Thrombotic Tendency In Patients Research Articles

Thrombosis Tendency After Splenectomy in a Danish Family With Hemoglobin Volga, and a Literature Review

Hemoglobin (Hb) Volga is a rare, unstable β-chain hemoglobin variant (β27 Ala→Asp), causing chronic hemolytic anemia. This study presents two members of a Danish family, splenectomized due to Hb Volga at and with multiple thrombotic events. The proband was diagnosed with Hb Volga 9 years old and splenectomy was performed as a part of treatment. Throughout his life, he experienced multiple superficial thrombophlebitis, two episodes of distal deep venous thrombosis (DVT) on lower extremities (age 32 and 33) and a transient ischemic attack (TIA) presented as amaurosis fugax (age 51). Thrombophilia investigation was normal. The proband’s son was diagnosed with Hb Volga and underwent splenectomy at the age of 6. Despite anticoagulation therapy, he suffered from multiple venous thromboembolic events in his youth and died of chronic pulmonary embolism (PE)/pulmonary hypertension combined with infection. Given the observed propensity for multiple thromboses in these two patients, a literature review was conducted investigating reported occurrence of thrombotic events in individuals with Hb Volga. Currently 25 cases of Hb Volga are reported worldwide. The clinical symptoms primarily described are related to hemolytic anemia. Splenectomy is reported in 15 patients. Thromboses have previously been reported in only three patients who were also splenectomized. These cases involved DVT and PE, myocardial infarction, and an unspecified thrombotic event. The proband represents the first reported Hb Volga case with both venous and arterial thrombotic disorders. The exact mechanism underlying thrombotic tendency in patients with Hb Volga remains unknown, but it is probably associated with splenectomy.

Neutrophil extracellular traps enhance procoagulant activity and thrombotic tendency in patients with obstructive jaundice.

Patients with obstructive jaundice (OJ) are considered to be prothrombotic with increased risk of thromboembolism complications. The role of neutrophil extracellular traps (NETs) in procoagulant activity (PCA) and thrombosis risk in patients with OJ is unclear. In this study, we investigated NETs formation in OJ patients and the role of elevated unconjugated bilirubin (UCB) in inducing NETs, resulting in enhanced PCA and endothelial injury. NETs of OJ patients and healthy controls were measured. NETs PCA was assessed via coagulation time (CT), fibrin formation and purified coagulation complex production assays. Visualization of NETs and mitochondrial reactive oxygen species (MitoROS) were performed with a fluorescence microscope. We further used confocal microscopy to quantify the exposure of phosphatidylserine (PS), fibrin strands and FVa/Xa on Human umbilical vein endothelial cells (HUVECs). Assessment of NETs components levels revealed greater NETs production in OJ patients than in healthy controls. Importantly, OJ-NETs were responsible for enhanced PCA. UCB induced NETs formation via MitoROS accumulation and mitochondrial mobilization. HUVECs cocultured with OJ NETs lost their cell-cell junctions and consequently converted to a procoagulant phenotype. The PCA was attenuated by using DNase I alone or in combination with lactadherin. Our results suggest that UCB-induced NETs play a prominent role in promoting the hypercoagulable and prothrombotic state in OJ patients. The increased MitoROS accumulation in neutrophils initiated NETosis. NETs are promising targets for indicating or improving coagulation disorders in OJ patients.

High Prevalence of Acquired Thrombophilia Without Prognosis Value in Patients With Coronavirus Disease 2019.

BackgroundRecent literature reports a strong thrombotic tendency in patients hospitalized for a coronavirus disease 2019 (COVID‐19) infection. This characteristic is unusual and seems specific to COVID‐19 infections, especially in their severe form. Viral infections can trigger acquired thrombophilia, which can then lead to thrombotic complications. We investigate for the presence of acquired thrombophilia, which could participate in this phenomenon, and report its prevalence. We also wonder if these thrombophilias participate in the bad prognosis of severe COVID‐19 infections.Methods and ResultsIn 89 consecutive patients hospitalized for COVID‐19 infection, we found a 20% prevalence of PS (protein S) deficiency and a high (ie, 72%) prevalence of antiphospholipid antibodies: mainly lupus anticoagulant. The presence of PS deficiency or antiphospholipid antibodies was not linked with a prolonged activated partial thromboplastin time nor with D‐dimer, fibrinogen, or CRP (C‐reactive protein) concentrations. These coagulation abnormalities are also not linked with thrombotic clinical events occurring during hospitalization nor with mortality.ConclusionsWe assess a high prevalence of positive tests detecting thrombophilia in COVID‐19 infections. However, in our series, these acquired thrombophilias are not correlated with the severity of the disease nor with the occurrence of thrombotic events. Albeit the strong thrombotic tendency in COVID‐19 infections, the presence of frequent acquired thrombophilia may be part of the inflammation storm of COVID‐19 and should not systematically modify our strategy on prophylactic anticoagulant treatment, which is already revised upwards in this pathological condition.RegistrationURL: https://www.clini​caltr​ials.gov; Unique identifier: NCT04335162.

Thrombophilia in systemic lupus erythematosus: A case-control study

To investigate the thrombotic tendency in patients with systemic lupus erythematosus (SLE) by evaluating congenital and acquired abnormalities with an increased risk of thrombosis. A total of 53 patients with SLE were included in the study. Fifty-three healthy controls paired by age and sex were assessed. Anticardiolipin antibodies (aCL), anti β2 glycoprotein (aβ2GP), lupus anticoagulant (LAC), protein C (PC), protein S (PS), antithrombin (AT), acquired activated protein C, and homocysteinemia were evaluated. Comparisons for categorical variables were analyzed by Chi2 and student tests. The patients were all female and had a mean age of 30.6 years (16/58). The healthy controls were all female and their mean age was 30.8 years (17/56). Five patients (9.4%) developed venous thrombosis during the 24 months of follow-up. The antiphospholipid antibodies were positive in 17 patients (32.1%) and negative in all healthy controls (P=0.01). PS deficiency was noted in 17 patients (32.1%) and in 5 controls (P=0.004). Hyperhomocysteinemia was noted in 16 patients (30.2%) versus 3 controls (5.6%) (P=0.002). Test for PC deficiency and acquired activated protein C showed no significant difference between the two groups. No AT deficiency was found in the patients. The study of clinical and biological correlations based on the presence and absence of thrombophilic parameters concluded to a significant association between Protein C deficit and thrombosis (P=0.02) and acquired activated protein C resistance and thrombosis (P=0.04). There was no significant association between the APL and thrombosis. Thrombophilic abnormalities were significantly more frequent in lupus patients than in healthy controls. Thrombotic events were significantly associated with PC deficit and acquired protein C resistance. There was no correlation between antiphospholipid antibodies and thrombosis.

The association between P selectin glycoprotein ligand 1 gene variable number of tandem repeats polymorphism and risk of thrombosis in Behçet's disease.

Behçet's disease (BD) has been recognized as an unclassified type of vasculitis with an accompanying tendency to thrombosis. No disease-specific pathology has been demonstrated so far to explain the prothrombotic state, and this predisposition is considered to be associated with endothelial activation/dysfunction. P-selectin glycoprotein ligand-1 (PSGL-1) variable number of tandem repeat (VNTR) polymorphism has an impact on the protein length, and heterozygosity affect of the PSGL-1 to P-selectin interaction, which has been found to be associated with an increased risk of thrombosis in patients with antiphospholipid syndrome. We aimed to analyze the association of PSGL-1 gene polymorphism, in a group of BD patients with and without thrombosis. The study group consisted of 136 BD patients (112 male, 24 female) with thrombosis, 120 BD patients without thrombosis (54 male, 66 female) during at least 5years disease course, and 190 healthy controls (103 male, 87 female) All patients fulfilled the International Study Group criteria for classification of BD. Genotyping for the PSGL-1 gene exon 2 VNTR polymorphism was carried out with the amplification of genomic DNA and running of the polymerase chain reaction product on agarose gel electrophoresis. The frequency of heterozygous genotypes (AB+AC+BC) was greater in BD patients with thrombosis compared to BD patients without thrombosis (33.1% vs. 20.8%, P=0.028, odds ratio=1.85). However, the increased frequency of heterozygous genotypes in BD patients with thrombosis did not reach a statistically significant level compared to healthy controls (33.1% vs. 32.6%). PSGL-1 VNTR polymorphism may have limited contribution to the thrombotic tendency in patients with BD.

Coagulation profile in patients with chronic kidney disease before and after kidney transplantation: A retrospective cohort study.

Patients with chronic kidney disease (CKD) tend to experience both thrombotic and hemorrhagic complications; however, the pathophysiology remains unclear. This study aimed to identify the underlying mechanisms and characteristics of hemostatic problems in patients with CKD and to demonstrate the role of kidney transplantation (KT) in correcting these hemostatic abnormalities. In this retrospective observational study, 557 KT recipients who did not receive perioperative plasmapheresis and who did not exhibit graft failure within 1month after KT were included. KT recipients demonstrated increased levels of homocysteine and D-dimer. A total of 80.9% of patients exhibited ≥1 thrombophilic factor at pre-transplantation, and the proportion of these patients decreased to 47% at 28th post-operative day (P<.001). The renal function of patients with no thrombophilic factors was better than that of patients with ≥1 thrombophilic factor at all post-operative assessments (P<.001). The duration of pre-operative dialysis significantly correlated with the thrombotic tendency of patients with CKD before and after KT. Patients with CKD can exhibit hypercoagulability, which might be caused by reduced renal function per se. Both HD and PD can aggravate the prothrombotic tendency of patients with CKD via different mechanisms. Most thrombophilic factors in patients with CKD were corrected after KT.

Is There a Thrombotic Tendency in Patients with Familial Mediterranean Fever? A Small Case Series and Review of the Literature

OBJECTIVES: Familial Mediterranean fever (FMF) is an auto-inflammatory disease characterized by fever, abdominal pain and pleuritic attacks. It is well-known that there is a relationship between inflammation and thrombosis. However, there is very limited knowledge about thrombotic tendency in familial Mediterranean fever (FMF). Here we reported two patients with FMF who developed thrombo-embolic events in the presence of acquired thrombophilic factors. We would also like to review additional published 5 FMF cases developed thromboembolic event as well as discuss haemostatic mechanisms in FMF patients briefly. METHODS: We conducted a comprehensive review of the English literature to analyze data on thrombotic or thromboembolic event in patients with FMF. The Pub-Med, Web of Science, Proquest, Ovid databases were searched for the articles using the terms FMF combined with one of the following terms: thrombosis, thromboembolism, deep venous thrombosis, pulmonary embolism. RESULTS: In four English articles, we identified 5 FMF patients plus our two cases with thrombotic complications. Hereditary or at least one acquired thrombophilic factor was determined in 6 cases. One patient had not had any thrombophilic factor. M694V mutation was determined in 5 patients. In 6 patients, thrombotic events developed under the age of 45 years. CONCLUSIONS: Thromboembolic events may rarely develop in FMF patients with the presence of congenital or inherited thrombophilic disorders.

Idiopathic intracranial hypertension: Can studies of obesity provide the key to understanding pathogenesis?

The pathogenesis of idiopathic intracranial hypertension (IIH) is poorly understood. Several mechanisms have been suggested, but no one mechanism has been able to account for all manifestations of the disease. Although IIH predominantly affects obese, premenopausal women, little is known about whether or how the obesity contributes to the IIH. Obesity is a heterogeneous condition, consisting of different phenotypes that are influenced by the regional distribution of adipose tissue. This review explores the literature to integrate current knowledge on the relationships between obesity and IIH. The review evaluates the hypotheses that dysregulation of insulin, glucose metabolism, sex hormones, adipokines, glucocorticoids, lipids and free fatty acids in obesity could predispose to IIH. One potential common pathway linking metabolic disorders to the pathogenesis of IHH is a thrombotic tendency due to dysregulation of haemostatic risk factors. This could cause either occult cerebral sinus thrombosis or partial thrombosis of the parasagittal venous lacunae, with subsequent impaired resorption of cerebrospinal fluid and venous hypertension. Investigations that evaluate obesity, fat metabolism, endocrinological dysregulation and thrombotic tendency in patients with IIH are required so that pathogenic mechanisms can be clarified and management strategies in IIH can be improved.

Identifying hypocoagulable states with a modified global assay of overall haemostasis potential in plasma

To test the sensitivity of the global assay of overall haemostasis potential (OHP) in detecting hypocoagulation, the OHP was assayed in plasma containing exogenous thrombin (0.04 IU/ml), tissue-plasminogen activator (330 ng/ml), Ca and a platelet reagent. Commercial plasmas with factor II, V, VIII, IX, X, XI, XII or VII deficiency were mixed with normal plasma in different proportions to imitate different severities. Samples from patients with haemophilia and factor XII deficiency were also examined. No clot was found in the absence of factor II/factor X, indicating that the tiny dose of thrombin worked solely as a trigger for the intrinsic pathway activation. Changed levels of the investigated coagulants, apart from factor XII, influenced the outcome. OHPs were decreased in patients with haemophilia but were unchanged or even increased in those with factor XII deficiency. This modified OHP method may therefore be useful for estimating the bleeding tendency in haemophilic patients and to find suitable doses and intervals for prophylactic treatment. It may also be of use in investigations of the effect of antifibrinolytic drugs as well as for identifying a thrombotic tendency in patients with factor XII deficiency. For detection of other coagulation factor deficiencies, our investigations with the commercial plasmas suggest that the OHP assay is also valuable, especially when the intrinsic pathway of the coagulation cascade is impaired.

Thrombosis in systemic lupus erythematosus: Congenital and acquired risk factors

To investigate the thrombotic tendency in patients with systemic lupus erythematosus (SLE) by evaluating congenital or acquired abnormalities associated with an increased risk of venous and/or arterial thrombosis. A total of 57 patients with SLE were included in the study. Twenty-one patients (37%) had a history of arterial and/or venous thrombosis and 36 patients (63%) did not have such a history. Sera from 50 healthy controls were examined. Protein C, protein S, antithrombin, D-dimer, fibrinogen, homocysteine, anticardiolipin antibodies (aCL), lupus anticoagulant (LAC), prothrombin G20210A, and methylenetetrahydrofolate reductase (MTHFR) C677T gene mutation were evaluated. Protein C, antithrombin, fibrinogen, D-dimer, and homocysteine levels were significantly higher in patients with SLE than in controls. A prothrombin mutation was observed in 2 (4%) of 50 controls and in 6 (11%) of 57 patients. A significantly higher prevalence (P = 0.036) of MTHFR homozygous mutation was observed in patients with SLE (14 [25%] of 57) in comparison with controls (4 [8%] of 50). IgG-aCL and IgM-aCL levels were significantly higher in patients with SLE than in controls (P < 0.0001). The presence of medium-high (> or = 20 IgG phospholipid units/ml) IgG-aCL antibody titers was significantly higher (P = 0.005) in patients with thrombosis (11 [52%] of 21) than in patients without (5 [14%] of 36) thrombosis. LAC was present in 22 (38.5%) of 57 patients and in none of 50 controls. In this study, we confirm the association between thrombosis and IgG-aCL at medium-high titers and suggest that the coexistence of other risk factors can affect the expression of thrombosis in patients with SLE.

Survey of factor V leiden and prothrombin gene mutations in systemic lupus erythematosus.

The two most common hereditary risk factors for thrombosis are factor V Leiden mutation and a prothrombin gene mutation. There is indeed a thrombotic tendency in patients with systemic lupus erythematosis (SLE) and it is not always associated with antiphospholipid antibodies. We aimed to determine the relationship between both factor V Leiden and prothrombin gene mutations and SLE. Using polymerase chain reaction (PCR) the factor V Leiden and prothrombin gene mutations were evaluated in 55 patients (20 children and 35 adults) with SLE. Although seven patients were found to have factor V Leiden mutation in the heterozygous state, two had the heterozygous G-->A (20210) prothrombin gene mutation. Although one had these two mutations concurrently, these two patients did not have thrombosis. The factor V Leiden mutation frequency (12.7%) was higher than that of our general population (7.1%). On the other hand, seven of the patients with SLE had a thrombotic event. Although of these seven, four (57%) had factor V Leiden mutation, three (43%) had no mutation. Of 48 patients with no thrombotic history, only three had the factor V mutation (6.25%). The prevalence of the factor V Leiden mutation in SLE patients with and without thrombosis was significantly different by Fisher's exact test (p<0.05). The risk of venous thrombosis in patients with factor V Leiden increased threefold compared to that in those without factor V Leiden mutation (odds ratio 20.1; CI 2.99-133.6). Although factor V Leiden mutation seems to play a role in the development of venous thrombosis in SLE, the development of thrombosis in SLE is multifactorial.

No evidence for an increased risk of venous thrombosis in patients with factor V Leiden by the homozygous 677 C to T mutation in the methylenetetrahydrofolate-reductase gene.

Hyperhomocysteinemia is an established risk factor for arterial and venous thrombosis. Recently, it has been shown that a C to T mutation at nt position 677 in the methylenetetrahydrofolate-reductase (MTHFR) gene is a common cause of moderately elevated levels of plasma homocysteine in adults. In order to investigate whether the newly recognized genetic alteration in the MTHFR gene potentiates the thrombotic tendency in patients with factor V Leiden, we studied 81 unrelated patients with a history of venous thrombosis and a heterozygous factor V Leiden mutation. In addition, we analyzed 111 family members of 34 families in which the proband had a heterozygous factor V Leiden mutation. In all individuals, factor V Leiden and the MTHFR mutation were tested and the occurrence of venous thrombotic events was evaluated retrospectively. Seventy-seven healthy subjects without the factor V Leiden mutation or any other known thrombotic risk factor served as a control group. The prevalence of the homozygous MTHFR mutation was similar in index patients (10 of 81, 12%) and in the control group (10 of 77, 13%). The median age at first thrombosis in index patients was 32 years (range 22-69 years) in 10 patients with heterozygous factor V Leiden and T/T MTHFR mutation, and 34 years (range 6-72 years) in 71 patients with the factor V Leiden mutation only. In the family members, the prevalence of thrombosis was not higher in patients with factor V Leiden and +/+ MTHFR genotype than in those with only the heterozygous factor V Leiden mutation. We conclude from these data that the 677 C to T mutation in the MTHFR gene does not represent a significant additional risk factor for venous thrombosis in patients with factor V Leiden mutation.

Apparent Different Thrombotic Tendency in Patients With Factor V Leiden and Protein C Deficiency Due to Selection of Patients

AbstractBoth activated protein C (APC) resistance and protein C deficiency are associated with an increased risk for venous thrombosis. To assess their tendencies to venous thrombosis, we compared the median age of first venous thromboembolism in patients with factor V Leiden or protein C deficiency, who were identified either within unselected consecutive cases with a first deep venous thrombosis derived from a population-based case-control study, or identified by selection of patients with a deep venous thrombosis, who were referred for thrombophilia work-up. The median age of onset for 92 unselected APC resistant cases was 43 years and for 13 unselected protein C-deficient cases 47 years. The median age at the first thrombotic event for 28 APC-resistant members of thrombophilia families was 29 years and for 50 protein C-deficient members of thrombophilia families 31.5 years. The median age of onset for all unselected patients (n = 105) was 45 years of age (range, 16 to 69 years) and the median age of onset for all selected patients from the thrombophilia families (n = 78) was 30.5 years (range, 16 to 67 years). These results show that within the case-control study and the family studies, the median age of onset is very similar in patients with APC resistance and patients with protein C deficiency. This suggests that APC resistance is not less severe with respect to risk of thrombosis than (heterozygous) protein C deficiency. In conclusion, the median age at which the first thrombosis occurs mainly depends on the way the patients are identified and not on the type of thrombophilia.

Apparent different thrombotic tendency in patients with factor V Leiden and protein C deficiency due to selection of patients

Both activated protein C (APC) resistance and protein C deficiency are associated with an increased risk for venous thrombosis. To assess their tendencies to venous thrombosis, we compared the median age of first venous thromboembolism in patients with factor V Leiden or protein C deficiency, who were identified either within unselected consecutive cases with a first deep venous thrombosis derived from a population-based case-control study, or identified by selection of patients with a deep venous thrombosis, who were referred for thrombophilIa work-up. The median age of onset for 92 unselected APC resistant cases was 43 years and for 13 unselected protein C-deficient cases 47 years. The median age at the first thrombotic event for 28 APC- resistant members of thrombophilia families was 29 years and for 50 protein C-deficient members of thrombophilia families 31.5 years. The median age of onset for all unselected patients (n=105) was 45 years of age (range, 16 to 69 years) and the median age of onset for all selected patients from the thrombophilia families (n=78) was 30.5 years (range, 16 to 67 years). These results show that within the case-control study and the family studies, the median age of onset is very similar in patients with APC resistance and patients with protein C deficiency. This suggests that APC resistance is not less severe with respect to risk of thrombosis than (heterozygous) protein C deficiency. In conclusion, the median age at which the first thrombosis occurs mainly depends on the way the patients are identified and not on the type of thrombophilia.

Lack of a Thrombotic Tendency in Patients with Acute Myocardial Infarction and Angiographically Normal Coronary Arteries

The hematological profile of 12 patients with acute myocardial infarction and normal coronary arteriographic findings was compared to that of 8 patients with acute myocardial infarction associated with obstructive coronary artery disease, and of 12 patients with no evidence of myocardial infarction and normal coronary arteriographic and left ventriculographic findings who served as control. There were no significant differences in the hematological profile among the 3 groups, suggesting lack of a thrombotic tendency in patients with acute myocardial infarction and normal coronary arteriographic findings.

Effects of the Lupus Anticoagulant in Patients with Systemic lupus Erythematosus on Endothelial Cell Prostacyclin Release and Procoagulant Activity

A disturbance in endothelial cell (EC) function may be pathogenetic in the thrombotic tendency of patients with the lupus anticoagulant (LA). The ability of serum from normal subjects and patients with systemic lupus erythematosus (SLE), with and without the LA, to modulate the release of prostacyclin (PGI2) and the expression of procoagulant activity by cultured human EC was investigated. Only the 10% and 20% serum concentrations from patients with SLE-LA produced a significantly greater inhibition of 6-keto-prostaglandin F1 alpha (6-keto-PGF1 alpha) release (the stable metabolite of PGI2) than control serum. However, when patients with SLE-LA having Raynaud's phenomenon were excluded from this group, there was then no significant difference between the effect of the patient and control serum. Serum from patients with SLE +/- LA caused a significant increase in EC procoagulant activity compared to healthy controls. The two-stage partial thromboplastin time expressed in seconds decreased from 66 (normal) to 34 (SLE - LA) and 31 (SLE + LA), but there was no significant difference between the patients with and without the LA. The significantly increased EC procoagulant activity induced by serum from patients with SLE +/- LA may account for the observed increased incidence of thrombotic events in patients with SLE. Our data suggest that factors other than decreased prostacyclin release are responsible for the altered hemostasis observed in patients with SLE + LA.

The incidence of thromboembolism and the hemocoagulative background in patients with rheumatic heart disease.

We discussed the existence of a thrombotic tendency and the relationship between the high incidence of thromboembolism and the thrombotic tendency in patients with rheumatic heart disease (RHD). The augmentation of platelet function was detected in all kinds of rheumatic valvular disease from the finding of high values of plasma beta-thromboglobulin (72 ng/ml, normal 29 ng/ml). The existence of hypercoagulation was also detected in patients with mitral stenosis by showing low levels of plasma antithrombin III (AT III), while fibrinolytic reaction remained normal. The degree of hypercoagulation became augmented in the order of cases of mitral stenosis (MS) complicated by both atrial fibrillation and chronic congestive heart failure, MS complicated only atrial fibrillation and MS with normal sinus rhythm (AT III: 19.6, 25.0, 26.7 mg/dl, respectively). On the contrary, hypercoagulation, the degree of which was almost the same as that in the respective MS groups, also existed in comparable controls of non-RHD, accompanied by the acceleration of fibrinolytic reaction as shown by the decrease in activity of plasma alpha 2-plasmin inhibitor. Therefore, it was concluded that thrombotic tendency certainly existed in patients with MS compared to those with non RHD and that it was one of the causes of the significantly high incidence of thromboembolism in comparison with non RHD.

A thrombotic tendency in patients with infective endocarditis.

An attempt was made to evaluate a thrombotic tendency in cases of infective endocarditis (IE) from the viewpoint of the changes of platelets and coagulo-fibrinolysis. Qualitative changes of platelets by thrombi formation were detected by showing activated responses of platelets to adenosine diphosphate or collagen and by showing a high level of plasma beta-thromboglobulin which is released by platelets during aggregation. A mild hypercoagulable state without acceleration of fibrinolysis was also detected by showing low levels of plasma antithrombin III which is the most potent antithrombin in the blood and normal levels of plasma alpha 2-plasmin inhibitor in the blood. From above findings, it was concluded that a thrombotic tendency in cases of IE was clearly detected by qualitative changes of platelets by thrombi formation and by mild hypercoagulability without acceleration of fibrinolysis.

Studies on thrombotic tendency in cerebral arteriosclerosis. The first report

ADP, collagen and epinephrine induced platelet aggregation was measured by the optical density method in patients with cerebral arteriosclersis (45 cases) and controls (25 cases) in order to clarify that patients with cerebral arteriosclerosis have a thrombotic tendency. In addition, platelet count, platelet adhesiveness, fibrinogen, cholesterol and triglyceride were measured. The results obtained are as follows.1) The time and rate of collagan induced platelet aggregation were higher in the patients than the controls (P<0.05).2) Neither ADP nor epinephrine induced platelet aggregation was significantly different in both groups.3) Platelet adhesiveness was higher in the patients than the controls (P<0.05).4) Epinephrine induced platelet aggregation correlated with serum cholesterol (r=0.469, P<0.05).These data have probably reflected a thrombotic tendency in patients with prolonged cerebral arteriosclerosis.

Platelet aggregation and thrombus formation in diabetes mellitus: An in vitro study

<h2>Summary</h2> The blood of 52 healthy subjects and 83 patients with diabetes mellitus was studied in a modified Chandler apparatus. Thrombus size was significantly greater in diabetic than in control subjects and was also greater in complicated than in uncomplicated diabetics. There was a significant correlation between thrombus size and plasma fibrinogen level in both control and diabetic subjects. Total serum cholesterol level and thrombus size were statistically related only in diabetic subjects. Plasma thrombus formation time was significantly shorter in diabetics than in healthy controls. Platelet aggregation was more frequent in diabetics than in control subjects. The findings suggest a possible thrombotic tendency in patients with diabetes mellitus.