Type Of Thrombosis Research Articles

Differential Diagnosis of Lemierre's Syndrome in a Patient with Acute Paresis of the Abducens and Oculomotor Nerves

Lemierre's syndrome is characterized by anaerobic septicemia, internal jugular vein thrombosis, and septic emboli associated with infections of the head and neck. We describe an unusual and clinically confusing case of a young woman with an acute paresis of the abducens nerve and partial paresis of the right oculomotor nerve. After an extensive imaging diagnostic procedure, we also documented a peritonsillar abscess and various types of thromboses in intracranial and extracranial veins. Furthermore, we found brain and lung abscesses, which led us to establish the diagnosis of Lemierre's syndrome. Despite intensive anti-coagulation and antibiotic therapy, the patient developed a mycotic aneurysm in the right internal carotid artery directly adjacent to the previously thrombosed cavernous sinus. In summary, we were able to confirm that Lemierre's syndrome may occur in conjunction with uncharacteristic symptoms. Due to the sometimes confusing clinical symptoms as well as clinical and radiological specialties, we had to work on an interdisciplinary basis to minimize the delay prior to establishing the diagnosis and therapy.

Polymorphisms in platelet glycoproteins Ia and IIIa are associated with arterial thrombosis and carotid atherosclerosis in type 2 diabetes

To determine the genotype distributions of the polymorphisms in platelet glycoproteins (GP) Ib-alpha, Ia/IIa and IIb/IIIa and their association with clinical arterial thrombosis and preclinical carotid atherosclerosis in type 2 diabetes we studied 229 patients with type 2 diabetes and 229 controls matched by age, gender and ethnicity. Biochemical and haemostasis analyses were performed. The GP Ib-alpha VNTR, GP Ia 807 C/T and GP IIIa Pl(A) polymorphisms were determined by PCR. Thrombotic events were registered and carotid atherosclerosis was evaluated by ultrasound examination. A total of 107 patients had clinical atherothrombosis (CA), 65 subclinical atherosclerosis (SA), and 57 had no evidence of atherosclerosis (NA). There were no differences in allele frequencies and the genotype distribution of platelet GP polymorphisms between diabetic patients and controls. The VNTR Ib-alpha polymorphism was not associated with CA. We found a significant association between CA and the 807T (odds ratio [OR]: 2.86, confidence interval [CI]: 1.65-4.93; p<0.001) and PlA2 (OR: 2.03, CI: 1.13-3.65; p=0.03) alleles (in GP Ia and GP IIIa, respectively) in comparison to SA and NA group. Diabetic patients with the coexistence of the 807T and PlA2 alleles presented the highest risk of CA (OR: 3.59, CI: 1.64-7.8; p<0.001). The coexistence of both 807T and PlA2 alleles was also associated with the presence of SA (OR: 9.00, CI: 1.10-73.42; p=0.04). In conclusion, the 807T allele of GP Ia and the PlA2 allele of GP IIIa, and specially its combination, may confer an additional risk for development of carotid atherosclerosis and arterial thrombosis in type 2 diabetes.

Polyurethane foam treatment of type II endoleaks promotes endoleak thrombosis and eliminates intraaneurysmal pressure in the canine model

Introduction: The impact on intraaneurysmal pressure of treatments for retrograde-collateral perfusion of AAA after endovascular repair (type II endoleak) has not been evaluated. Using a canine model the effect of polyurethane induced thrombosis of type II endoleaks was measured. Methods: Prosthetic aneurysms with multiple collateral branches (lumbar, caudal mesenteric) were created in the infrarenal aorta of 10 mongrel dogs. Type II endoleaks were generated by excluding the aneurysm from antegrade arterial flow with an impermeable stent graft. Implantation of thrombogenic polyurethane foam (reticulated polycarbonate scaffold, pores 250–600um) was performed in 4 animals via a transfemoral catheter delivery system. In 4 control animals no side branches and no endoleaks were present. Intra-aneurysmal and systemic pressures were measured using a solid-state, strain gauge pressure transducer for 14 days before and 30–90 days after stent graft exclusion. Results: Type II endoleaks generated considerable intraaneurysmal pressurization that was significantly reduced from systemic pressure (P < 0.001)(table). Treatment with polyurethane foam induced thrombosis of the endoleak and feeding arteries in all 4 animals. It resulted in nearly complete elimination of intraaneurysmal pressure (P < 0.001) making it indistinguishable from control aneurysms with no endoleaks (P = NS). Cine MRA, Duplex and angiography documented persistent patency up to the time of euthanasia (mean, 64 days) for untreated type II endoleaks and confirmed thrombosis of polyurethane treated endoleaks. ∗. Systolic pressure∗ Mean pressure∗ Pulse pressure∗ Endoleak patency Patent type II endoleak 0.702 0.784 0.406 Patent Polyurethane treated type II endoleak 0.183 0.142 0.054 Thrombosed Control (no endoleak/no branches) 0.172 0.137 0.089 Thrombosed Systemic pressure 1.0 1.0 1.0 NA p value (patent vs polyurethane treated) <0.001 <0.001 <0.001 <0.001 ∗ All pressures listed were measured after antegrade AAA exclusion and are indexed as a percentage of the systemic pressure. Conclusions: Untreated type II endoleaks result in intraaneurysmal pressures 70–80% of systemic pressure. Thrombosis of endoleaks by polyurethane foam occurs rapidly and results in near abolition of intraaneurysmal pressure.

Hyperhomocysteinaemia and risk of thrombosis in systemic lupus erythematosus patients.

Hyperhomocysteinaemia is strongly associated with increased relative risk of occlusive vascular disease, mainly of the carotid and coronary arteries. The aim of our study was to assess whether raised plasma homocysteine is a risk factor for thrombotic events in patients with systemic lupus erythematosus (SLE), a condition known to be associated with premature atherothrombotic complications. The study included 34 consecutive consenting SLE patients who were seen in the Rheumatology Unit of Al-Amiri hospital, one of the main teaching hospitals in Kuwait. Twenty consenting healthy subjects were included in the control group. Twenty-four patients were grouped as SLE without thrombosis and 10 had different types of thromboses. Vitamin B(12), folate, anticardiolipin antibodies (IgG and IgM), activated partial thromboplastin time (APTT) and total homocysteine level were measured for both patients and controls. A raised homocysteine concentration was defined as plasma homocysteine level above 9.4 mmol/l. Hyperhomocysteinaemia was found in 21 (61.8%) SLE patients. Low levels of folate and vitamin B(12) were significantly associated with high concentrations of plasma homocysteine (r = -0.35 and -0.39, respectively, P<0.01). SLE patients with elevated homocysteine concentration have a threefold increase in odds ratio of thrombotic events after adjusting for other risk factors (male sex, shortened APTT, treatment with prednisone, low folate and vitamin B(12) levels). We concluded that homocysteine is an independent risk factor for thrombosis in patients with SLE and is potentially modifiable.

Multifactorial aspects of the treatment of the type II diabetic patient

People with type II diabetes have a twofold to fourfold increased risk of dying from the complications of cardiovascular disease. Atherosclerosis and vascular thrombosis are major contributors. The increased risk is present before fasting hyperglycemia is seen. These individuals often have a sedentary life-style, poor physical conditioning, insulin resistance, centripetal obesity, hypertension, dyslipidemia, and a prothrombotic state. Chronic hyperglycemia is then added to these risk markers. Microalbuminuria may precede hyperglycemia in type II diabetes, occurs in 30% to 40% of these individuals after diabetes is established, and is a predictor of cardiovascular events. Early intervention in high-risk individuals may delay or prevent fasting hyperglycemia. An all-inclusive approach that focuses on early risk factor (or marker) identification and management to prevent or delay accelerated atherosclerosis and thrombosis in type II diabetes is an attractive strategy. However, the database to support this strategy is limited. In particular, large-scale prospective trial data are not available to support the concept of intensive glycemic regulation to prevent progression of macrovascular disease in type II diabetes. This is in contrast to the situation regarding microvascular disease of the eyes and kidneys. Recently, indirect data of a correlative nature have emerged, and short- and long-term prospective trials at early and late stages of type II diabetes are now being reported. These studies are analyzed and interpreted in this report. In contrast, the database to support an intensive antiplatelet regimen to prevent vascular thrombotic events in people with type II diabetes is large, and these studies are reviewed. They are of a type and magnitude to allow definite recommendations for aspirin therapy in type II diabetes. Aggressive therapy directed at hypertension, hyperlipidemia, and elevated urinary albumin in people with type II diabetes appears to be indicated. Increased attention to the multifactorial aspects of treatment of the type II diabetic patient is needed. Our present challenge is to translate these findings for patients and primary health care providers so that effective actions may be implemented.

Type I Congenital Plasminogen Deficiency Is not a Risk Factor for Thrombosis

The risk of thrombosis in type I congenital plasminogen (PLG) deficiency has been suggested, but is still not confirmed. We studied 40 members of two unrelated families with this disease, and found that 21 were heterozygotes of type I congenital PLG deficiency. Three of them had thrombosis, but the other 18 had no thrombosis. The percentages of family members with no history of thrombosis up to a given age among subjects with type I congenital PLG deficiency and healthy controls were analyzed by the Kaplan-Meier method. No significant difference between the two groups was observed by the generalized Wilcoxon test (p = 0.23). These results suggest that there is no significant correlation between type I congenital PLG deficiency and thrombosis.

NERVOUS REGULATION OF CLOTTING MECHANISM

In a previous communication 1 I described a simple clinical test of the clotting mechanism which consists of the injection of 10 mg. (1 cc.) of purified heparin intravenously and the determination of capillary coagulation times before and ten, twenty, thirty and forty minutes after the injection. It was found that the reaction to heparin is rather constant in the normal person but that it significantly changes to a diminished response in the first few days after major operations, in Buerger's disease and following all types of thromboses. Under the influence of sulfur compounds the hyporeactivity to heparin could be temporarily corrected. 2 In this report I wish to submit some observations regarding the effect of autonomic nervous stimuli on the heparin curve. Cannon and his co-workers 3 have convincingly shown that epinephrine injected in small amounts intravenously or in larger doses subcutaneously will shorten the coagulation time from one