Influence of blood collection systems on coagulation tests.

OBJECTIVE: Coagulation tests are influenced by pre-analytic conditions such as blood collection systems. Change of glass collection tubes with plastic ones will cause alteration of the test results. The aim of this study was to compare three plastic blood collection tubes with a standard glass blood collection tube and each plastic collection tube with the other two for possible additional tube-to- tube differences. MATERIAL AND METHODS: A total of 284 blood samples were obtained from 42 patients receiving warfarin during their routine controls, besides 29 healthy volunteers. Subgroup analyses were done according to health status. RESULTS: Our study demonstrated that different blood collection tubes have a statistically significant influence on coagulation tests. The magnitude of the effect depends on the tube used. However most of the tests performed on samples obtained from any tube correlated significantly with results obtained from other tube samples. CONCLUSION: Although blood collection tubes with different brands or properties will have distinct effects on coagulation tests, the influence of these blood collection tubes may be relatively small to interfere with decision-making on dose prescription, therefore lack clinical importance. Correlations between the results showed that, one of these plastic blood collection tubes tested in our study, can be used interchangably for a wide variety of coagulation assays. CONFLICT OF INTEREST: None declared.

Plasma levels of tumor necrosis factor-alpha and its receptors in patients with mitral stenosis and sinus rhythm undergoing percutaneous balloon valvuloplasty.

This study aimed to determine whether plasma levels of tumor necrosis factor-alpha (TNF-alpha) and soluble TNF receptor (sTNF-R) increases in rheumatic mitral stenosis (MS) patients with sinus rhythm and to examine the effect of percutaneous mitral balloon valvuloplasty (PMBV) on these parameters. Twenty-six patients with MS and sinus rhythm (study group, 20 female, mean age 33 +/- 8 years), who were scheduled for PMBV, and a well-matched control group consisting of 21 healthy volunteers (15 female, mean age 35 +/- 6 years) were enrolled in the study. Tumor necrosis factor-alpha and sTNF-R levels were compared between study patients and controls, and between peripheral and left atrium (LA) blood. Changes in TNF alpha and sTNF-R levels 24 h and 4 weeks after PMBV were analyzed. Significantly higher baseline TNF-alpha and sTNF-R levels were noted in the study group. In the study group, TNF-alpha and its receptors were also found to be higher in LA blood than in baseline peripheral blood. After PMBV, mitral valve area (MVA) increased and transmitral pressure gradient decreased significantly. At the 24th hour after PMBV, the TNF-alpha level decreased from 29.61 +/- 12.22 pg/ml to 22.42 +/- 8.81 pg/ml (P < 0.0001) and at the 4th week, from 22.42 +/- 8.81 pg/ml to 18.92 +/- 7.37 pg/ml (P < 0.0001). Similar reductions were observed in the sTNF-R level. Regression analysis between the difference in sTNF-R level measured 24 h after and before PMBV and the difference in MVA measured 24 h after and before PMBV showed a significant direct relationship between these variables. This study suggests that isolated rheumatic MS without atrial fibrillation is accompanied by increased TNF-alpha and sTNF-R level. The successful PMBV establishes a significant reduction in TNF-alpha and its receptors, probably due to improved postprocedural hemodynamic parameters.

Increased platelet activity in patients with isolated coronary artery ectasia.

BACKGROUND: The common coexistence with coronary artery disease has led to the suggestion that coronary artery ectasia (CAE) is a variant of coronary artery disease. The mechanisms, however, responsible for CAE formation during the atherosclerotic process and the exact clinical significance are not well known. In this study, we aimed to investigate platelet activity in patients with isolated CAE by using specific markers of platelet activation as P-selectin, beta-thromboglobulin (beta-TG) and platelet factor 4 (PF4). METHODS: Thirty-two patients with isolated CAE without significant stenosis and 30 control participants with angiographically normal coronary arteries were included in this study. According to the angiographic definition used in the Coronary Artery Surgery Study, a vessel is considered to be ectasic when its diameter is > or = 1.5 times that of the adjacent normal segment in segmental ectasia. Plasma P-selectin, beta-TG and PF4 levels were measured in all patients and control participants using enzyme-linked immunosorbent assay method. RESULTS: Patients with isolated CAE were detected to have significantly higher levels of plasma P-selectin, beta-TG and PF4 in comparison with control participants with angiographically normal coronary arteries (P-selectin: 248+/-46 vs. 154+/-32 ng/ml, respectively, P<0.001; beta-TG: 51+/-19 vs. 21+/-9 ng/ml, respectively, P<0.001; PF4: 58+/-23 vs. 33+/-11 ng/ml, respectively, P<0.001). CONCLUSION: In conclusion, we have shown for the first time that patients with isolated CAE have raised levels of plasma P-selectin, beta-TG and PF4 compared with control participants with angiographically normal coronary arteries, suggesting increased platelet activation in patients with CAE.

Vascular endothelial growth factor receptor-1 levels in hepatocellular carcinoma and correlations with clinicopathological features.

BACKGROUND/AIMS: To determine the serum vascular endothelial growth factor receptor-1 (VEGFR-1) levels in hepatocellular carcinoma patients and its correlations with the clinical and laboratory parameters. METHODOLOGY: Serum VEGFR-1 levels were measured in 18 biopsy-proven treatment-naive hepatocellular carcinoma patients (female/male: 5/13; mean age: 59.22 +/- 13.15 years) and in age- and sex-matched healthy controls. Possible associations were also evaluated between serum VEGFR-1 levels and etiology and severity of chronic liver disease, serum alpha-fetoprotein levels, presence of ascites and portal vein thrombosis, and tumor number, size and stage. RESULTS: Serum VEGFR-1 levels were undetectable in all healthy subjects, while all of the patients with hepatocellular carcinoma had increased VEGFR-1 (p < 0.001). Serum VEGFR-1 levels did not correlate with the clinical and laboratory parameters and tumor characteristics in hepatocellular carcinoma. CONCLUSIONS: VEGFR-1 is involved in the regulation of carcinogenesis in hepatocellular carcinoma.

Coagulation, fibrinolytic system activation and endothelial dysfunction in patients with mitral stenosis and sinus rhythm.

Anticoagulation treatment can prevent systemic embolism in patients with mitral stenosis (MS) and atrial fibrillation (AF), but this treatment is under debate if patients are in sinus rhythm. The authors aimed to determine the hemostatic changes in patients with MS and sinus rhythm. Forty-six patients (28 in sinus rhythm and 18 in AF) with mitral stenosis were enrolled in this study. They studied systemic venous fibrinogen, D-dimer, antithrombin-III, tissue plasminogen activator (tPA), plasminogen activator inhibitor-I (PAI-I), von Willebrand factor (vWF), and platelet factor 4 (PF 4) in these patients. The patients were first classified according to their rhythm as sinusal and AF, and then according to the presence of left atrial spontaneous echo contrast (LASEC). Fibrinogen, D-dimer, antithrombin-III, vWF, and PF 4 levels were significantly greater in patients with MS and sinus rhythm or atrial fibrillation compared to the control group (p < 0.05). Whether the rhythm was sinus or AF, fibrinogen, D-dimer, antithrombin-III, vWF, and PF 4 levels were significantly higher in patients with LASEC than in the control group (p < 0.05). Only PF 4 was higher in the AF group than in those with sinus rhythm (p < 0.05). As to plasminogen activator and PAI-I levels, only tissue plasminogen activator levels were found to be higher in the AF group than in those with sinus rhythm and the control group (p < 0.05). In patients with mitral stenosis and sinus rhythm, if LASEC is present, coagulation activation, platelet activation, and endothelial dysfunction are similar in patients with AF, and anticoagulation should be considered in these patients.

Serum level of lipoprotein (a) is inversely associated with the development of coronary collateral circulation.

BACKGROUND: This study sought to determine the relationship between serum lipoprotein (a) levels and angiographically visible coronary collateral circulation and to evaluate whether lipoprotein (a) exerts any effect on vascular endothelial cell growth factor. METHODS: The study population included 60 patients (39 men, mean age 59+/-13 years) with angiographically documented total occlusion in one of the major coronary arteries. Development of collaterals was classified by Rentrop's method. Patients were defined as having poorly developed collaterals for grades 0 and 1 (group 1), or well-developed collaterals for grades 2 and 3 (group 2). Serum lipoprotein (a) and vascular endothelial cell growth factor levels were determined by enzyme-linked immunosorbent assay. RESULTS: In group 1, lipoprotein (a) levels were significantly higher and vascular endothelial cell growth factor levels were significantly lower than in group 2 (34+/-19 vs. 20+/-12 mg/dl, P<0.001, and 2.5+/-0.7 vs. 3.4+/-0.8 ng/dl, P<0.001, respectively). Poorly developed collaterals were significantly more frequent in patients with lipoprotein (a) levels >or=30 mg/dl than in patients with levels <30 mg/dl (72 vs. 37%, P=0.008). A strong negative correlation was observed between lipoprotein (a) and vascular endothelial cell growth, factor (r=-0.708, P<0.0001). Multivariate analysis revealed that a high level of lipoprotein (a) negatively affected the development of collaterals, whereas the duration of angina had a positive effect. CONCLUSION: This study demonstrated for the first time that the high level of lipoprotein (a) negatively affects the formation of coronary collateral vessels in human beings. Reduced production or bioactivity of vascular endothelial cell growth factor caused by high levels of lipoprotein (a) may be the possible responsible mechanisms of hyperlipoprotein (a)-related poor collateral formation.

Increased plasma soluble adhesion molecules; ICAM-1, VCAM-1, and E-selectin levels in patients with slow coronary flow.

BACKGROUND: Inflammation has been reported to be a major contributing factor to many cardiovascular events. In the present study, we aimed to evaluate plasma soluble adhesion molecules; intercellular adhesion molecule-1 (ICAM-1), vascular cell adhesion molecule-1 (VCAM-1) and E-selectin as possible indicators of endothelial activation or inflammation in patients with slow coronary flow. METHOD: Study population included 17 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 11 male, 6 female, mean age=48+/-9 years), and 20 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 11 male, 9 female, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviation above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. Serum levels of ICAM-1, VCAM-1, and E-selectin were measured in all patients and control subjects using commercially available ELISA kits. RESULTS: Serum ICAM-1, VCAM-1, and E-selectin levels of patients with slow coronary flow were found to be significantly higher than those of control subjects with normal coronary flow (ICAM-1: 545+/-198 ng/ml vs. 242+/-113 ng/ml respectively, p<0.001, VCAM-1: 2040+/-634 ng/ml vs. 918+/-336 ng/ml respectively, p<0.001, E-selectin: 67+/-9 ng/ml vs. 52+/-8 ng/ml respectively, p<0.001). Average TIMI frame count was detected to be significantly correlated with plasma soluble ICAM-1 (r=0.550, p<0.001), VCAM-1 (r=0.569, p<0.001) and E-selectin (r=0.443, p=0.006). CONCLUSION: Increased levels of soluble adhesion molecules in patients with slow coronary flow may be an indicator of endothelial activation and inflammation and are likely to be in the causal pathway leading to slow coronary flow.

Serum transforming growth factor beta 1 levels in multiple myeloma patients.

Cytokinesis plays an important role in the etiology of multiple myeloma. The transforming growth factor (TGF) beta 1 levels in 82 sera from 60 patients with multiple myeloma were analyzed by ELISA. Fourty one sample were obtained before treatment from newly diagnosed patients, 22 after treatment from the same patients and 19 from relapsed/refractory patients. Serum median TGF level of newly diagnosed patients was 769.5 ng/mL (126-1853), and the relapsed/refractory patients had similar levels. TGF levels after chemotherapy were not different between patients that reached plateau phase and those who remained refractory. We found a negative correlation between TGF and C-reactive protein and blood urea nitrogen and a positive correlation between TGF and hemoglobin level in newly diagnosed patients. After treatment, it was determined that TGF levels at diagnosis were higher in patients who reached plateau phase than in the refractory patients. Elevated serum TGF concentration at diagnosis in multiple myeloma patients may be a favorable predictor of response.

Late saphenous vein graft occlusion in patients with coronary bypass: possible role of aspirin resistance.

BACKGROUND: Late venous graft thrombosis, leading to recurrent ischemia, is frequently encountered in old, degenerated vein grafts with advanced atherosclerotic plaque formation. Aspirin has been indicated to maintain venous graft patency in the post-operative period. However, there is considerable evidence that aspirin resistance is of concern in patients with venous grafts. MATERIAL AND METHOD: Prospectively enrolled 14 patients (11 male, 3 female, Group 1), who were shown to have at least one occluded saphenous vein graft on their late control coronary angiogram after bypass operation, were compared for the presence of aspirin resistance by PFA-100 with age- and sex-matched 14 patients (10 male, 4 female, Group 2), who were found patent and well-functioning vein grafts without wall irregularities on late post-operative coronary angiograms (mean 6.5+/-2.5 years), enrolled as a control group. RESULTS: Mean CT of collagen/epinephrine cartridge in Group 1 was 197+/-85 s and significantly less than in Group 2 (279+/-44 s; p=0.011). It was found that 50% of patients in Group 1 were so-called aspirin resistant, whereas in Group 2, this ratio was 7.1% (p=0.033). BMI (p=0.038, Beta=-0.322), uric acid level (p=0.023, Beta=-0.355), and CT by collagen/epinephrine cartridge (p=0.008, Beta=0.431) were independently predicting late occlusion of saphenous vein graft. CONCLUSION: Aspirin resistance is highly prevalent in patients with occluded venous grafts at a relatively late period.

Elevated level of plasma homocysteine in patients with slow coronary flow.

BACKGROUND: Elevated plasma levels of homocysteine are currently considered a major, independent risk factor for cardiovascular diseases. Recently, several investigators have suggested that even mild elevation in plasma homocysteine level can severely disturb vascular endothelial function and subsequently impair coronary blood flow. Accordingly, we investigated plasma homocysteine level in patients with slow coronary flow. METHOD: Study population included 53 patients with angiographically proven normal coronary arteries and slow coronary flow in all three coronary vessels (group I, 21 females, 32 males, mean age=48+/-9 years), and 50 subjects with angiographically proven normal coronary arteries without associated slow coronary flow (group II, 22 females, 28 males, mean age=50+/-8 years). Coronary flow rates of all patients and control subjects were documented by Thrombolysis In Myocardial Infarction frame count (TIMI frame count). All patients in group I had TIMI frame counts greater than two standard deviations above those of control subjects (group II) and, therefore, were accepted as exhibiting slow coronary flow. The mean TIMI frame count for each patient and control subject was calculated by adding the TIMI frame counts for each major epicardial coronary artery and then dividing the obtained value into 3. Plasma homocysteine level was measured in all patients and control subjects using commercially available homocysteine kits. RESULTS: There was no statistically significant difference between two groups in respect to age, gender, hypertension, diabetes mellitus, hyperlipidemia and cigarette smoking (p>0.05). Plasma homocysteine level of patients with slow coronary flow were found to be significantly higher than those of control subjects (15.5+/-5.7 vs. 8.7+/-4.2 microM/l, respectively, p<0.001). Moreover, we found a significant positive correlation between plasma homocysteine level and mean TIMI frame count (r=0.660, p<0.001). CONCLUSION: We have shown that patients with slow coronary flow have raised level of plasma homocysteine compared to control subjects with normal coronary flow. This data suggests that elevated level of plasma homocysteine may play a role in the pathogenesis of slow coronary flow.

[Thrombotic, fibrinolytic and proliferative activities of pulmonary vascular bed in secondary pulmonary hypertension]. / Sekonder pulmoner hipertansiyonda pulmoner vasküler yatagin trombotik, fibrinolitik ve proliferatif aktiviteleri.

OBJECTIVE: To determine whether pulmonary vascular bed contributes to the development of in situ thrombosis and vascular remodelling in secondary pulmonary hypertension (SPH) via changes in its local secretory activities. METHODS: Seventy-one patients with the diagnosis of secondary pulmonary hypertension (38 females, mean age 40.36+/-1.05 years) were included in the study. Selective right and left heart catheterization was performed to each patient for diagnostic purposes. Blood samples obtained from left ventricle (LV) and pulmonary artery (PA) of each patient were analyzed for levels of plasminogen activator inhibitor-1 (PAI-1), platelet derived growth factor (PDGF), vascular endothelial growth factor (VEGF), D-dimer, von Willebrand factor (vWF), protein-C, antithrombin-III, fibrinogen, and plasminogen. Results were compared between LV and PA. Correlation analysis between each parameter and mean pulmonary artery pressure (MPAP) was performed. RESULTS: Although mean level of VEGF in LV and PA were found to be in normal range, it was significantly higher in LV than in PA (p<0.001). Mean PDGF and D-dimer levels, which remained in normal range were also higher in LV (p<0.001 and p<0.001, respectively) than in PA;.vWF showed similar degree of elevation in both LV and PA. Only one parameter, PAI-1, was found to be significantly higher in PA than in LV (p=0.012). Antithrombin-III, protein C, plasminogen, and fibrinogen levels showed no significant differences between two chambers. They also remained in normal range, except for fibrinogen, which was slightly elevated in both LV and PA. Correlation analysis revealed strong positive correlation between D-dimer level in both LV and PA and MPAP (r=0.775, p<0.001 and r=0.649, p<0.001, respectively). CONCLUSION: In SPH, pulmonary vascular bed shows increased thrombotic, hypofibrinolytic, and proliferative activities, which are partially related to the severity of illness.

Predictors of left ventricular thrombus formation in patients with dilated cardiomyopathy: role of activated protein C resistance.

OBJECTIVES: The aim of this study was to investigate the association between left ventricular thrombus formation and natural anticoagulant systems including the protein C, protein S and antithrombin in patients with dilated cardiomyopathy. MATERIALS AND METHODS: Sixty patients with dilated cardiomyopathy who met the inclusion criteria were included in the study. Patients were divided into two groups: group I consisted of 22 patients with left ventricular thrombus and group II consisted of 38 patients without left ventricular thrombus. Our main inclusion criteria were ejection fraction /= 6.0 cm. These two groups were compared for clinical and hematologic parameters (activated protein C resistance, protein S and antithrombin). RESULTS: There were no statistically significant differences between patients with or without left ventricular thrombi with respect to left ventricular end-diastolic and end-systolic dimensions, ejection fraction, fractional shortening and left atrial diameter. There were no statistically significant differences between patients with and without left ventricular thrombus with respect to platelet count (252 +/- 64/mm3 x 10(3) compared with 260 +/- 74/mm3 x 10(3) respectively, P=0.68), prothrombin time (12.94 +/- 1.9 s compared with 12.86 +/- 1.3 s respectively, P=0.82), activated partial thromboplastin time (32 +/- 5 compared with 30 +/- 4 s respectively, P=0.32) and fibrinogen levels (36 +/- 9 mg/dl compared with 34 +/- 8 mg/dl respectively, P=0.41). None of the patients had protein S and antithrombin deficiency. Activated protein C resistance was found in 12 patients (12 out of 22, 54%) in group I and four patients (four out of 38, 9.5%) in group II (P < 0.01). It was also shown to be an independent predictor of left ventricular thrombus (P < 0.05). CONCLUSION: Activated protein C resistance is found to be an independent predictor of left ventricular thrombus in patients with dilated cardiomyopathy who have ejection fractions less then 35% and left ventricular end-diastolic dimensions > 6.0 cm.

Decreased platelet activation and endothelial dysfunction after percutaneous mitral balloon valvuloplasty.

OBJECTIVE: This study was conducted to assess the changes in platelet activation and endothelial dysfunction in patients with mitral stenosis (MS) and sinus rhythm (SR) following percutaneous mitral balloon valvuloplasty (PMBV). BACKGROUND: Systemic thromboembolism is a serious complication in patients with valvular heart disease, and its incidence is highest in those with mitral stenosis. A hypercoagulable state has also been reported in patients with mitral stenosis and sinus rhythm. A recent study has shown that patients with previous PMBV had a lower incidence of thromboembolism. METHODS AND RESULTS: The study was conducted in 21 patients (two men, 19 women, mean age=34+/-6 years) with mitral stenosis and sinus rhythm (SR) who underwent percutaneous mitral balloon valvuloplasty and 17 healthy control subjects (two men, 15 women, mean age=33+/-6 years). Biochemical markers of platelet activity (beta thromboglobulin, BTG, and soluble P-selectin, sPsel) and endothelial dysfunction (von Willebrand Factor, vWF) were measured in both control subjects' and patients' serum samples taken immediately before PMBV and 24 h after PMBV procedure. All patients underwent successful PMBV. Significant improvement of mitral valve area, pulmonary artery pressure, mean mitral gradients, and left atrial diameter were achieved in all patients after PMBV. Compared with control subjects, patients with MS had higher plasma levels of BTG (66+/-26 ng/ml vs. 14+/-6 ng/ml, P<0.001), vWF (177+/-67 units/dl vs. 99+/-37 units/dl, P<0.0001), sPsel (226+/-74 ng/ml vs. 155+/-66 ng/ml, P<0.001). There was a significant reduction of plasma levels of BTG (66+/-26 ng/ml vs. 48+/-20 ng/ml, P=0.002), vWF (177+/-67 units/dl vs. 134+/-60 units/dl, P=0.001) and P-selectin (226+/-74 ng/ml vs. 173+/-71 ng/ml, P=0.008,) 24 h after PMBV. CONCLUSION: We have shown that patients with severe MS and SR have increased platelet activation and endothelial dysfunction compared with control subjects and PMBV results in decreased platelet activity and improvement of endothelial injury.

Relationship between control of ventricular rate in atrial fibrillation and systemic coagulation activation in patients with mitral stenosis.

BACKGROUND AND AIM OF THE STUDY: Systemic thromboembolism is a major complication in patients with mitral stenosis (MS), especially in those who have atrial fibrillation (AF). It has been suggested that systemic coagulation activity may be increased in these patients. The study aim was to investigate the relationship between control of ventricular rate and systemic coagulation factors in patients with MS and AF by measuring plasma levels of prothrombin fragment (PF) 1+2, thrombin-antithrombin III complex (TAT) and plasminogen activator inhibitor-1. METHODS: Fifty-four consecutive patients with moderate to severe MS and AF were included in the study. Patients with resting heart rates < 100 beats per min were considered as having a controlled ventricular response rate (group A; n = 28) and those with > 100 beats per min as an uncontrolled ventricular response rate (group B; n = 26). RESULTS: Group A patients had a lower mean mitral gradient and pulmonary artery pressure than group B patients (11 +/- 6 versus 15 +/- 5 and 35 +/- 7 versus 39 +/- 8; p < 0.05, respectively). Plasma concentrations of PF 1+2 (4.17 +/- 2.1 versus 2.95 +/- 1.21; p < 0.01) and TAT III (4.61 +/- 1.75 versus 3.12 +/- 1.01; p < 0.01) were elevated in group B compared with group A. Similarly, group B patients had higher plasminogen activator inhibitor-1 levels than group A patients (7.87 +/- 3.8 versus 5.8 +/- 2.9; p < 0.05). A significant correlation was found between heart rate and plasma PF 1+2 and TAT levels. Multiple logistic regression analysis revealed that heart rate and mean mitral gradient were independent predictors of systemic coagulation activation. CONCLUSION: Besides contributing towards hemodynamic and symptomatic relief, the control of AF rate in MS patients induces a drastic decline in coagulation activation, and may also reduce the incidence of thromboembolism.

Increased systemic and regional coagulation activity in patients with mitral stenosis and sinus rhythm.

A hypercoagulable state has been reported in patients with mitral stenosis (MS) and sinus rhythm (SR). However it has been suggested that the coagulation activity may be increased only within the left atrium in MS, with normal peripheral blood levels. The aim of the present study was to assess regional left atrial and systemic coagulation activities by measuring PF1+2 in patients with severe mitral stenosis and sinus rhythm, normal blood clotting times, and no left atrial thrombus. The study was conducted in 25 consecutive patients with moderate-to-severe MS and sinus rhythm who underwent percutaneous balloon mitral valvuloplasty. Transesophageal echocardiography was performed before the valvuloplasty procedure in all patients to exclude the presence of left atrial thrombus and left atrial spontaneous echo contrast (LASEC). There were no statistically significant differences between LASEC-positive and LASEC-negative patients with respect to age, gender, fibrinogen levels, prothrombin time, mitral valve area, mean mitral gradient, pulmonary artery pressure (in all p > 0.05). Regional (left atrial) PF1+2 levels of both LASEC-positive and LASEC-negative patients were significantly elevated when compared to control subjects (p < 0.01). Statistically significant elevated systemic level of PF1+2 was observed only in LASEC-positive patients when compared to control subjects (p < 0.01, p > 0.05, respectively). In conclusion patients with severe mitral stenosis and SR have increased regional coagulation activity in both LASEC-negative and LASEC-positive groups. Although this increased regional coagulation activity has been reflected in peripheral blood of LASEC-positive patients, it has not been reflected in peripheral blood of LASEC-negative patients.

Antineutrophil cytoplasmic autoantibodies and anti-Saccharomyces cerevisiae antibodies in inflammatory bowel diseases.

BACKGROUND/AIMS: Perinuclear antineutrophil cytoplasmic autoantibody is a marker for ulcerative colitis, and anti-Saccharomyces cerevisiae antibody is known to be associated with Crohn's disease. The purpose of this study was to search the value of detecting perinuclear antineutrophil cytoplasmic autoantibody and anti-Saccharomyces cerevisiae antibody for the diagnosis of Turkish inflammatory bowel disease patients. METHODS: Serum samples were obtained from 80 patients with ulcerative colitis, 61 patients with Crohn's disease and 40 healthy controls. Determination of both anti-Saccharomyces cerevisiae antibody and antineutrophil cytoplasmic autoantibody was performed with the standardized enzyme-linked immunosorbent assay. RESULTS: In cases with ulcerative colitis, 65% tested seropositive for antineutrophil cytoplasmic autoantibody, whereas the controls showed 2.5% positivity. In cases with Crohn's disease, 63.9% tested seropositive for anti-Saccharomyces cerevisiae antibody, whereas the controls showed 2.5% seropositivity. The combination of a positive anti-Saccharomyces cerevisiae antibody test and a negative antineutrophil cytoplasmic autoantibody yielded a sensitivity and specificity of 32.0% and 97.5%, respectively. The combination of a positive perinuclear antineutrophil cytoplasmic autoantibody and a negative anti-Saccharomyces cerevisiae antibody test yielded a sensitivity and specificity of 44.2% and 97.5%, respectively. CONCLUSIONS: Both serologic tests may aid in the differential diagnosis of inflammatory bowel disease.

Hemostatic abnormalities in cirrhosis and tumor-related portal vein thrombosis.

In order to investigate the relationship between hemostatic abnormalities and portal vein thrombosis (PVT) in hepatocellular carcinoma (HCC), platelets, prothrombin time (PT), activated partial thromboplastin time (aPTT), thrombin time, fibrinogen, d-dimer, fibrinogen degradation products (FDPs), protein C, protein S, antithrombin, plasminogen, antiplasmin, coagulation factors (CFs) V, VII, VIII, IX, XI, and XIII, von Willebrand factor (vWF), prothrombin fragment 1 + 2 (PF 1 + 2), tissue-type plasminogen activator (tPA), and plasminogen activator inhibitor 1 (PAI-1) were studied in patients with HCC, cholangiocarcinoma, and metastatic liver tumors and in cirrhosis patients with or without PVT. Platelet, antithrombin, protein C, plasminogen, and CFs V, VII, IX, XI, and XIII levels of HCC group were found lower and PT, aPTT, thrombin time, vWF, FDPs, PF 1 + 2, tPA, and PAI-1 levels were higher than the control group. Our findings suggested that the abnormalities of coagulation and fibrinolysis systems have some role in provoking thrombosis of portal veins in HCC, in addition to the invasion of portal veins by hepatoma cells.

Continuous active state of coagulation system in patients with nonthrombotic inflammatory bowel disease.

This study was planned for searching possible changes of the total coagulation and fibrinolysis system in inflammatory bowel disease (IBD) in order to obtain some clues for explaining the relation between IBD and hypercoagulability. A total of 24 patients with ulcerative colitis, 12 patients with Crohn disease, and 20 healthy controls were studied. Platelets; prothrombin time (PT); partial thromboplastin time (PTT); fibrinogen; D-dimer; fibrinogen degradation products; protein C; protein S; antithrombin; thrombin time; von Willebrand factor; coagulation factors V, VII, VIII, IX, XI, and XIII; plasminogen; antiplasmin; tissue plasminogen activator; plasminogen activator inhibitor 1; and prothrombin fragments 1 + 2 were studied. Most of the procoagulants (platelets, fibrinogen, von Willebrand factor, coagulation factor IX, and plasminogen activator inhibitor 1) were found increased together with decreases in some anticoagulants (protein S and antithrombin) in IBD. Also the activation markers of coagulation (D-dimer, fibrinogen degradation products, and prothrombin fragments 1 + 2) were all increased. The parameters of the total coagulation-fibrinolysis system were increased in IBD, regardless of the form and the activity of the disease.

Basic hemostatic parameters in patients with long-term oral anticoagulation undergoing cholecystectomy.

BACKGROUND: The current hemostatic data in relation to laparoscopic cholecystectomy (LC) is limited particularly for patients receiving chronic oral anticoagulant treatment. The aim of this study is to assess hemostatic alterations before, during and after LC for the patients placed on long-term oral anticoagulant treatment. PATIENTS AND METHODS: A prospective, nonrandomized, controlled study was designed to compare the characteristics, hemostatic system, and postoperative complications of patients maintained on long-term anticoagulation with those who did not receive such therapy. In the period from January 2009 to December 2009, a total of 31 patients who underwent elective LC for symptomatic cholelithiasis were enrolled in the study. Sixteen of these patients were on long-term anticoagulation therapy with warfarin (OAC group). The other 15 patients did not receive anticoagulant or antiaggregant drugs and served as the control group. RESULTS: Five patients (31.5%) of the OAC group had postoperative bleeding, whereas no bleeding occurred in the control group. Significant reductions in postoperative hemoglobin levels were observed in the OAC group when compared with the control group (P<.05). Although within normal ranges, international normalized ratio values and the tissue plasminogen activator activity were significantly higher, whereas factor II, VII, IX, and X levels were significantly lower in the OAC group when compared with the control group (P<.05). CONCLUSION: Patients receiving oral anticoagulant treatment are at risk of postoperative bleeding and the basic parameters of coagulation appear unable to predict which patients undergoing anticoagulant therapy are candidates for bleeding after surgery. More sensitive methods should be developed to measure the degree of hemorrhagic risk.

Natural anticoagulant protein levels in Turkish patients with inflammatory bowel disease.

Thromboembolism is an important cause of morbidity and mortality in patients with inflammatory bowel disease (IBD). The aim of this study was to investigate common thrombophilic markers in patients with IBD and to search for a relation between these predisposing factors and activity of disease. Seventy-four patients with ulcerative colitis, 22 patients with Crohn's disease and 20 healthy volunteers were enrolled into the study. Plasma levels of protein C, protein S, antithrombin III and activated protein C resistance were determined in patients with IBD and healthy controls. Mean values of protein C, protein S and antithrombin III were significantly lower in patients with ulcerative colitis and Crohn's disease compared with the healthy control group. Patients with active ulcerative colitis had lower protein C, protein S and antithrombin III level than patients in remission (P < 0.001, P < 0.001, P < 0.001). Levels of protein C, S and antithrombin III were also decreased in patients with active Crohn's disease compared with those in remission (P < 0.05, P < 0.001, P < 0.05). Differences in all natural anticoagulant levels between patients in remission and healthy individuals in both ulcerative colitis and Crohn's disease groups were not statistically significant (P > 0.05). No significant difference was observed in activated protein C resistance (APCR) between patients with active disease, those in remission and the control group (P > 0.05). Abnormalities in natural anticoagulants are common in patients with IBD during active disease.