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

Haemostatic changes in 16 patients with Crohn's disease were studied from active disease into clinical remission and beyond. Elevated concentrations of fibrinopeptide A (FpA) and prothrombin fragments F1 + 2 (F1 + 2) were found at times of both active (FpA median 3.2, range [0.3-40] ng/ml and F1 + 2 median 2.3, range [0.3-18] nm/l) and inactive disease (FpA median 2, range [0.4-40] ng/ml and F1 + 2 median 1.3, range [0.2-20) nm/l]. We also measured the physiological inhibitors of coagulation and fibrinolysis; there was no significant difference in the levels of antithrombin III, protein C or the Exner ratio between active and inactive disease. Free protein S levels were significantly lower in active disease (median 34, range 9-54 U/dl) than in remission (median 40, range 12-65 U/dl). Plasminogen activator inhibitor type 1 (PAI-1) was significantly raised in remission (median 11, range 3-32 ng/ml) when compared to active disease (median 7, range 3-42 ng/ml). The D-dimer correlated significantly with fibrinopeptide A (P < 0.001), suggesting reactive fibrinolysis in some patients. Most (35/52, 67%) samples showed evidence of persistent haemostatic activation (elevated FpA and/or F1 + 2) during phases of apparent clinical remission in Crohn's disease, a factor that is not reflected by clinical activity scores. This study supports the hypothesis that coagulation is activated in the mesenteric vasculature of patients with Crohn's disease.
 ...
PMID:Evidence for activation of coagulation in Crohn's disease. 148 98

Following liver transplantation, the decision to retransplant in cases in which graft function is marginal must be taken early. Plasma coagulation factor monitoring was evaluated as an early predictor of graft failure requiring retransplantation in the first posttransplant week. Plasma levels of fibrinogen, factors V, VII, VIII, IX, antithrombin III, protein C, and plasminogen were measured in all patients at 0, 12, 24, 48, 72, 96, and 120 hours posttransplant in 46 patients who received 56 grafts and results were compared between livers that failed early (group 1) and those that functioned adequately (group 2). Six grafts were included in group 1: one patient died before retransplantation, four were retransplanted once, and one patient was retransplanted twice. Three grafts had primary nonfunction (PNF), 2 had obstructed portal veins, and 1 had a long period of warm ischemia during the initial transplant. In group 1, plasma levels of factor V were significantly lower than in group 2 at 24, 48, and 72 hours posttransplant (21.2% +/- 14.2%, 12.4% +/- 4.5%, and 13.0% +/- 5.0% v 39.1% +/- 23.9%, 48.8% +/- 31.9%, and 60.9% +/- 25.9%; P less than .05, P less than .01, and P less than .005, respectively). Similarly, plasma levels of factor VII were significantly lower in group 1 over the same period of time (7.3% +/- 2.7%, 4.2% +/- 1.8%, and 4.7% +/- 2.5% v 27.4% +/- 17.1%, 34.1% +/- 21.6%, and 34.8% +/- 18.6%, respectively; P less than .005).(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Coagulation plasma factor levels are early indicators of graft nonfunction following liver transplantation in children. 150 Oct 1

The levels of protein C (PC) and antithrombin III (AT III) antigens (ag) were measured in the plasma of 39 patients with various histologic types of primary nephrotic syndrome (NS) and in 12 patients with amyloidosis secondary to familial Mediterranean fever (FMF). The controls comprised 15 healthy children. Normal or elevated PC levels were observed in primary NS patients (mean 64%, range 36-98%) and in amyloidosis patients (mean 58%, range 48-70%). There was no difference found between PC ag levels in primary NS and in amyloidosis patients. In addition, no correlation existed between protein selectivity and the PC ag levels in the primary NS patients. Normal and decreased levels of AT III were observed (mean 29 mg/dl, range 11.1-39 mg/dl) in the patients with primary NS and amyloidosis (mean 31 mg/dl range, 21-39 mg/dl). The AT III ag levels of these two groups did not differ and no correlation was found between protein selectivity and AT III levels in primary NS patients. These results suggest that in patients with primary NS, or amyloidosis secondary to FMF, hypercoagulability is not related to a deficiency in PC ag levels due to a dynamic balance between urinary losses, increased rate of hepatic synthesis, catabolism and the distribution of PC in the body compartments. Patients with low AT III levels may be more susceptible to thromboembolic complications than patients with normal levels.
 ...
PMID:Evaluation of the hypercoagulable state by measuring protein C and antithrombin III levels in nephrotic syndrome and in familial Mediterranean fever-related amyloidosis. 150 25

Previous studies of patients with thromboembolic disease have revealed an association either with hereditary anticoagulant protein deficiencies or with defects in the fibrinolytic system. To obtain a more comprehensive picture and to investigate which analyses are useful in the evaluation of such patients, we have performed an extensive laboratory investigation in 439 individuals with thromboembolic disease. Anticoagulant protein deficiencies were found in 24 patients. Deficiencies of protein C (n = 10) and protein S (n = 9) were most common followed by deficiencies of antithrombin III (n = 3) and plasminogen (n = 2). Six of the nine protein S deficient patients demonstrated a selective deficiency of free protein S with normal total protein S concentrations. To diagnose protein C and S deficiencies among the 201 patients receiving oral vitamin K antagonists, the concentrations of protein C and S were compared with the mean concentration of several other vitamin K-dependent proteins. One protein C and three protein S deficiencies were identified among the treated patients. The number of protein C deficiencies found in this group was significantly lower than the number found among untreated patients. Although fewer protein S deficiencies were also identified among the treated patients, than in the untreated group, the difference was not statistically significant. The results suggest that protein C deficiencies went undetected in the treated group and that oral anticoagulant therapy should be discontinued before efforts to diagnose protein C deficiency are made. We found no cases with heparin cofactor II deficiency. Lupus anticoagulant was present in 10 patients.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Thromboembolic disease--critical evaluation of laboratory investigation. 832 78

Four hemodialysis patients (1 male and 3 females, aged 29-40 years) with unusual recurrent vascular access or dialyzer thrombosis were studied to find out whether a hypercoagulable state exists. Measurements of euglobulin clot lysis time (ELT), fibrinogen, antithrombin III (AT III), protein C (PC), protein S (PS), tissue plasminogen activator (tPA), and plasminogen activator inhibitor (PAI) were done. Results indicated that all patients had prolonged ELT, low tPA, elevated PAI, normal AT III, and PS. Three patients had elevated fibrinogen level and two had low PC. Danazol 200 mg orally once a day effectively prevented any further thrombosis. In 4 weeks' time, all the abnormal coagulation studies normalized in addition to elevation of AT III, PC and PS. Only 1 female patient had a prolonged menstrual period, which was reversed by lowering the daily dose of danazol to 100 mg. No other side effects were encountered. These data indicate that hypofibrinolysis may play a major role in vascular access or dialyzer thrombosis and that low-dose danazol may provide an effective prophylaxis and treatment. Larger controlled studies are needed to confirm these findings.
 ...
PMID:Low-dose danazol for vascular access and dialyzer thrombosis in hemodialysis patients. 152 23

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)
 ...
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

Hereditary deficiency of protein C, protein S or antithrombin III has been associated with an increased incidence of venous thrombosis or pulmonary embolism. The relationship between these deficiencies and the development of arterial thrombosis is a matter of current investigation. We retrospectively studied the occurrence of arterial thrombosis in 92 symptomatic patients belonging to a group of 160 with a confirmed diagnosis of hereditary deficiency of one of the physiologic clotting inhibitors. Seventeen of them experienced at least one arterial thrombotic event. This indicates that about one out of five of the symptomatic patients had experienced arterial thrombosis. The control group consisted of 92 sex and age matched (+/- 5 years) patients with no clotting deficiency who had experienced in the same period at least one episode of deep vein thrombosis or pulmonary embolism. Only one of them had developed arterial thrombosis. Ischemic stroke, myocardial infarction, upper and lower limb arterial thrombosis, and mesenteric artery occlusion occurred regardless of the type of defect taken into account; mean age of about 37.05 +/- 23 years (mean +/- SD). In some cases, arterial thrombosis was fatal. The overall number of venous thrombotic events in the 92 symptomatic patients of this study was much higher than that of arterial thrombosis, with a ratio of 24 to 1. The use of long-term anticoagulant therapy in our group of patients seemed to be able to prevent recurrences of both arterial and venous thrombosis.
 ...
PMID:Occurrence of arterial thrombosis in a cohort of patients with hereditary deficiency of clotting inhibitors. 153 14

We examined the relationship between free protein S deficiency and cerebrovascular disease by reviewing the records of all patients with the diagnoses of cerebral thrombosis, cerebral embolism, and cerebral vascular occlusion who were referred for coagulation studies over a 12-month period. We assayed for free protein S antigen, protein C antigen, and antithrombin III and tested for lupus-like anticoagulant and anticardiolipin antibody. Twenty-two of 267 patients (8.2%) admitted with thrombotic strokes were referred for coagulation studies. Free protein S antigen was significantly lower in women than in men (62 +/- 25% versus 88 +/- 24%, p = 0.03; n = 11 in each group). Six women had free protein S antigen levels below the range recorded for a contemporary group of 24 age-matched normal women (17 to 59% versus 70 to 102%, p less than 0.001); four of these women had cerebral arterial thrombosis and two had venous dural sinus thrombosis. The six women were aged 29 to 55 at the time of their first strokes; two had family members with protein S deficiency, and one of these had died of a stroke at age 52. Other abnormalities in this population included a positive test for lupus-like anticoagulant or anticardiolipin in five patients, a modest decrease in protein S in two men, and one patient with an isolated deficiency of antithrombin III. We conclude that protein S deficiency may be an important risk factor for stroke in middle-aged women but this requires confirmation by prospective studies in unselected patients.
 ...
PMID:Protein S deficiency in middle-aged women with stroke. 153 5

To investigate levels of coagulation inhibitors in sera from patients with Clostridium difficile-associated diarrhoea and colitis, commercially available antigen assays were used for immunochemical determination of antithrombin III, protein C and free protein S. Sera from patients with Clostridium difficile-associated diarrhoea and colitis showed significantly lowered levels of all measured inhibitors as compared to controls (Student's t test). Protein C (mean +/- SD): 0.70 +/- 0.30 vs. 1.28 +/- 0.23, t = 6.61, p less than 0.001; antithrombin: 0.70 +/- 0.21 vs. 0.90 +/- 0.17, t = 3.12, p less than 0.01; free protein S: 0.27 +/- 0.06 vs. 0.37 +/- 0.08, t = 3.7, p less than 0.001. Infection with C. difficile may lead to loss of coagulation inhibitors and constitutes a risk for thromboembolic complications.
 ...
PMID:Low levels of coagulation inhibitors in patients with Clostridium difficile infection. 153 51

In 107 asymptomatic and untreated patients with inherited syndromes associated with thrombophilia (antithrombin III, protein C and protein S deficiencies), we compared in parallel two plasma peptides which reflect activation of the common coagulation pathway: the prothrombin fragment 1 + 2 (F1 + 2) and fibrinopeptide A (FPA). Both F1 + 2 and FPA were measured with simple, commercially available ELISA methods. High levels of F1 + 2 or FPA were found in about one fourth of the patients as a whole. When patients were divided according to the type of inherited thrombophilic syndrome, it appeared that F1 + 2 was more frequently elevated in protein C and protein S deficiencies than in antithrombin deficiency; and that, in general, it was no more frequently elevated than FPA. Although our data confirm the existence of a procoagulant imbalance in inherited thrombophilic syndromes due to defects of natural anticoagulant proteins, they do not confirm that such imbalance can be more frequently diagnosed by measuring F1 + 2 levels, particularly in patients with antithrombin deficiency.
 ...
PMID:Markers of procoagulant imbalance in patients with inherited thrombophilic syndromes. 153 36


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>