Pathogenesis of venous thromboembolism.
ABSTRACT Three factors are related with the pathogenesis of venous thrombosis: (1) blood stasis, (2) hypercoagulability, and (3) vessel damage. Local and systemic factors are implicated in blood stasis. Remarkable advances have been recently achieved regarding the understanding of the concept of hypercoagulability, with special emphasis to thrombophilic molecular abnormalities. Increased thromboembolic risk has been described in patients with antithrombin III, protein C, or protein S deficiencies as well as factor V Leiden, prothrombin mutation G20210A, or hyperhomocystinemia. Vessel wall has a remarkable role in protecting against and in promoting thrombosis. The role of inflammation on venous thrombosis is under investigation.
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ABSTRACT: In COPD, the systemic effects of the disease reflect the structural and/or biochemical alterations occurring in the structures or organs other than the lungs in relation to the characteristics of the primary disease. The disorders of endothelial structures due to COPD may lead vascular pathologies, such as ischemic heart disease, stroke, to occur more commonly in those with COPD. On consideration of the fact that the vascular endothelium is a major site in which the systemic effect of the inflammation occurs, should von Willebrand Factor, a clotting factor of endothelium origin, and the plasma level of fibrinogen vary with the severity of the disease in COPD, the variability of arterial blood gas values, and the stability or exacerbation of the disease? Considering the fact that microalbuminuria is an indirect manifestation of the renal endothelial permeability and/or renal perfusion; should there be an association between microalbuminuria and the severity of COPD? Therefore, in order to assess the effect of the systemic inflammation in COPD on the vascular endothelium, we compared the levels of the plasma vWF, fibrinogen, 24-h urine microalbuminuria of those with stable COPD (33 patients) and exacerbation of COPD (26 patients) with those of the controls (16 healthy subjects). The mean age was 63.42 -/+ 10.29, 68.00 -/+ 9.77 and 59.63 -/+ 14.10 years in SCOPD, COPDAE, and CG, respectively. The level of microalbuminuria was found to increase significantly in COPDAE group, compared to that of the controls (P = 0.004). When we investigated the relation between smoking burden and microalbuminuria, vWF, fibrinogen levels, the amount of consumption and positive relationship were found significant. (r = 0.336, P = 0.003 between smoking pack-years and vWF, r = 0.403, P = 0.001 between smoking pack-years and fibrinogen, and r = 0.262, P = 0.02 between smoking pack-years and microalbuminuria). The levels of vWF and fibrinogen are AECOPD > SCOPD > CG, with the highest being in AECOPD, and the difference among the groups was statistically significant. The relationship between the level of hypoxemia and microalbuminuria, fibrinogen and vWF was found to be significant (r = -0.360, P = 0.005 between oxygen saturation and microalbuminuria, r = -0.359, P = 0.005 between the level of PaO(2) and fibrinogen, and r = -0.336, P = 0.009 between PaO(2) and vWF). In conclusion, the levels of plasma vWF, fibrinogen, and microalbuminuria may be helpful in grading the severity of COPD exacerbation. The related increase in these markers may represent a possible pathophysiological mechanism behind the increased vascular morbidity of patients with COPD and detecting indirectly the endothelial dysfunction as a manifestation of systemic outcomes due to COPD and in detecting earlier the cases in which the risk for developing the associated complications are higher. We suggest that further studies are necessary to investigate the impact of antithrombotic treatment on microalbuminuria, plasma vWF and fibrinogen as markers of endothelial dysfunction coexisting COPD exacerbation.Journal of Thrombosis and Thrombolysis 08/2007; 26(2):97-102. · 1.99 Impact Factor
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ABSTRACT: A 40-year-old male smoker presented with a 3-week history of painful digital infarction involving the hands. Histology was unhelpful, showing lichen simplex chronicus. A provisional diagnosis of a vasculitic disease was made. Treatment included aspirin, azathioprine, iloprost, methylprednisolone, nifedipine and prednisolone. After failure of these treatments an alternative clinical diagnosis of Buerger's disease was made. Treatment was to advise the patient of the importance of continuing to abstain from smoking, to perform bilateral video-assisted thoracoscopic sympathectomies and to commence folate supplementation. This led to marked improvement of his symptoms and healing of the digital infarction.Australasian Journal of Dermatology 06/2008; 49(2):94-7. · 0.97 Impact Factor
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ABSTRACT: The incidence of venous thrombosis (VT) increases sharply with age: it is very rare in young individuals (<1 per 10,000 per year) but increases to ∼ 1% per year in the elderly, which indicates that aging is one of the strongest and most prevalent risk factor for venous thrombosis. The cause of this steep age gradient is as yet, unexplained. The aim of this review was to provide an overview of studies on the effect of conventional risk factors as well as age-specific risk factors for thrombosis in the elderly. Limited data are available on risk factors for thrombosis in the elderly, i.e. all results are based on small study groups. Results indicate that, of the conventional risk factors, malignant disease, the presence of co-morbidities and the genetic risk factors factor (F)V Leiden and the prothrombin mutation seem to be associated with an increased risk of venous thrombosis. In the elderly, the population attributable risk (PAR) of malignancy is approximately 35%, for co-morbidities a PAR up to 25% is found, and the contribution of genetic risk factors to the thrombosis incidence is estimated to be 7-22%. Age-specific risk factors of thrombosis, i.e. endothelial dysfunction and frailty may be important in the explanation of the increased incidence of VT in the elderly. In conclusion, as aging is a major risk factor for thrombosis, further identification of the risk factors for thrombosis in the elderly is needed to elucidate the age gradient of the incidence of VT and to target preventive measures.Journal of Thrombosis and Haemostasis 10/2010; 8(10):2105-12. · 6.08 Impact Factor