Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: EC:3.4.21.69 (APC)
 16,337 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The Progetto Lombardo Atero-Trombosi (PLAT) Study was a prospective, multicenter, multidisciplinary study of the association among hemostatic variables, conventional risk factors, and atherothrombotic events in four groups of patients with preexisting vascular ischemic disease (335 myocardial infarction survivors, 123 patients with stable angina pectoris, 160 with transient ischemic attacks, and 335 with peripheral vascular disease). In the myocardial infarction group, univariate analysis showed that atherothrombotic events were associated with high fibrinogen (p = 0.001), factor VIII:C (p less than 0.001), and von Willebrand factor antigen (vWF:Ag) (p = 0.004) levels and with low high density lipoprotein cholesterol (p = 0.043), factor VII (p = 0.019), and protein C (p = 0.044) levels; multivariate analysis produced associations with high fibrinogen and factor VIII:C levels and low protein C levels. By both univariate and multivariate analysis, events in the angina pectoris group were associated with high vWF:Ag (p = 0.026) and leukocyte (p = 0.033) levels and the presence of carotid arterial stenosis (p = 0.063); associations with high leukocyte (p = 0.037) and factor VIII:C (p = 0.186) levels, family history (p = 0.031), and diabetes (p = 0.061) were also found in the group with transient ischemic attacks. In those with peripheral vascular disease, events were associated with Fontaine stage greater than or equal to IIB (p = 0.024), high factor VIII:C levels (p = 0.073), and low protein C (p = 0.028), fibrinogen (p = 0.030), antithrombin III (p = 0.054), and factor VII (p = 0.057) levels by univariate analysis and with Fontaine stage and low fibrinogen levels by multivariate analysis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:The PLAT Study: hemostatic function in relation to atherothrombotic ischemic events in vascular disease patients. Principal results. PLAT Study Group. Progetto Lombardo Atero-Trombosi (PLAT) Study Group. 152 21

Pulmonary embolus can have insidious onset and unusual etiology. This case report of a 35-year-old woman with hyperthyroidism, atrial fibrillation, and an above-knee amputation demonstrates the subtle presentation of pulmonary emboli. On the rehabilitation ward of a tertiary care hospital, the patient developed undulating fever to 39.6C, rapidly worsening peripheral vascular disease, and pulmonary emboli. Eventually, a protein C deficiency was found; institution of appropriate therapy resulted in rapid improvement. This case reminds physiatrists to evaluate thoroughly the cause of pulmonary thrombi. Currently available assays permit rapid elucidation of factor deficiencies in the workup of the hypercoagulable state.
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PMID:Above-knee amputation with insidious pulmonary embolism and hypercoagulability secondary to protein C deficiency. 277 90

Blackfoot disease is a peripheral vascular disease causally related to the fluorescent humic acid found in the drinking water of endemic areas in Taiwan. We compared the effects of humic acid (HA) purified from the well water of Blackfoot disease endemic areas with the effects of commercial humic acid (Aldrich) as well as trivalent arsenic (As2O3) on protein C activity, which plays an important role in regulation of blood coagulation and fibrinolysis. Humic acid, either purified from drinking water or obtained commercially, dose-dependently inhibited both activated protein C activity and the activation of protein C induced by Protac, a snake venom-derived protein C activator. In contrast to humic acid, arsenic oxide dose-dependently enhanced both activated protein C activity and the Protac-stimulated activation of protein C. In the presence of humic acid the enhancement effect of arsenic oxide was completely abolished, resulting in concentration-dependent inhibition of protein C activity. Therefore, the results of this study indicate that humic acid is a potent protein C inhibitor even in the presence of arsenic, which enhances the protein C activity. Since protein C is a potent anticoagulant and profibrinolytic agent, acquired defects of protein C induced by humic acid might cause a thrombophilic or hypercoagulable state. Whether this is one of the possible mechanisms of humic acid-induced thrombotic disorders in Blackfoot disease needs to be further characterized.
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PMID:Plasma protein C activity is enhanced by arsenic but inhibited by fluorescent humic acid associated with blackfoot disease. 803 75

Hypercoagulable states are found in up to 10 per cent of patients with a history of unexplained venous thrombosis. To investigate the prevalence in arterial thrombosis, thrombophilia screening was performed on 124 patients who had previously undergone lower-limb revascularization, 45 claudicants and 27 controls. Of the patients who had undergone revascularization 40 per cent had a hypercoagulation abnormality (low levels of protein C, protein S and antithrombin III or presence of the lupus anticoagulant) in comparison with 27 per cent of claudicants and 11 per cent of controls (P < 0.01). Furthermore, patients who had suffered reocclusion after revascularization were significantly more likely to have a hypercoagulation abnormality than those who had not (P < 0.05), even if the occlusion had occurred more than 6 months previously. Lupus anticoagulant was the abnormality most frequently detected and, like low protein C levels, was found only in patients with peripheral vascular disease. It appears that hypercoagulable states are common in patients with arterial disease and may predispose to failure of revascularization.
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PMID:Hypercoagulable states in patients with leg ischaemia. 804 89

Diabetic patients have increased morbidity and mortality attributable to myocardial infarction, cerebrovascular disease and peripheral vascular disease, due to a high incidence of premature atherosclerosis. Abnormalities of hemostasis have been reported in many studies on diabetes over almost thirty years, but unfortunately the results have often appeared contradictory. The hemostatic alterations could lead to increased risk of vascular disease in diabetic patients. We have studied some coagulation factors (Fibrinogen, Factor II, Factor VII) and coagulation inhibitors (Protein C, Protein S), and plasminogen in fifty-four type 2 diabetic patients. The possible relationship between coagulation factors and coagulation inhibitors and parameters for glyco-metabolic control (glycosylated hemoglobin, fructosamine) and disturbed lipid metabolism (cholesterol, triglycerides) have ben analyzed. Our results show increase of fibrinogen, correlated with the metabolic control of the disease, positive correlation between plasminogen, factor II, protein S and hypertriglycerides, decreased levels of protein C correlated neither with metabolic control of disease neither with disturbed lipid metabolism.
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PMID:[Evaluation of the coagulation and fibrinolysis system in 54 patients with type 2 diabetes mellitus: correlations with lipid metabolism and blood glucose control]. 876 54

Activated protein C resistance caused by factor V Leiden is an important thrombophilia disorder which predisposes to venous thromboembolism. Some studies also suggest a role in the pathogenesis of arterial thrombosis and atherosclerosis. The authors have investigated the prevalence of activated protein C resistance and factor V Leiden in a series of 45 patients with peripheral vascular disease. Twelve patients were receiving warfarin. The activated protein C resistance ratios were significantly lower in the group of 33 non-warfarinized patients with peripheral vascular disease (median 2.82 (range 1.36-3.83)) compared with 33 age- and sex-matched controls (median 2.97 range 2.24-4.11); P<0.005; Wilcoxon rank sum). Eight patients (24%) had activated protein C resistance (ratio <2.2). The prevalence of factor V Leiden in patients with peripheral vascular disease was 17.8% (8/45). This is significantly increased compared with the local population and UK published frequency of 3.5% for this genotype. The presence of factor V Leiden did not affect the late outcome of arterial reconstructive surgery in terms of graft patency (P=0.5, Fisher's Exact test).
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PMID:Activated protein C resistance, factor V Leiden and peripheral vascular disease. 921 1

Beriplex, a prothrombin complex concentrate (PCC), was administered to 42 patients requiring immediate reversal of their oral anticoagulant therapy. The dose administered was determined using the pretreatment International Normalized Ratio (INR). Blood samples were obtained before treatment and at 20, 60 and 120 min after treatment. The following investigations were performed on all samples - INR, clotting factors II, VII, IX and X, coagulation inhibitors protein C (PC) and antithrombin (AT), and other markers of disseminated intravascular coagulation, plasma fibrinogen, D-dimer and platelet count. Immediate reversal of the INR, the vitamin K-dependent clotting factors and PC was achieved in virtually all patients. Reduced AT levels were present in 18 patients before treatment. Further slight AT reductions occurred in four patients, but other associated abnormalities of haemostasis were observed in only one of the four patients. One patient with severe peripheral vascular disease, sepsis and renal and cardiac failure died of a thrombotic stroke following leg amputation, 48 h after receiving Beriplex. No other arterial and no venous thromboembolic events occurred within 7 d of treatment. Beriplex is effective in rapidly reversing the anticoagulant effects of warfarin, including PC deficiency, without inducing coagulation activation. Caution should continue to be exercised in the use of these products in patients with disseminated intravascular coagulation, sepsis or liver disease.
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PMID:Rapid reversal of oral anticoagulation with warfarin by a prothrombin complex concentrate (Beriplex): efficacy and safety in 42 patients. 1184 21

There is limited evidence that certain heritable thrombophilias may be associated with an increased risk of peripheral vascular disease. In particular, increased activated protein C resistance and FV Leiden have been described as being more prevalent in patients with peripheral arterial disease. There is no clear evidence at present, however, that other heritable thrombophilias are associated with an increased risk of arterial occlusive disease. Heritable thrombophilia, in particular FV Leiden, may be associated with an increased risk of vascular reconstruction failure but there is a lack of evidence to show that intervention with anticoagulants influences the outcome of graft surgery in these patients.
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PMID:Inherited thrombophilia. 1567 88

To determine whether exercise increases endothelial progenitor cells (EPCs) in patients with peripheral vascular disease, we developed a multi-parameter flow cytometry assay to rigorously assess EPCs and mature endothelial cells (ECs) in control subjects and patients with peripheral artery disease (PAD) subjected to graded exercise. Blood was collected from young healthy subjects (n = 9, mean age 33 years), older healthy subjects (n = 13, mean age 66 years), and older subjects with PAD (n = 15, mean age 69 years) before and 10 minutes after exercise. White blood cells were isolated and stained with a five-color antibody panel: FITC-anti-CD31, PE-anti-CD146, PE-anti-CD133, PerCP-Cy5.5-anti-CD3,-CD19,-CD33, PE-Cy7-anti-CD34, and APC-anti-VEGF-R2. Viability was assessed by propidium iodide exclusion. Viable, low, side scatter singlets that were CD3-, 19-, and 33-negative were counted. While baseline levels of EPCs and ECs were similar among all subjects, young healthy subjects demonstrated significantly greater (p < 0.05) levels of progenitor cells (PCs) than older healthy and PAD subjects. Levels of EPCs and ECs tended to increase in all subjects after exercise; however, increases in PCs were only observed in young healthy and PAD subjects. Further, trends in the magnitude of change of subsets with exercise were most similar between young and PAD subjects. Our findings suggest that aging may reduce baseline circulating levels of PCs, but not EPCs or ECs, and that exercise-induced mobilization of subsets may differ depending on age and presence of PAD.
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PMID:Effect of acute exercise on endothelial progenitor cells in patients with peripheral arterial disease. 1739 May 50

Many factors contribute to the pathogenesis of leg ulcer. Most patients have venous leg ulcer due to chronic venous insufficiency. Less often, patients have arterial leg ulcer resulting from peripheral arterial occlusive disease, the most common cause of which is arteriosclerosis. Leg ulcer may be of a mixed arteriovenous origin. In diabetic patients, distal symmetric neuropathy and peripheral vascular disease are probably the most important etiologic factors in the development of diabetic leg ulcer. Other causes of chronic leg ulcers are hematologic diseases, autoimmune diseases, genetic defects, infectious diseases, primary skin diseases, cutaneous malignant diseases, use of some medications and therapeutic procedures, and numerous exogenous factors. Diagnosis of leg ulcer is based on medical history, inspection, palpation of skin temperature, palpation of arteries, fascia holes, presence and degree of edema, firm painful cords, and functional testing to assess peripheral occlusive arterial disease or identify superficial and deep venous reflux of the legs. Knowledge of differential diagnosis is essential for ensuring treatment success in patients with leg ulcer. There are many possible etiologic factors of leg ulcers and sometimes, clinical findings are similar. Additional testing should be performed, e.g., serologic testing such as blood count, C-reactive protein, HBA1c, erythrocyte sedimentation rate, differential blood count, total proteins, electrolytes, coagulation parameters, circulating immune complex, cryoglobulins, homocysteins, AT, PAI-1, APC resistance, proteins C and S, paraproteins, ANA, ENA, ANCA, dsDNA, antiphospholipid antibodies, urea, creatinine, blood lipids, vitamins and trace elements. Also, biopsy of the lesion for histopathology, direct immunofluorescence, bacteriology and mycology should be included. Other tests are Raynaud (cold stimulation) test and pathergy test. Device-based diagnostic testing should be performed for future clarification. Ankle brachial pressure index, color duplex sonography, plethysmography, MSCT and MR angiography, digital subtraction angiography, phlebography, angiography, x-ray, and capillaroscopy in lupus erythematosus are indicated. Except for bacteriologic analyses of wound biopsies, there is no test to provide specific information on the wound condition.
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PMID:[List of diagnostic tests and procedures in leg ulcer]. 2437 72


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