend to be those most frequently used for catheterization. Other documented risk factors for the development of neonatal thrombosis include asphyxia, septicemia, dehydration, maternal diabetes and cardiac disease. Main laboratory findings for the diagnosis of hypercoagulable states, include shortened aPTT, decreased levels of inhibitors (AT III, Protein C and Protein S), increased resistance to activated protein C, defective fibrinolysis (basal and after stimuli), increased levels of clotting factors (fibrinogen, factor VII, factor VIII, etc.), increased and/or hyperactive platelets, increased whole blood and/or plasma viscosity, Antiphospholipid antibodies and presence of prothrombotic molecular defects like FV Leiden, P20210 and MTHFR. Approximately 4% and 2% respectively of Caucasians are heterozygous for these gene defects. Their causative role in neonatal thrombosis is unknown but they may have a contributory role in the pathogenesis of thrombosis in neonates.

Disseminated Intravascular Coagulation↗
PubMed1998

Variations and clinical significance of coagulation and fibrinolysis parameters in patients with diabetes mellitus.

We observed the changes of parameters of coagulation and fibrinolytic system in order to understand the clinical implication of these variations in type II diabetic patients. Subjects consisted of 22 patients with type II diabetes mellitus and 25 healthy controls. Compared with the control, activated partial thromboplastin time, prothrombin time were shortened in the patients. The diabetic subjects also displayed higher levels of D-dimer, serum fibrin degradation products, median concentrations of fibrinogen (3.99 vs 2.96 g/L, P < 0.01) and von Willebrand factor (149% vs 87%, P < 0.01). Levels of antithrombin III activity or antigen were not different from control values. Simple linear regression analysis revealed a negative correlation between antithrombin III activity and fast blood glucose. Diabetic patients with vascular complications had significantly higher levels of fibrinogen and D-dimer than those without diabetic angiopathy. Our data demonstrated that patients with type II diabetes mellitus had a hypercoagulable state. We believed the activation of coagulation might contribute to the vascular complications in diabetics.

Adult↗
PubMed1999

Detection of the level of urinary FPA in chronic nephritis with renal failure and its clinical implication.

The level of urinary FPA was assayed by high performance liquid chromatography (HPLC) in 42 normal controls, 57 cases of chronic glomerulonephritis, including 24 with normal renal function, 12 with renal insufficiency and 21 with uremia. Their levels were 24.40 +/- 10.30 micrograms/L, 26.99 +/- 5.77 micrograms/L, 38.81 +/- 6.28 micrograms/L, 79.74 +/- 18.76 micrograms/L, respectively. The level of urinary FPA in renal insufficiency function group was significantly higher than those of the control group and normal renal function group (P < 0.01). The patients with uremia presented dramatically higher level of urinary FPA than those in the renal insufficiency group (P < 0.01). A positive correlation was found between the level of urinary FPA and the blood creatine (r = 0.9120, P < 0.01). It was suggested that a hypercoagulable state existed in the patients with chronic nephritis with renal failure, in which the severity was closely related with the occurrence and development of the disease. The urinary FPA could serve as a good indicator for renal function.

Biomarkers↗
PubMed2001

Secondary mitral valve replacement in antiphospholipid syndrome and chronic renal failure.

A 48-year-old woman admitted with progressive dyspnea had previously been diagnosed with systemic lupus erythematosus, antiphospholipid syndrome, and chronic renal failure, and had undergone mitral valve replacement with a Carpentier-Edwards pericardial bioprosthesis for mitral insufficiency 9 years before. She suffered a cerebral infarction 5 years earlier, despite appropriate anticoagulant therapy. On admission, echocardiography showed severe bioprosthetic stenosis. Repeat mitral valve replacement was conducted using a Mosaic bioprosthesis. On postoperative day 2, when heparinization was commenced, she suddenly had an epileptic fit. She also developed ischemic necrosis of the fingers and toes, considered secondary to microthrombosis. Aspirin was administered and heparin replaced by warfarin sodium. Necrosis gradually disappeared, and she was discharged 3 months after surgery. The original bioprosthesis showed degenerative changes with significant thrombus formation on cusps, thought to be mainly due to her hypercoagulable state. Considering the thrombophilic tendency in patients with antiphospholipid syndrome, strict management of anticoagulant therapy is required.

Adult↗