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)

Serum level of vitamin K1 (= phylloquinone, hereinafter K1) and K dependent blood coagulation factors were determined by HPLC in normal subject, liver cirrhosis, hepatocellular carcinoma, acute hepatitis, chronic hepatitis, chronic renal failure with hemodialysis and patients under warfarin therapy. Normal range of serum K1 concentration was decided on 0.20-2.30 (0.87 +/- 0.53, n = 96) ng/ml. Serum K1 level showed no significant differences among normal subject, various diseases and warfarin therapy. Correlation between serum K1 level and F-VII (r = 0.879, p less than 0.001) or protein C activity (r = 0.839, p less than 0.01) was found in patients whose thrombotest was 20% and less. However serum K1 level didn't correlate with any K dependent coagulation factors in patients if thrombotest was over 20%.
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PMID:[Study on changes of serum vitamin K1 level and K dependent coagulation factors in patients with coumarin derivatives (warfarin) therapy]. 150 98

The cause of the thrombotic tendency in nephrotic patients is unknown. Recent reports of thrombotic complications in patients with deficiencies of protein C or protein S (natural inhibitors of coagulation) have raised the possibility that decreased levels of these proteins may play a role in the hypercoagulable state of nephrotic patients. We measured the levels of protein C, total protein S, and free protein S antigens in 42 patients (21 nephrotic and 21 non-nephrotic) with one of four types of glomerular pathology: diabetic nephropathy (DM), focal glomerular sclerosis (FGS), membranous glomerulonephritis (MGN), and chronic renal failure due to hypertension (CRF). Protein C and total protein S antigen levels were significantly higher in FGS and MGN than they were in DM or CRF. Free protein S levels were lower in DM than they were in MGN. Protein C, total protein S, and free protein S levels did not significantly correlate with either serum albumin or degree of proteinuria. The mean levels of the three proteins did not differ between nephrotic and non-nephrotic patients. Free protein S and protein C were, however, significantly correlated (P less than .005 and P less than .002, respectively) with the type of glomerular pathology, independent of differences in age, sex, serum albumin, or degree of proteinuria. These data suggest that abnormalities of free protein S and protein C are related to the nature of the underlying renal disease, rather than to the degree of proteinuria.
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PMID:Protein S and C antigen levels in proteinuric patients: dependence on type of glomerular pathology. 252 34

Longitudinal Cohort Study: Electrocardiogram and blood pressure were taken biannually along with history taking, physical examination and other laboratory studies. 6,690 subjects were included in this study in whom at least 7 out of 9 biannual check up examinations were performed. At the end of the study period, their ages ranged from about 40 to 90 years. The incidence of atrial fibrillation was about 0.2% in the forties and early fifties and increased to 0.6% by the late fifties. The incidence of atrial fibrillation was then increased almost linearly up to 2.5% at the end of the eighties. Likewise, incidence of CRBBB and LBBB was also increased with age even after the age of sixty; 1.0% at the fifties to 7.5% at the eighties in CRBBB and 0.05% at the fifties to 1.4% at the eighties in LBBB, respectively. Holter ECG Study: Holter ECG was recorded in 164 healthy subjects aged 14 to 87 years in whom no arrhythmias were found in the routine 12 leads ECG at entry to the study. In 96.9% of the subjects APC was recorded in the 24-hour Holter ECG irrespective of their age. The total number of APCs in 24 hours significantly increased with age, especially after age sixty. The incidence of couplet or short run APCs was 21.4% under age sixty and 74.2% above age sixty. Electrophysiologic Studies in Patients with Paroxysmal Atrial Fibrillation (Paf): Repetitive atrial firing (RAF) elicited by premature atrial stimulation, and prolonged intra-atrial electrogram (PAE) with multiple (more than 7) spikes recorded during sinus rhythm were taken as indicators of atrial vulnerability. RAF and PAE was observed in more than 60% of Paf patients with or without sick sinus syndrome (SSS), but only approximately 25% in the control group (without SSS). It was also noted that in patients with SSS, who were generally of old age, RAF was observed in about 63% even without Paf. These results suggest that the atrial vulnerability might be an expression of the common electrophysiologic properties of the atrial muscle in the elderly with atrial arrhythmias and/or SSS. Syncopal Episodes due to Transient Severe Hyperkalemia in the Elderly: Two patients with mild to moderate chronic renal failure developed transient severe hyperkalemia (9.9, 7.3 mEq/L, respectively), severe sinus bradycardia with sinus arrest and syncopal episodes. These transient findings almost completely improved in a few days by kayexatete and bicarbonate, and temporary back-up atrial pacing. Hyperkalemia was disproportionately severe compared to BUN and serum creatinine.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Arrhythmias in the elderly]. 267 51

Chronic renal failure causes elevations of factor VIII coagulant activity and Factor VIII-related antigen even before the patients enter chronic hemodialysis. The change from control of Factor VIII ristocetin cofactor does not reach significance. The elevations are not effected by entering onto hemodialysis. These parameters are the same for non-diabetic and diabetic patients. Protein C, plasminogen and total fibrinolytic capacity are normal in diabetic and non-diabetic patients, with or without hemodialysis for chronic renal failure. However, before entering onto hemodialysis some of these parameters had negative correlation coefficients with parts of the factor VIII complex among the diabetic and non-diabetic patients. These negative correlates turned positive after hemodialysis. Thus, there are differences in these catabolic mechanisms for factor VIII when hemodialysis is used for diabetic and non-diabetic patients with chronic renal failure.
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PMID:Factor VIII complex in chronic renal failure: influence of protein C, fibrinolysis and diabetes mellitus. 613 88

A pathogenetic role for fibrin deposition and platelet activation in the kidney is thought to play a role in the pathogenesis of acute renal failure (ARF). Thus, some fibrinolytic parameters and platelet function have been studied in 17 patients with ARF and compared to healthy volunteers and subjects with chronic renal failure (CRF). Since serotonin may participate in pathological processes resulting from platelet/vessel wall interactions, its level in the whole blood and plasma was also assayed. In ARF and CRF platelet aggregatory responses in both whole blood and in platelet rich plasma upon stimulation with various agonists (collagen, arachidonic acid, ADP, ristocetin) were lower than those obtained in healthy volunteers. Increased levels of lipoprotein (a), von Willebrand factor (vWF) and fibronectin were found in ARF relative to controls. Protein C activity was significantly lower in patients with ARF. Euglobulin clot lysis time was prolonged in ARF and CRF, reflecting a decreased overall fibrinolytic activity. Activity of tissue plasminogen activator (tPA) inhibitor (PAI) and PAI:Ag were higher in ARF, whereas tPA:Ag, urokinase, tPA/PAI complexes, thrombin-antithrombin complexes (TAT), plasmin-antiplasmin (PAP) complexes, fibrinogen, and F1+2 did not differ between ARF and controls. In CRF elevated levels of TAT, PAP, fibrinogen and prothrombin fragments F1+2 were found, whereas concentration of fibronectin was lowered when compared to controls. In both groups of renal failure patients increased levels of fibrin monomers and d-dimer were found relative to healthy volunteers. Whole blood serotonin was significantly lower, whereas plasma serotonin was significantly higher in patients with ARF and CRF relative to controls. Serotonin uptake and its release from platelets were markedly diminished in patients with ARF and CRF. Chronic renal failure exhibit a slightly different pattern of coagulopathies that acute renal failure.
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PMID:Hemostasis, platelet function and serotonin in acute and chronic renal failure. 887 44

To clarify the abnormalities of coagulation and fibrinolytic systems on predialysis patients with chronic renal failure, we measured indices of coagulation and fibrinolytic systems in 33 predialysis patients whose creatinine (Cr) levels were over 3.0 mg/dl. We termed twenty-four patients with chronic glomerulonephritis the "CGN group". We also termed nine patients wit diabetes mellitus the "DM group". We measured thrombin.antithrombin III complex (TAT), alpha 2-plasmin inhibitor plasmin complex (PIC), D-dimer, protein C, protein S, thrombomodulin (TM), vitronectin, tissue plasminogen activator.plasminogen activator inhibitor-1 complex (tPAI-C) in theses two groups. Furthermore, we measured the same indices after 6 months in the CGN group. As a result, the plasma levels of both TAT, PIC, TM/Cr ration in the DM group were significantly higher that those in the CGN group, changes in both protein S activities and plasma levels of tPAI-C were reduced significantly after 6 months. In conclusion, the abnormalities of coagulation and fibrinolytic systems in predialysis diabetic patients were stronger than those in predialysis patients with CGN. Furthermore, these abnormalities were worsened after 6 months in predialysis patients with chronic renal failure.
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PMID:[Study on coagulation fibrinolytic systems in predialysis patients with chronic renal failure--comparison between patients with chronic glomerulonephritis and patients with diabetic nephropathy]. 928 13

The study enclosed 30 dogs with severe or end stage chronic renal failure showing distinctly increased concentrations of urea and creatinine. In most of the 15 cases, where a pathologic-histological investigation of the kidney was carried out, a glomerulonephritis was observed (n = 11), partly accompanied by an interstitial nephritis or tubulonephrosis, respectively. Compared to the control group (n > or = 100) the most significant changes were the distinctly increased concentrations of fibrinogen (6.22 [2.95-11.83] g/l; median [minimum-maximum]) and activity of the coagulation factors V (median = 165%), VII (198%), X (176%), VIII:C (154%), and IX (178%) as well as of protein C (147%) (each: p < 0,0001 [Mann-Whitney-Test]). Thereby, the latter does not contribute to hypercoagulability in dogs with chronic renal insufficiency. The activity of antithrombin III was clearly diminished (69[41-112]%), and was closely correlated to the albumin concentration (r = 0.7000; p = 0.001) reflecting the joint renal loss of these proteins of nearly a size. Surprisingly a reagent dependent prolongation of the activated partial thromboplastin time appeared. Against that, a corresponding diminution of the activity of single coagulation factors was demonstrated only seldom, reaching only a small degree, and related almost exclusively to the contact activating system. Compared to the respecting reference range the concentrations of soluble fibrin or fibrin degradation products were increased in 15 or 21 (of 29) samples, and were, thereby, significantly higher than in the control group (p < 0.0001). This reflects the enhanced intravascular coagulation occurring possibly limited to the region of the renal alteration that should be more noticed in therapy.
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PMID:[Changes in hemostasis in dogs with chronic renal insufficiency]. 945 45

Genetic abnormalities in two metabolic steps in homocysteine degradation: transsulfuration and remetylation can cause raised plasma homocysteine concentration. Homocysteine appeared to be an independent arteriosclerotic risk factor in the coronary, cerebral and peripheral circulation and elevated homocysteine levels have been found in chronic renal failure patients undergoing hemodialysis treatment and in transplant patients as well. Homocysteine has a direct toxic effect on endothelial cells, reduces normal activation of protein C by endothelial cells, increases the binding of Lp(a) to plasmin-modified fibrin, induces tissue factor procoagulant activity and inhibits the cofactor activity of thrombomodulin. Treatment with folic acid and piridoxine can lower the high level of homocysteine and should be associated with a clinical benefit.
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PMID:[Homocysteine as a nonlipid factor in the pathogenesis of atherosclerosis]. 978 35

Calciphylaxis is a rare disorder of small-vessel calcification and cutaneous infarction associated with chronic renal failure. Rare cases of calciphylaxis not associated with chronic renal failure have been reported with breast cancer, hyperparathyroidism, and alcoholic cirrhosis. To our knowledge, we report the first case of calciphylaxis without chronic renal failure associated with cholangiocarcinoma and the first attempt to treat calciphylaxis with vitamin K. A 56-year-old woman presented with necrotic leg ulceration. She was treated initially with low-molecular-weight heparin, with no effect. A coagulation work-up showed vitamin K deficiency. During vitamin K therapy, the patient had fulminant progression of the calciphylaxis. She died, and an autopsy showed metastatic cholangiocarcinoma. Thrombosis and protein C deficiency have been implicated in the pathophysiology of calciphylaxis. Functional protein C deficiency may be one of several factors contributing to the development of calciphylaxis. Vitamin K therapy was ineffective in our patient and may have been detrimental.
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PMID:Calciphylaxis associated with cholangiocarcinoma treated with low-molecular-weight heparin and vitamin K. 1144 9

Hyperleptinemia is also common in chronic renal failure, particularly in CAPD. On the other hand, cardiovascular events related to thrombosis are a predominant cause of death and account also for an important morbidity in uremic patients. Treatment with recombinant human erythropoietin (rHuEPO) may shift the precarious hemostatic balance towards thrombosis. Therefore, the aim of the study was to assess the relationships between leptin and platelet aggregation and some hemostatic parameters in CAPD patients treated with rHuEPO. The study was performed on 15 patients maintained on CAPD given rHuEPO and 13 subjects without rHuEPO therapy served as a control group. Platelet aggregation was studied in both platelet-rich plasma (PRP) and in the whole blood. Tissue factor (TF) and tissue factor pathway inhibitor (TFPI) (antigens and activities), von Willebrand factor, trombomodulin, protein C, thrombin activatable fibrinolysis inhibitor (TAFI) and leptin (serum and dialysate) were assayed by using commercially available kits. Patients in both groups studied did not differ significantly with respect to age, BMI, duration of renal replacement therapy, and other hematological and hemostatic parameters studied as well as leptin serum and dialysate leptin. In CAPD patients treated with rHuEPO serum and dialysate leptin significantly correlated with tissue factor pathway inhibitor, protein C, thrombomodulin, ristocetin-induced platelet aggregation in the whole blood and PRP. In CAPD patients not treated with rHuEPO the significant correlations were observed between serum and dialysate leptin and protein C. Positive correlations between platelet aggregation and leptinemia in CAPD patients might indicate that hyperleptinemia could be associated with the cardiovascular disease in dialyzed patients. Leptin might contribute at least in part to the thrombotic complications observed in CAPD patients.
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PMID:Leptin correlates with some hemostatic parameters in CAPD patients. 1237 66


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