Clinical correlation between coagulation disorders and sepsis in patients with liver failure

OBJECTIVE: This study aimed to explore the clinical detection and prognosis of coagulation function in patients with liver failure and sepsis. METHODS: The plasma fibrinogen (FIB), factor II, factor VII, factor V, factor IV, antithrombin III (ATIII), platelet (PLT), mean PLT volume (MPV), D-dimer, prothrombin activity (PTA), and fibrin degradation product (FDP) levels and thromboelastogram values were detected in patients with liver failure complicated with sepsis and compared with those in the liver failure and liver cirrhosis groups. The patients with liver failure complicated with sepsis were analyzed by univariate and multivariate logistic regression, and the regression equation was established. RESULTS: The levels of FIB, factor II, factor VII, factor V, ATIII, PLT, MPV, D-dimer, and FDP in the patients with liver failure complicated with sepsis were compared with those in the control group patients, and the differences were statistically significant (p < 0.05). Among the thromboelastography parameters in the patients with liver failure and sepsis, the differences in the K-value, R-value, angle, maximum amplitude, and coagulation index values compared with those of the control group were statistically significant (p < 0.05). The logistic regression model obtained was as follows: p = 1/(1 + e [–0.128×X1–0.058×X2 + 0.211×X3 + 0.2×X4 + 0.25]). The specificity, sensitivity, and accuracy values of the regression equation in determining the prognosis were 92%, 93.9%, and 92.8%, respectively. Among the 11 factors, factor VII, PLT, FDP, and D-dimer were included in the regression equation. CONCLUSION: Coagulation disorder is exacerbated in patients with liver failure and sepsis. Among the 11 coagulation-related factors, factor VII, PLT, FDP, and D-dimer may be the independent factors influencing the prognosis of patients with acute liver failure and sepsis.

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Coagulation Findings in Rats with Experimental Hypersplenism and Their Changes after Splenectomy and after Administration of Adrenaline

Thrombosis and Haemostasis ◽

10.1055/s-0038-1654190 ◽

1970 ◽

Vol 23 (03) ◽

pp. 593-600

Author(s):

P Pudlák ◽

I Farská ◽

V Brabec ◽

V Pospíšilová

Keyword(s):

Factor Viii ◽

Normal Control ◽

Normal Values ◽

Coagulation Factors ◽

Factor Vii ◽

Factor V ◽

Thrombin Time ◽

Factor Ii ◽

Recalcification Time

Summary1. The following coagulation changes were found in rats with experimental hypersplenism: a mild prolongation of the recalcification time, shortened times in Quick’s test, a lowered activity in plasma thrombin time and shortened times in the partial thromboplastin test. Concentrations of factor II, V, VII (+X), VIII and X did not differ from those of normal control rats.2. The administration of adrenaline to hypersplenic rats induced the correction of the partial thromboplastin test, Quick’s test and plasma thrombin time to normal values. Concentrations of coagulation factors were not significantly changed. An increase was found in factor V.3. Splenectomy performed in hypersplenic rats was followed by a shortened recalcification time, a prolongation of the partial thromboplastin test and of the test with partial thromboplastin and kaolin. A prolongation was also observed in Quick’s test. Complete correction of plasma thrombin time was not observed. The concentration of factor VII increased.4. The administration of adrenaline to splenectomized rats with experimental hypersplenism did not induce any significant changes with the exception of a corrected plasma thrombin time and a decreased concentration of factor VIII.5. A different reaction of factor VIII to adrenaline in normal and hypersplenic rats is pointed out.

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FACTOR II ACTIVATING ACTIVITY IN EXTRACTS OF TUMORAL NECROSIS FROM TWO MURINE BREAST ADENOCARCINOMAS

10.1055/s-0038-1643206 ◽

1987 ◽

Author(s):

A Blanco ◽

R Bonfil ◽

O Bustoabad ◽

M Lazzari

Keyword(s):

Coagulation Factors ◽

Factor Vii ◽

Factor V ◽

Factor X ◽

Extrinsic Pathway ◽

Factor Ii ◽

Metastatic Capacity ◽

Plasma Recalcification Time ◽

Recalcification Time ◽

Breast Adenocarcinomas

Increased deposition and lysis of fibrin, associated with malignant tissue, has led to look for activators of both the coagulation and fibrinolytic systems produced by tumor cells. We report the evidences of a procoagblant activity (PA) in the extracts of intratumoral necrosis from two experimental breast adenocarcinomas in murine model (BALB/c). The tumors have different metastatic capacity (MC). M3 without MC and MM3 with high MC.The addition of the extracts to: 1- Normal Plasma, 2- Deficient substrates in coagulation factors, 3- Purified, fibrinogen (I), showed: 1- Shortening of the plasma recalcification time (PRT) and APTT, without ;modification on prothrombin time (PT), 2- Reduction of the PRT on deficient substrates in factors: VIII; VII; VII and X; V; V, VII and X; without modification on II deficient substrate, 3- No PA on I. Table:C: Control, s: seconds, m: minutes. The PA was not affected by heparin. The results suggest that the PA is independent of the presence of either factor VIII or factor VII (intrinsic or extrinsic pathway respectively), as well as presence of either factor V or factor X. Any effect was observed either on factor II deficient substrate or on I, so, there was no evidence of thrombin activity The PA could be act directly on factor II, suggesting that fibrin formation could be induced by a “non-classical” activation pathway. No significant differences (p>0.5) in PA were observed between both tumoral necrosis extracts. The necrotic area in M3 (37%) is bigger than in MM3 (18%). So, much more PA could be present in MM3 and this could play a role in the MC of this tumor.

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Multidimensional Similarity of Letters

Perceptual and Motor Skills ◽

10.2466/pms.1969.28.1.3 ◽

1969 ◽

Vol 28 (1) ◽

pp. 3-12 ◽

Cited By ~ 32

Author(s):

Teodor Kuennapas ◽

Anne-Jeanette Janson

Keyword(s):

Factor Viii ◽

Factor Ix ◽

Factor Vii ◽

Similarity Analysis ◽

Factor V ◽

Factor I ◽

Considerable Portion ◽

Lower Case ◽

Factor Ii

28 lower-case letters of the Swedish alphabet were studied by the method of multidimensional similarity analysis. 57 Ss participated in the experiment. 9 factors were found. Factor I is called ‘t’ or ‘Vertical linearity,’ Factor II: ‘o’ or ‘Roundness,’ Factor III: ‘n’ or ‘Parallel vertical linearity,’ Factor IV: ‘i’ or “Vertical linearity with dot,’ Factor V: ‘p’ or ‘Roundness attached to vertical linearity,’ Factor VI: ‘k’ or ‘Vertical linearity with crossness,’ Factor VII: ‘a’ or ‘Roundness attached to a hook,’ Factor VIII: V or ‘Angularity open upward’ and Factor IX: ‘z’ or ‘Zigzaggedness.’ ‘Vertical linearity’ and ‘Roundness’ are the most important of these factors and account for a considerable portion of the similarity among many letters.

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Assessment of Thalidomide Therapy Effect on Platelet Activation and Selected Blood Coagulation Parameters in Multiple Myeloma Patients

Blood ◽

10.1182/blood.v112.11.5181.5181 ◽

2008 ◽

Vol 112 (11) ◽

pp. 5181-5181

Author(s):

Marta Robak ◽

Jacek Trelinski ◽

Krzysztof Chojnowski

Keyword(s):

Multiple Myeloma ◽

Platelet Count ◽

Factor Viii ◽

Platelet Activation ◽

Factor Vii ◽

Control Group ◽

High Dose ◽

Closure Time ◽

Therapy Effect ◽

D Dimer

Abstract Background: Patients with multiple myeloma are at relatively high risk of developing thromboembolic events (TEE). These life-threatening complications may arise from hypercoagulability associated with malignancy and/or may be connected with anticancer therapy. The risk of developing TEE appears to be particularly high during treatment with thalidomide alone or combined with chemotherapy and/or high-dose dexamethasone. The pathogenesis of thalidomide-related thrombosis in myeloma patients remains unexplained. Some authors suggest that platelet activation can contribute to development of this complication in multiple myeloma patients on thalidomide therapy but until now it has not been a subject of investigation. Patients and methods: The study was performed in 20 patients with multiple myeloma. The tests were done at diagnosis and after one month of thalidomide therapy at a dose of 100–200 mg/24h. All patients had normal renal function and did not take drugs affecting platelet function. The control group consisted of 15 healthy subjects of similar age. In each patient closure time with ADP/Collagen and Epinephrine/Collagen cartridges by PFA-100 method was assessed. Platelet expression of membrane activation marker P-selectin (CD62p) on resting platelets and after stimulation with ADP/Collagen and Epinephrine/Collagen was analyzed by flow cytometry. Additionally, activity of factor VII, factor VIII and von Willebrand factor (vWF), concentration of fibrinogen and D-dimer, and platelet count were evaluated. Results: The mean PFA-100 closure time was significantly shortened with ADP/Collagen (87.2 ±17.1 s vs 100.4 ± 19.3 s, p=0.008) and Epinephrine/Collagen cartridges (118.5 ± 20.3 s vs 132.2 ± 27.9 s, p=0.04) after one month of therapy in comparison to baseline. The median CD62p percentage increased markedly after treatment-on resting platelets 5.1 (0.76–22.2) vs 3.6 (0.1–21.5) p=0.03. and after stimulation with Epinephrine/Collagen 16.6 (2.3–57.3) vs 11.1 (1.4–19.5) p=0.03. The observed increased P-selectin expression after ADP/Collagen stimulation 26.3 (8.5–42.8) vs 19.7 (1.0–35.4) was not statistically significant. The median values of P-selectin expression at diagnosis and after thalidomide therapy were also higher than in the control group. The results of factor VIII, vWF activity, fibrinogen and D-dimer concentration did not differ markedly before and after therapy. Significantly lower mean activity of factor VII (p=0.004) and higher mean platelet count (p=0.03) after therapy were observed. Conclusions: These results demonstrate that platelet activation is one of the pathogenetic factor of thalidomide-related thrombotic complications and can explain some observations that acetylsalicylic acid may protect against TEE during myeloma treatment with thalidomide.

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Etiopathogenesis of Sheehan’s Syndrome: Roles of Coagulation Factors and TNF-Alpha

International Journal of Endocrinology ◽

10.1155/2014/514891 ◽

2014 ◽

Vol 2014 ◽

pp. 1-6 ◽

Cited By ~ 3

Author(s):

Halit Diri ◽

Elif Funda Sener ◽

Fahri Bayram ◽

Nazife Tascioglu ◽

Yasin Simsek ◽

...

Keyword(s):

Gene Polymorphisms ◽

Venous Blood ◽

Hormone Deficiency ◽

Control Group ◽

Pituitary Hormone ◽

Factor V ◽

Sheehan’S Syndrome ◽

Factor Ii ◽

Sheehan's Syndrome ◽

Pai 1

Sheehan’s Syndrome (SS) is defined as pituitary hormone deficiency due to ischemic infarction of the pituitary gland as a result of massive postpartum uterine hemorrhage. Herein, we aimed to investigate the roles ofFactor II(G20210A),Factor V(G1691A),MTHFR(C677T and A1298C),PAI-14G/5G, andTNF-α(-308 G>A) gene polymorphisms in the etiopathogenesis of SS. Venous blood samples were obtained from 53 cases with SS and 43 healthy women. Standard methods were used to extract the genomic DNAs.Factor II(G20210A),Factor V(G1691A), andMTHFR(C677T and A1298C) polymorphisms were identified by real-time PCR.PAI-14G/5G andTNF-α(-308 G>A) gene polymorphisms were detected with polymerase chain reaction (PCR) and restriction fragment length polymorphism (RFLP) methods. According to statistical analysis, none of the polymorphisms were found to be significantly higher in the SS group compared to the control group. Hence, we suggest that genetic factors other thanFactor II, Factor V, MTHFR, PAI-1, andTNF-αgene polymorphisms should be researched in the etiopathogenesis of SS.

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The Influence of Ethanol Feeding on the Activities of Factors II, VII, VIII, IX and X in Rats

Thrombosis and Haemostasis ◽

10.1055/s-0038-1648073 ◽

1976 ◽

Vol 36 (03) ◽

pp. 532-536 ◽

Cited By ~ 2

Author(s):

Jørg Mørland ◽

Turid Holm ◽

Hans Prydz

Keyword(s):

Chronic Administration ◽

Fold Increase ◽

Coagulation Factors ◽

Factor Vii ◽

Control Group ◽

Factor Viii Activity ◽

Dietary Polyunsaturated Fatty Acid ◽

Factor Ii ◽

Ethanol Feeding ◽

Experimental Group

SummaryThe effect of chronic administration of ethanol to rats in a controlled regimen upon the activities of the coagulation factors II, VII, VIII, IX and X has been studied.No significant differences were found for factor II, IX and X between the ethanol-treated rats and the control group given an isocaloric diet with carbohydrate replacing ethanol. Factor VII activity was somewhat higher and factor VIII activity decreased significantly in the experimental group when ethanol treatment was combined with an approximately two-fold increase in dietary polyunsaturated fatty acid.

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Intravascular Clotting After Endotoxin in Rabbits With Impaired Intrinsic Clotting Produced by a Factor VIII Antibody

Blood ◽

10.1182/blood.v42.4.523.523 ◽

1973 ◽

Vol 42 (4) ◽

pp. 523-534 ◽

Cited By ~ 4

Author(s):

S. M-C. Shen ◽

S. I. Rapaport ◽

D. I. Feinstein

Keyword(s):

Factor Viii ◽

Rabbit Model ◽

Saline Group ◽

Factor Vii ◽

Test Material ◽

Control Group ◽

Inert Material ◽

Factor V ◽

Mean Values ◽

Human Factor Viii

Abstract A rabbit model in which intrinsic clotting was selectively impaired by injection of a human factor VIII antibody was used to evaluate the mechanism of endotoxin-induced intravascular clotting in cortisone-treated rabbits. Three groups of animals were studied: a control group given factor VIII antibody followed by saline; a second control group given an inert material followed by endotoxin; and an experimental group given factor VIII antibody followed by endotoxin. The following parameters were measured: 125I-fibrinogen kinetics, fibrinogen levels, factor VIII, factor VII, factor V, WBC, platelets, and hematocrit. The kidneys were examined for deposition of fibrin. Mean values for factor VIII at the time of injection of the second test material and mean values for fibrinogen consumed in the 6 hr after the second injection were as follows: antibody-saline group, 8.5% and 11.0 mg/kg; control material-endotoxin group, 90% and 29.6 mg/kg; and antibody endotoxin group, 7.0% and 32.7 mg/kg. Factor V, factor VII, granulocytes, and platelets fell in both groups of animals given endotoxin. One animal in each group given endotoxin developed gross renal cortical necrosis. These data establish that selective impairment of the intrinsic clotting reactions does not reduce the amount of clotting induced by a single injection of endotoxin in the cortisone-treated rabbit.

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A Case of FVII Inhibitor.

Blood ◽

10.1182/blood.v116.21.3655.3655 ◽

2010 ◽

Vol 116 (21) ◽

pp. 3655-3655

Author(s):

Michael Joshua Levitt ◽

Arthur A. Topilow ◽

William Lerner ◽

Peter Mencel ◽

Carl Henningson ◽

...

Keyword(s):

Research Funding ◽

Immunosuppressive Treatment ◽

Factor Ix ◽

Factor Vii ◽

Factor V ◽

First Line ◽

Immunosuppressive Medications ◽

Factor Ii ◽

Plasma Factor ◽

History Of

Abstract Abstract 3655 Acquired inhibitors of coagulation are bleeding disorders that require prompt recognition, diagnosis, and management. Antibodies against factor VII are extremely rare with only a few cases reported in the literature. We present a case of a patient with an acquired Factor VII inhibitor. This is an 87 year old female with a past medical history of breast cancer, hypertension, and hyperlipidemia who presented to the emergency room with right flank pain and hematuria. A CT scan of the abdomen and pelvis showed bilateral hydronephrosis with no evidence of nephrolithiasis. The patient denied hematemesis or hematochezia but was noted to have hemoccult positive stools. The patient denied any anticoagulant use. Admission laboratories revealed a coagulopathy with a normal partial thromboplastin time (PTT) of 28 seconds and prolonged prothrombin time (PT) of greater than 50 seconds and INR of 19.59. The patient received vitamin K without improvement in coagulation parameters. A mixing study revealed a markedly prolonged PT that did not correct with 1:1 (18.9 seconds) and 4:1 (27.3 seconds) mix normal plasma. Factor assays shows an abnormal Factor VII level of less than 1%, and normal Factor II 121%, Factor V 140%, Factor VIII 201%, Factor IX 99%, and Factor XI 126% levels. A FVII inhibitor was 1.66 Bethesda units per milliliter. Immunosuppressive treatment was initiated with prednisone 1 milligram per kilogram daily and cyclophosphamide 200 milligrams daily. Factor VII levels normalized without evidence of inhibitor. The patient clinically improved and immunosuppressive medications were gradually tapered off. This case emphasizes the importance of prompt recognition in a patient with a rare acquired inhibitor of coagulation. Treatment with immunosuppressive therapy consisting of corticosteroids and cyclophosphamide resulted in normalization of factor VII levels and resolution of bleeding symptoms and should be considered as first-line management for such patients. Disclosures: Philipp: Baxter: Research Funding; Wyeth: Research Funding; Octapharma: Research Funding.

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Thrombophilic Polymorphisms Are Common in Women with Fetal Loss without Apparent Cause

Thrombosis and Haemostasis ◽

10.1055/s-0037-1614620 ◽

1999 ◽

Vol 82 (07) ◽

pp. 6-9 ◽

Cited By ~ 127

Author(s):

G. Sarig ◽

Z. Weiner ◽

J. Younis ◽

Z. Blumenfeld ◽

N. Lanir ◽

...

Keyword(s):

Pregnancy Termination ◽

Fetal Loss ◽

Factor V Leiden ◽

Late Pregnancy ◽

Mthfr C677t ◽

Control Group ◽

Factor V ◽

Third Trimester ◽

Factor Ii ◽

Significant Difference

SummaryAn association between fetal loss and thrombophilia has recently been described but has not been yet fully elucidated. We have evaluated prospectively the prevalence of the three common thrombophilic polymorphisms (TP) factor V G1691A (Leiden), thermolabile-methyl-enetetrahydrofolate reductase (TL-MTHFR) C677T and factor II G20210A mutations, in 76 women with fetal loss (≥3 in first, ≥2 in second, ≥1 in third trimester) without apparent cause and 106 controls without fetal loss. Thirty seven out of 76 (49%) of the women in the fetal loss group had at least one TP compared to only 23/106 (22%) in the control group (p = 0.0001). Factor V-Leiden was more common in the fetal loss group 24/76 (32%) compared to the control group 11/106 (10%) (OR = 4.0, 95% CI: 1.8-8.8, p <0.001). Five of the 76 patients (7%) were homozygous for factor V-Leiden compared to none of the controls (p = 0.012). A trend, albeit no statistically significant difference was found between women with fetal loss and control groups regarding factor II G20210A (8% vs. 4% respectively, OR = 2.2, 95% CI: 0.6-8.0, p = 0.23) and MTHFR C677T (18% vs. 10% respectively, OR = 1.95, 95% CI: 0.83-4.6, p = 0.12). Combined TP were documented in 6/76 (8%) patients compared to 1/106 (1%) in controls (OR = 9.0, 95% CI: 1.1-76, p = 0.02). Second or third trimester fetal loss were more common cause of pregnancy termination in 37 patients with TP compared to 39 patients without TP (57/158 (36%) vs. 23/135 (17%) respectively, (p = 0.0004). Thrombophilic polymorphisms are common in women with fetal loss without apparent cause and are associated with late pregnancy wastage. Combinations of TP increase the risk for fetal loss.

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Hemostatic Markers in Congestive Heart Failure Dogs with Mitral Valve Disease

Journal of Veterinary Medicine ◽

10.1155/2014/589873 ◽

2014 ◽

Vol 2014 ◽

pp. 1-6 ◽

Cited By ~ 3

Author(s):

Kreangsak Prihirunkit ◽

Amornrate Sastravaha ◽

Chalermpol Lekcharoensuk ◽

Phongsak Chanloinapha

Keyword(s):

Heart Failure ◽

Congestive Heart Failure ◽

Mitral Valve ◽

Mitral Valve Disease ◽

Valve Disease ◽

Factor Vii ◽

Control Group ◽

Total Plasma Protein ◽

At Iii ◽

D Dimer

Prothrombin time (PT), activated partial thromboplastin time (APTT), fibrinogen, D-dimer, antithrombin III (AT III), protein C (PC), factor VII (F.VII), and factor VIII (F.VIII), as well as hematocrit (HCT), platelets number (PLT), total plasma protein (TP), and albumin (ALB), were studied on fifty-eight congestive heart failure (CHF) dogs with mitral valve disease (MVD) and fifty control dogs. All of variables of MVD group, except APTT, were significantly different (P<0.5) from control group. The variables were also compared among functional classes of CHF dogs and control dogs. It was determined that the higher the functional class of CHF dogs was, the greater the levels of fibrinogen and D-dimer were, whereas the lesser the activities of AT III and PC were presented. Additionally, TP had linear correlation with fibrinogen, D-dimer, HCT, and PLT (r=0.31, 0.30, 0.43, and 0.38, resp., P<0.5). These findings suggested that fibrinogen and D-dimer were the factors predisposing hypercoagulability through an increase in blood viscosity. The hemorheological abnormalities would shift an overall hemostatic balance toward a more thrombotic state in CHF dogs with MVD.

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