Changes In Blood Coagulability Research Articles

Characterization of thromboelastography of patients with different pathological types of nephrotic syndrome.

To investigate the changes in blood coagulability as measured by thromboelastography (TEG) in patients with nephrotic syndrome of different etiologies as well as in patients with venous thromboembolic events (VTE).From January 2013 to October 2017, patients who were diagnosed as idiopathic membranous nephropathy (IMN), minimal change disease (MCD) and focal segmental glomerulosclerosis (FSGS) were enrolled into this retrospective study in which their clinical characteristics, including TEG variables, were investigated. According to the presence or absence of VTE, the patients with IMN were divided into 2 groups of VTE and non-VTE. The risk factors of VTE were analyzed with logistic regression.Significant differences in TEG parameters were found among the 3 groups of patients with R and K values lower, while the α-angle, maximum amplitude (MA) and confidence interval (CI) values higher, in the IMN group than those in the MCD and FSGS groups (P < .01). Multiple linear regression analysis indicated that the histologic subtype was an independent relevant factor of K time, angle, MA, and CI values. Multivariate logistic regression analysis revealed that serum albumin and CI value were independent risk factors of VTE (P < .05).The results showed that IMN patients may have higher whole blood coagulability than MCD and FSGS patients. The hypercoagulability in IMN patients may be attributed to platelet hyperactivity and the accelerated fibrin-platelet interaction. Hypoproteinemia and increased CI value were independent risk factors of VTE in IMN.

Compression in acute stroke: nursing considerations

British Journal of Neuroscience NursingVol. 11, No. Sup2 CommentCompression in acute stroke: nursing considerationsEmma GeeEmma GeeSearch for more papers by this authorEmma GeePublished Online:27 Apr 2015https://doi.org/10.12968/bjnn.2015.11.Sup2.20AboutSectionsView articleView Full TextPDF/EPUB ToolsAdd to favoritesDownload CitationsTrack CitationsPermissions ShareShare onFacebookTwitterLinked InEmail View article References CLOTS trial collaboration (2009) Effectiveness of thigh-length graduated compression stockings to reduce the risk of deep vein thrombosis after stroke (CLOTS Trial 1): a multicentre, randomised controlled trial. Lancet 373(9679): 1958–65 Crossref, Google ScholarCLOTS trials collaboration (2010) Thigh-length versus below-knee stockings for DVT prophylaxis after stroke: a randomised trial. Ann Intern Med 153(9): 553–62 Crossref, Google ScholarCLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration et al. (2013) Effectiveness of intermittent pneumatic compression in reduction of risk of deep vein thrombosis in patients who have had a stroke (CLOTS3): a multicentre randomised controlled trial. Lancet 382(9891): 516–24 Crossref, Google ScholarCLOTS (Clots in Legs Or sTockings after Stroke) Trials Collaboration (2014) Effect of intermittent pneumatic compression on disability, living circumstances, quality of life, and hospital costs after stroke: secondary analyses from CLOTS 3, a randomised trial. Lancet Neurol 13(12): 1186–92 Crossref, Google ScholarKearon C (2003) Natural History of Venous Thromboembolism. Circulation 107(23): 122–30 Google ScholarKelly J, Rudd A, Lewis RR, Coshall C et al. (2004) Venous Thromboembolism after acute ischaemic stroke; a prospective study using magnetic resonance direct thrombus imaging. Stroke 35: 2320–25 Crossref, Google ScholarKohro S, Yamakage M, Sato K et al. (2005) Intermittent pneumatic foot compression can activate blood fibrinolysis without changes in blood coagulability and platelet activation. Acta Anaesthesiologica Scandinavica 49: 660–4 Crossref, Google ScholarLankeit M, Konstantinides S (2011) Mortality risk assessment and the role of thrombolysis in pulmonary embolism. Critical Care Clinics 27(4): 953–67 Crossref, Google ScholarNational Institute for Health and Care Excellence (2010) NICE clinical guidance 92. Venous thromboembolism: reducing the risk: Reducing the risk of venous thromboembolism (deep vein thrombosis and pulmonary embolism) in patients admitted to hospital. https://www.nice.org.uk/guidance/cg92 (accessed 26 March 2015) Google ScholarNational Institute for Health and Care Excellence (2015) Addendum to NICE clinical guidance CG92. Reducing the risk of venous thromboembolism in patients admitted to hospital (Chapter 24-stroke patients). Draft for consultation. http://tinyurl.com/pdyk9xz (accessed 26 March 2015) Google ScholarStevens S, Woller S (2013) Intermittent pneumatic compression in patients with stroke. Lancet 382(9891): 484–6 Crossref, Google Scholar FiguresReferencesRelatedDetails 1 April 2015Volume 11Issue Sup2ISSN (print): 1747-0307ISSN (online): 2052-2800 Metrics History Published online 27 April 2015 Published in print 1 April 2015 Information© MA Healthcare LimitedPDF download

Seasonal variations in physical activity and implications for human health

This review explores the implications of seasonal changes in physical activity for fitness and human health. Photosensitivity and nutrient shortages mediate animal hibernation via the hypothalamus and changes in leptin and ghrelin concentrations. Opportunities for hunting and crop cultivation determine seasonal activity in under-developed human societies, but in developed societies temperature and rainfall are dominant influences, usually over-riding innate rhythms. Both questionnaire data and objective measurements show that many groups from children to the elderly increase their physical activity from winter to spring or summer. Measurements of maximal oxygen intake and muscle strength commonly show parallel seasonal changes. However, potential effects upon body mass and body fat may be counteracted by changes of food intake; subsistence agriculturists sometimes maintain or increase physical activity at the expense of a decrease in body mass. In developed societies, body fat commonly increases during the winter, with parallel changes in blood lipids, blood pressure and blood coagulability; moreover, these changes are not always fully reversed the following summer. Most developed societies show increased all-cause and cardiac mortalities in the winter. Health consequences of seasonal variations in physical activity including an increased vulnerability to cardiac catastrophe and a year-by-year increase in total body fat seem most likely if the average level of physical activity for the year is low. Public health recommendations should underline the importance of maintaining physical activity during adverse environmental conditions by adapting clothing, modifying behaviour and exploiting any available air-conditioned indoor facilities.

Changes in Blood Coagulability as It Traverses the Ischemic Limb

Changes in Blood Coagulability as It Traverses the Ischemic Limb

Intermittent pneumatic foot compression can activate blood fibrinolysis without changes in blood coagulability and platelet activation

Intermittent pneumatic foot compression (IPC) is a useful technique for prophylaxis of peri-operative venous thromboembolism. The aim of this study was to determine the effect of IPC on blood coagulation/fibrinolysis and platelet function using a blood viscometer (Sonoclot) and a platelet aggregation monitor (WBA analyzer(TM)), respectively. Using the same blood samples, serum levels of tissue-type plasminogen activator (t-PA), thrombomodulin (TM) and activated protein C (APC) were also measured. The soles and legs of each subject (n = 8) were compressed for 3 s (130 mmHg) at a 0.3-Hz interval using an IPC device. Parameters were measured 2 min before and at the end of 60-min compression. Parameters of the Sonoclot time-to-peak were shortened and clot retraction rate was increased significantly by IPC, whereas the other parameters did not change. These results indicate that IPC can activate blood fibrinolysis but not coagulability. A parameter of the WBA analyzer PATI (platelet aggregatory threshold index) did not change, indicating that IPC cannot activate platelet function per se. The concentration of t-PA decreased slightly but significantly. A decrease in the concentration of t-PA can lead to activation of fibrinolysis. Other humoral parameters did not change, indicating that IPC has no effect on endothelial function. Although neither blood coagulability nor platelet function were affected by IPC, fibrinolytic activity increased slightly, probably by activation of t-PA function. IPC is useful for prophylaxis for thromboembolism by activation of blood fibrinolysis as well as inhibition of blood stasis.

Changes in blood coagulability as it traverses the ischemic limb

Objective We undertook this study to determine whether changes in blood coagulability associated with peripheral arterial occlusive disease are due to contact with the atherosclerotic arterial wall or passage through distal ischemic tissue. Methods Thirty patients with peripheral arterial occlusive disease undergoing angiography participated in the study. Ankle-brachial pressure index was recorded before intervention. Blood samples taken from the aorta, common femoral artery, and common femoral vein were analyzed at thromboelastography. Angiograms were scored for stenotic disease by a radiologist blinded to the other results. Results When femoral artery samples were compared with aortic samples there was a decrease in reaction time (R; P < .05), an increase in maximum amplitude (MA; P < .05), and an increase in coagulation index (CI; P < .002), indicating an increase in coagulability as blood flowed down the iliac segment. These changes also correlated (ΔR, r = 0.442, P < .05; ΔMA, r = 0.379, P < .05; ΔCI, r = 0.429, P < .05) with the severity of disease in the ipsilateral iliac segment. Significant differences in R ( P < .05), angle ( P < .05), MA ( P < .005), and CI ( P < .001) between common femoral arterial and venous samples confirmed that venous samples were more coagulable in this group of patients. This difference in Thromboelastography parameters across the arteriovenous segment correlated inversely with the degree of ischemia (represented by ankle-brachial pressure index; ΔCI, r = −0.427, P < .05; ΔMA, r = −0.370, P < .05) in the puncture side limb. Conclusion Passage of blood down an atherosclerotic artery leads to an increase in coagulability proportional to the degree of stenosis in that vessel. Passage of blood through ischemic tissue may also contribute to increased coagulability in peripheral arterial occlusive disease.

Thromboembolism.

Venous thomboembolism (VTE) causes only about 2% of maternal deaths in the developing world but is a leading cause of direct maternal deaths in developed countries. Pregnancy increases the risk of VTE through venous stasis, changes in blood coagulability and damage to vessels. Early diagnosis of VTE depends crucially on awareness of the condition but clinical diagnosis is unreliable in pregnancy and objective testing is essential. Compression or duplex ultrasonography is used to diagnose deep venous thrombosis and a ventilation/perfusion scan for pulmonary embolism. Low molecular weight heparins are safe and effective for treatment and for thromboprophylaxis in pregnancy. All women should undergo risk assessment in early pregnancy or preferably before pregnancy. Identifying risk factors such as obesity, or a past or family history of thromboembolism, allows at-risk women to be offered thromboprophylaxis. Guidelines on thromboprophylaxis have reduced deaths after caesarean section and are now being developed for all women.

Neurotrauma &amp; Deep Vein Thrombosis

Neurotrauma &amp; Deep Vein Thrombosis

Experimental Investigation of Hypercoagulant Conditions Associated with Angiography

To evaluate changes in blood coagulability after high-velocity intravascular fluid injections under conditions relevant to angiography. In 101 rabbits, fluids were injected at 1,000 psi (6,890 kPa) via a multiple-side-hole catheter in the abdominal aorta, while blood was simultaneously aspirated via a second downstream catheter. The fluids injected included saline, contrast media, blood, tissue plasminogen activator, and heparin. The aspirate was evaluated for clotting time with an activated clotting time (ACT) device, for elevated levels of plasma hemoglobin to confirm capture of at least part of the injection bolus in the sample, and sometimes for hematocrit or fibrin degradation products (FDP). A single high-pressure injection of 2 mL of saline briefly accelerated the ACT of a blood-saline bolus (mean, 38% +/- 4). The mean volume of the hypercoagulable bolus was 15 mL. Systemic FDP levels became elevated within a few minutes after initial injection, suggesting activation of the fibrinolytic system by intravascular clot formation. Subsequent injections produced less hypercoagulability, probably reflecting the anticoagulant effects of FDP. Pressure-injected contrast agents had anticoagulant effects. The ACT was accelerated by up to 80% after injection of blood that had remained within the catheter for 3-10 minutes. Glove powder or gauze lint from wiping the guide wire markedly accelerated intracatheter clotting. Hypercoagulability after injection of clotting blood was partially prevented by injections with contrast agent and was completely inhibited by low-dose systemic heparinization. A hypercoagulable bolus may occur after angiographically relevant high-pressure fluid injections. The major contributing factors appear to be high jet velocities and injection of small amounts of clotting blood. Heparinization provides a simple and effective means of prevention.

Prevention of venous thrombosis and pulmonary embolism

Deep vein thrombosis (DVT) leads to hospitalization for up to 600,000 persons each year in the United States. Venous thrombosis in itself may be benign, but the condition can lead to dangerous complications and has a high recurrence rate. Strategies to prevent DVT involve prevention of stasis and reversal of changes in blood coagulability that allow thrombi to form. Pharmacologic agents have been effective in reducing the incidence of DVT and pulmonary embolism. Low-dose subcutaneous heparin is considered a nearly ideal DVT preventative for surgically treated patients. The risk of hemorrhage is the main limitation to routine use of subcutaneous anticoagulants for DVT, but careful patient selection can minimize that risk. After anticoagulant therapy with heparin, generally for 7 to 10 days, oral warfarin is the drug of choice for maintenance anticoagulation to prevent DVT recurrence. Therapy for pulmonary embolism is the same as for DVT—immediate anticoagulation with heparin followed by maintenance with warfarin.

Tumor necrosis factor infusions have a procoagulant effect on the hemostatic mechanism of humans

Several investigators have reported that tumor necrosis factor (TNF) can alter the hemostatic properties of vascular endothelial cells in vitro. We have examined the in vivo effects on the hemostatic mechanism of recombinant human TNF administered as a continuous intravenous infusion to 23 cancer patients with active disease. A battery of sensitive and specific immunochemical techniques were used to monitor changes in blood coagulability. Serial determinations of F1 + 2, the protein C activation peptide (PCP), and fibrinopeptide A (FPA) were obtained prior to the initiation of the TNF infusions and at three and 24 hours after the start of therapy in 12 individuals who received greater than 3 x 10(5) U/m2/24h. The mean levels of F1 + 2, PCP, and FPA were significantly elevated at both time points as compared to the baseline values. The metabolic behavior of 125I-F1 + 2 in an animal model was not affected by infusions of the cytokine. We therefore conclude that the observed elevations in the concentration of this marker in humans receiving TNF result from hemostatic system hyperactivity. In 11 subjects infused with 1 x 10(5) to 2.4 x 10(5) U/m2/24 h of the cytokine, the mean levels of F1 + 2, PCP, and FPA were not significantly greater at 24 hours as compared with the baseline values, indicating that there is a threshold dose at which the cytokine can exert a biochemical effect on the coagulation system. Our studies demonstrate that TNF is able to provide a substantial net procoagulant stimulus to the hemostatic mechanism, and suggest that this cytokine may be a mediator of certain hypercoagulable states in humans.

Tumor Necrosis Factor Infusions Have a Procoagulant Effect on the Hemostatic Mechanism of Humans

AbstractSeveral investigators have reported that tumor necrosis factor (TNF) can alter the hemostatic properties of vascular endothelial cells in vitro. We have examined the in vivo effects on the hemostatic mechanism of recombinant human TNF administered as a continuous intravenous infusion to 23 cancer patients with active disease. A battery of sensitive and specific immunochemical techniques were used to monitor changes in blood coagulability. Serial determinations of F1+2, the protein C activation peptide (PCP), and fibrinopeptide A (FPA) were obtained prior to the initiation of the TNF infusions and at three and 24 hours after the start of therapy in 12 individuals who received greater than 3 × 105 U/m2/24 h. The mean levels of F1+2, PCP, and FPA were significantly elevated at both time points as compared to the baseline values. The metabolic behavior of 125I-F1+2 in an animal model was not affected by infusions of the cytokine. We therefore conclude that the observed elevations in the concentration of this marker in humans receiving TNF result from hemostatic system hyperactivity. In 11 subjects infused with 1 × 105 to 2.4 × 105 U/m2/24 h of the cytokine, the mean levels of F1+2, PCP, and FPA were not significantly greater at 24 hours as compared with the baseline values, indicating that there is a threshold dose at which the cytokine can exert a biochemical effect on the coagulation system. Our studies demonstrate that TNF is able to provide a substantial net procoagulant stimulus to the hemostatic mechanism, and suggest that this cytokine may be a mediator of certain hypercoagulable states in humans.

The pathophysiology of the prethrombotic state in humans: insights gained from studies using markers of hemostatic system activation

Numerous investigators have postulated that a hypercoagulable state exists in humans for a period of time before the development of thrombotic episodes. A clear biochemical definition of the prethrombotic state, however, has proved elusive due in part to the lack of reliable techniques for monitoring pertinent changes in blood coagulability. Based on recent advances in our knowledge of the biochemistry of the coagulation system, a series of highly sensitive and specific immunochemical tools has been developed that can quantitate the activities of various steps of the hemostatic mechanism in vivo at the subnanomolar level. We have established assays for F1+2 and the protein C activation peptide, which measure the cleavage of the prothrombin molecule by factor Xa and the scission of protein C by the thrombin-thrombomodulin complex, respectively. Nossel and coworkers had previously constructed similar assays for fibrinopeptide A (FPA) and fragment B beta 1–42, which monitor the cleavage of fibrinogen by thrombin and the proteolysis of fibrin I by plasmin, respectively. Substantial elevations in the levels of these markers have been found in patients with disseminated intravascular coagulation and many subjects with acute deep venous thrombosis. The F1+2 and FPA assays have been used to demonstrate that significant increments in factor Xa activity but not thrombin activity regularly occur in the blood of nonanticoagulated individuals with congenital deficiencies of antithrombin or protein C. These two disorders are known to be correlated with the subsequent development of thrombosis. Patients with protein C deficiency have also been noted to have significantly reduced plasma levels of protein C activation peptide. By using the immunoassays for FPA and B beta 1–42 in studies of postoperative patients, it has been shown that an imbalance between the procoagulant action of thrombin and the anticoagulant effect of plasmin on fibrin I polymer may induce an acquired thrombotic diathesis. Finally, we have recently demonstrated that prothrombin activation as measured by the F1+2 assay is suppressed by oral anticoagulants in the blood of patients with thrombotic diatheses. These investigations suggest that these assay techniques can be used to improve our understanding of the hypercoagulable state as well as to develop more effective treatment strategies for the prevention of thromboembolic events.

The Pathophysiology of the Prethrombotic State in Humans: Insights Gained From Studies Using Markers of Hemostatic System Activation

Numerous investigators have postulated that a hypercoagulable state exists in humans for a period of time before the development of thrombotic episodes. A clear biochemical definition of the prethrombotic state, however, has proved elusive due in part to the lack of reliable techniques for monitoring pertinent changes in blood coagulability. Based on recent advances in our knowledge of the biochemistry of the coagulation system, a series of highly sensitive and specific immunochemical tools has been developed that can quantitate the activities of various steps of the hemostatic mechanism in vivo at the subnanomolar level. We have established assays for F1+2 and the protein C activation peptide, which measure the cleavage of the prothrombin molecule by factor Xa and the scission of protein C by the thrombin-thrombomodulin complex, respectively. Nossel and coworkers had previously constructed similar assays for fibrinopeptide A (FPA) and fragment B beta 1-42, which monitor the cleavage of fibrinogen by thrombin and the proteolysis of fibrin I by plasmin, respectively. Substantial elevations in the levels of these markers have been found in patients with disseminated intravascular coagulation and many subjects with acute deep venous thrombosis. The F1+2 and FPA assays have been used to demonstrate that significant increments in factor Xa activity but not thrombin activity regularly occur in the blood of nonanticoagulated individuals with congenital deficiencies of antithrombin or protein C. These two disorders are known to be correlated with the subsequent development of thrombosis. Patients with protein C deficiency have also been noted to have significantly reduced plasma levels of protein C activation peptide. By using the immunoassays for FPA and B beta 1-42 in studies of postoperative patients, it has been shown that an imbalance between the procoagulant action of thrombin and the anticoagulant effect of plasmin on fibrin I polymer may induce an acquired thrombotic diathesis. Finally, we have recently demonstrated that prothrombin activation as measured by the F1+2 assay is suppressed by oral anticoagulants in the blood of patients with thrombotic diatheses. These investigations suggest that these assay techniques can be used to improve our understanding of the hypercoagulable state as well as to develop more effective treatment strategies for the prevention of thromboembolic events.

Changes of Blood Coagulability and Effects of the Platelet Aggregation Inhibitor (Ticlopidine) in Experimental Subarachnoid Hemorrhage in Dogs

It has been reported that vasospasms are frequently associated with changes in blood coagulability, which may play an important role in symptomatic vasospasms. To verify this point experimental studies were performed to analyze the changes of blood coagulability after subarachnoid hemorrhage (SAH) and to investigate the effect of the platelet coagulation inhibitor. SAH was produced by cisternal injection of autogeneous arterial blood in 50 mongrel dogs. Blood sampling and angiography were carried out every 1-3 days and the basilar artery was histologically examined 7-8 days after the bleeding. No changes of prothrombin time, partial thromboplastin time and activated coagulation time were noted before or after the bleeding and also by the oral administration of the platelet aggregation inhibitor. Increase of the platelet aggregation rate was noted from one day after SAH. Increase of fibrinogen on day 1-3 and return to the basal value on day 7-8 after SAH were also observed. These changes were prevented by oral administration of the platelet aggregation inhibitor though no angiographical and histological changes were induced. These findings indicate that this drug has the potential of preventing symptoms of vasospasms after SAH.

Assays for hypercoagulability.

Many investigators have attempted to determine whether a relationship exists between excessive activity of the hemostatic mechanism and the atherosclerotic process. A major difficulty encountered in unraveling this puzzle has been the lack of reliable techniques for quantifying pertinent changes in blood coagulability. We have focused our attention on detecting alterations in the zymogens and protease inhibitors of the coagulation system which might occur prior to the development of overt thrombotic phenomena. Measurement of these early changes may be critical, if we wish to dissect the molecular events which are ultimately responsible for the atherosclerotic lesion and intervene with appropriate therapy prior to the onset of gross pathologic changes. In the sections below, we outline the difficulties associated with developing this methodology. Furthermore, we describe two new radioimmunoassays that may serve as prototype techniques for monitoring the activity of the hemostatic mechanism.

Intermediate product I of prothrombin proteolysis as a natural factor of the anticoagulating system stimulation

Injection of Intermediate product I (P-I) resulting from prothrombin proteolysis by thrombin, into the systemic circulation of frog leads to mobilization of the anticoagulating and fibrinolytic potential of the organism. No effect is observed in animals with destroyed central nervous system. Perfusion of humorally isolated carotid labyrinth of frog by P-I considerably increases the bioelectric activity of carotid chemoreceptors and induces changes in blood coagulability in the systemic circulation. The resulting changes are accompanied by an increase in total coagulation time, overall fibrinolytic activity and non-enzymic fibrinolysis. The data obtained are indicative of reflex excitation of the anticoagulating system by P-I, which possesses no coagulating activity, but is structurally similar to thrombin.

Blood coagulation studies in a long-term experiment on dietary prevention of ischemic heart disease

In a long-term investigation the serum cholesterol level was lowered with the aid of an exchange of dietary saturated fatty acids for polyunsaturated fatty acids. After 6 years of diet, the experimental and control populations were reversed. Blood coagulation tests were made both before and after reversal of the diets. Whole blood clotting time (WBCT) and stypven time were determined twice, heparin tolerance time (HTT) and fibrinolysis in euglobulins only prior to the reversal of the diet. 150 male subjects were included in the first phase of the study; 129 of them were available for the second phase. On both occasions, the stypven time was shorter in the same group, in spite of the intervening reversal of the diets. There was no difference in WBCT and HTT, but the fibrinolysis was shorter in the control group. The intraindividual changes diverged: WBCT became more prolonged in the group changing from polyunsaturated to saturated fat intake, while stypven time was shortened more among the same group. WBCT was positively correlated with cholesterol and lipid phosphorus. Stypven time had negative correlations with relative body weight (RBW), systolic and diastolic blood pressure, and with serum cholesterol, triglyceride and lipid phosphorus. HTT was also negatively correlated with systolic pressure. Fibrinolysis time showed positive correlations with RBW, cholesterol and triglycerides. The observed lower incidence of ischemic heart disease in the group on the polyunsaturated diet evidently was not mediated by any changes in blood coagulability revealed by the tests used.

An Experimental Study on the Effect of Transfusion and Various Fluid Therapy upon Blood Coagulability in Acute Blood Loss

Fourty-eightmongrel dogs were bled to half the level of their control aystolic blood pressures and infused with Hartmanns solution, low molecular weight dextran, whole blood, or with Hartmann''s solution, low molecular weight dextran (1:1 or 1:3) in the amount equivalent to the blood loss. Bleeding time, coagulation time, platelet count and erythrocyte sedimentation rate were examined 6 hours and 24 hours after the completion of infusion. The results are as follows: 1) No changes in blood coagulability other than due to hemodilution were observed in dogs infused with Hartmann''s solution, whole blood, or 1: 1 Hartmann''s solution+low molecular weight dextran. 2) Significant changes in blood coagulability were noted, however, in dogs infused with low molecular weight dextran alone or 1:3 Hartmann''s solution+low molseular weight dextran. These changes seem to be related rather to decreased platelet function than to the decease in platelet number.

Correlative study of blood coagulation and serum lipids in diabetics without clinically recognizable complications

Blood coagulability and serum lipids have been studied in 28 diabetic patients without clinically recognizable complications. Changes of plasma FFA were correlated with platelet adhesiveness and thromboplastic activity. Positive correlation was also obtained between serum phospholipids on one hand and whole blood coagulation and recalcification times on the other hand. Although these results showed that changes in blood coagulability and blood lipids are closely associated yet they are probably two separate phenomena coexisting in the same disease.