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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

To study the possible role of an "increased thrombotic tendency" in the vascular complications of diabetes several tests of haemostatic function were carried out on 91 men and 63 women with diabetes aged 35-54 years and the results compared with findings in 686 men and 393 women of the same age in the Northwick Park Heart Study. Mean values for factors VII and X, fibrinogen, and platelet adhesiveness were higher in the diabetics, but mean fibrinolytic activity and whole blood platelet counts were lower. Antithrombin III values were also higher in the diabetics, which may have constituted a protective response to other changes favouring the onset of vascular disease. Diabetics with retinopathy had higher factor VII and antithrombin III values, and those with proteinuria had higher values for factor VII, fibrinogen, and platelet adhesiveness than those without these complications. These findings suggest a potentially important association between a thrombogenic tendency and vascular disease in diabetes. Nevertheless, prospective data are needed to clarify whether the haemostatic abnormalities precede the onset of clinically manifest vascular complications or are a consequence of them.
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PMID:Haemostatic variables associated with diabetes and its complications. 50 77

Plasma Antithrombin III (At III), a natural inhibitor of coagulation, was determined using a single radial immunodiffusion technique. In 116 diabetics, plasma At III levels were significantly decreased (26.6 +/- 0.4 mg/100 ml) compared with those in 64 controls (31.0 +/- 0.3 mg/100 ml, P less than 0.001). An elevation of plasma fibrinogen degradation products in 42 per cent of our patients, and a positive linear relationship between platelet counts and At III levels ( r = 0.29, P less than 0.01), provided additional evidence for chronic disseminated intravascular clotting in diabetes mellitus. Diabetic retinal complications were more frequent in patient with low plasma At III levels (50.6 per cent of cases) than in those exhibiting At III concentrations within a normal range: 32.4 per cent of cases (X2 = 6.09, P less than 0.02). It is postulated that the low levels of At III encountered in diabetes result from excessive consumption, and that the deficiency may be responsible for the onset and/or aggravation of intravascular clotting. At III deficiency may therefore contribute to vascular degenerative complications, particularly those leading to diabetic retinopathy.
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PMID:Antithrombin III deficiency in diabetes mellitus: influence on vascular degenerative complications. 74 66

Antithrombin III activity was determined in 100 patients with diabetes mellitus (24 type I and 76 type II) residing on the Ivory Coast. Results showed a significant decrease of antithrombin III in the diabetic subjects as compared to a normal Ivorian population and an inverse correlation was found between antithrombin III activity and hyperglycemia.
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PMID:Antithrombin III activity and diabetes mellitus in the Ivory Coast population. 133 72

The aim of this study was to evaluate the balance between thrombin and plasmin activity in a group of 79 diabetic patients (IDDM and NIDDM). For this purpose we determined fibrinopeptide A (FPA) and B beta 15-42, specific products of thrombin and plasmin activity. Moreover we investigated the behaviour of antithrombin III and alpha 2 antiplasmin, important inhibitors of blood coagulation and fibrinolysis. Results show an increase both in FPA and B beta 15-42 in IDDM and NIDDM patients when compared to healthy controls. However the ratio between B beta 15-42 and FPA was lower than in controls indicating an imbalance between thrombin and plasmin activity. Antithrombin III levels were not different from the controls and no correlation was found with Hb A1c. alpha 2 antiplasmin was found to be higher in IDDM when compared both with NIDDM and controls. A non linear correlation was found between Hb A1c and alpha 2 AP in both diabetic groups. We conclude that the imbalance between thrombin and plasmin activity may have a role in determining fibrin deposition. These subclinical abnormalities, unrelated to vascular complications and duration of the disease, may progressively contribute to the development of the vascular complications in diabetes.
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PMID:Is the imbalance between thrombin and plasmin activity in diabetes related to the behaviour of antiplasmin activity? 169 51

The pathogenesis of Limited Joint Mobility (LJM) in diabetes is unknown, but the abnormality is said to be associated with an increased incidence of microangiopathy. To examine the possibility that LJM may be a manifestation of microvascular disease, fibrinolysis and blood prostacyclin metabolites were measured in diabetic patients with and without LJM, and compared with patients who have systemic sclerosis (PSS). The concentrations of plasma fibrinogen (p less than 0.01) and Plasminogen Activator Activity (PAA) (p less than 0.02) were increased in both diabetic groups, compared with non-diabetic controls, and were of similar magnitude to the changes observed in PSS. Antithrombin III (AT III) activity was significantly lower in diabetic patients with LJM than in those without LJM, but not significantly different from controls. Prostacyclin concentrations were raised in PSS patients compared to controls (p less than 0.02) but were not raised in diabetic subjects. Thus abnormal fibrinolysis was demonstrated in diabetic patients compared to non-diabetic controls, and prostacyclin concentrations in diabetics were lower than in PSS patients. The diabetic patients with LJM had lower AT III activity than diabetics without LJM, but overall a convincing difference between the two groups of diabetics was not proven. No sure inferences could be drawn on the vascular aetiology of LJM, while the impaired prostacyclin activity might contribute to the development of diabetic microangiopathy.
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PMID:Microvascular disease and limited joint mobility in diabetes. A comparison of fibrinolysis and prostacyclin in diabetes and systemic sclerosis. 296 29

The effect of nonenzymatic glycosylation on the kinetics and structure-function relationships of antithrombin III were investigated at normal physiologic concentrations of antithrombin III and glucose, which are 5.2 microM and 5 mM, respectively. The results were compared with antithrombin III incubated at the glucose concentration expected to be found in severely diabetic patients (15 mM). Antithrombin III incubated at 5 mM lost 33% of the heparin cofactor activity after 7 days, whereas antithrombin III incubated at 15 mM lost 50% for the same period. Under both conditions, half of the heparin cofactor activity was lost after 15 days. When D-[U-14C]glucose was used as tracer, approximately 0.6 mol glucose/mol protein was incorporated after 10 days at both concentrations of glucose. A detailed evaluation of the kinetics of inhibition of thrombin by glycosylated antithrombin III revealed that the second-order rate constant is three times smaller than that of normal antithrombin III. On the basis of these data, it is concluded that glycosylated antithrombin III with 50% depressed heparin cofactor activity is three times weaker than normal antithrombin III as an inhibitor of thrombin. The implications of these observations with respect to the possible pathogenesis of thrombosis in diabetes are discussed.
Diabetes 1988 Aug
PMID:Demonstration of altered antithrombin III activity due to nonenzymatic glycosylation at glucose concentration expected to be encountered in severely diabetic patients. 339 45

Plasma Antithrombin III (AT III) has been shown to be elevated in certain conditions like diabetes mellitus and coronary artery disease as well as in situations where there is increased platelet turnover. This study attempts to define the role of platelet injury in Clinical Nephrology and assesses the clinical value of ATT III. In IgA Nephritis, plasma AT III levels (105 +/- 10%) in 97 patients were higher than those of normal controls (96 +/- 5%) (p less than 0.0005). AT III levels were significantly correlated with proteinuria (p less than 0.0001), segmental sclerosis (p less than 0.01), crescents (p less than 0.01), medial hypertrophy (p less than 0.001) and intensity of IgA staining on IMF (p less than 0.02). Patients with IgA nephritis with raised AT III had more proteinuria (p less than 0.003), more segmental sclerosis (p less than 0.007) as well as a greater intensity of IgA on IMG (p less than 0.02) when compared to patients with normal AT III levels. The data suggest that plasma AT III may serve as a marker of disease activity in IgA nephritis. Plasma AT III levels in hemodialysis patients, low prior to dialysis, improved after dialysis (p less than 0.01). Pre and post hemodialysis platelet counts however did not change significantly. In peritoneal dialysis patients, AT III levels which were normal before dialysis, increased significantly after peritoneal dialysis (p less than 0.01). The platelet counts before and after peritoneal dialysis also improved (p less than 0.005). No correlation was found between AT III levels and platelet counts. Although platelet damage has a contributory role in increasing AT III levels during hemodialysis, the data on peritoneal dialysis suggest that there may be other factors affecting platelets and AT III during dialysis.
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PMID:Galloway memorial lecture. Platelet injury and antithrombin III in clinical nephrology. 389 86

Antithrombin III (AT III) levels have been reported to be low, normal, and high in diabetes mellitus. Furthermore, a discrepancy between AT III activity and antigen concentration was reported. We have evaluated the behaviour of AT III activity and antigen level both in type 1 and type 2 diabetes, either in uncontrolled or in well controlled patients. AT III activity and antigen levels showed values similar to normal. No difference was seen between type 1 and type 2 diabetes. Similar results were observed in the group of well controlled diabetic patients. AT III activity and antigen did not correlate with blood glucose and glycosylated haemoglobin (HbA1). No difference was observed between AT III activity and antigen levels in any group. Therefore the hypercoagulable state found in diabetes mellitus does not depend on AT III modifications. A discrepancy between AT III activity and antigen was not confirmed. A dysantithrombinaemia, explained on the basis of an inactivation of protein glycosylation in diabetes mellitus has not been confirmed.
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PMID:Antithrombin III activity and concentration in diabetes mellitus. 393 13

Plasma beta-thromboglobulin, platelet factor 4, fibrinogen, fibrinopeptide A, antithrombin III, factor VIII related antigen, alpha 2-macroglobulin, platelet count, and total glycosylated haemoglobin were measured in three well matched groups of subjects: non-diabetic controls, diabetics without retinopathy, and diabetics with proliferative retinopathy. beta-thromboglobulin and platelet factor 4 concentrations were significantly higher in the diabetics with retinopathy than in the controls and platelet factor 4 was also increased in the diabetics without retinopathy compared with controls. Fibrinogen concentration was raised in diabetics without retinopathy compared with controls, diabetics with retinopathy compared with controls, and diabetics with retinopathy compared with those without. Fibrinopeptide A concentration did not differ significantly between groups. Antithrombin III levels were increased in diabetics with retinopathy compared with controls, and in diabetics with retinopathy compared with those without. Factor VIII related antigen values were higher in both the diabetic groups when compared with the controls. Fibrinopeptide A concentration correlated with both beta-thromboglobulin and platelet factor 4 in each of the three groups. Haemostatic abnormalities in diabetes have been shown, although a hypercoagulable state has not been confirmed. These changes in platelet and coagulation function may be secondary to the development of microvascular disease and their role in the pathogenesis of retinopathy remains uncertain.
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PMID:Platelet and coagulation factors in proliferative diabetic retinopathy. 620 21

Fibrin catabolism was measured during the pregnancy of insulin-dependent diabetic women in both a longitudinal and cross sectional fashion. Samples of maternal peripheral venous blood were obtained in 20 pregnant diabetic women between 26 and 38 weeks' gestational age. Fibrinopeptide A, the first peptide cleaved from fibrinogen during thrombin-mediated catabolism, was measured by radioimmunoassay. Intra-assay and interassay variation for fibrinopeptide A in this laboratory were 2% and 4% respectively. Antithrombin III activity was determined by the method of Odegaard. The patients ranged from 23 to 36 years. Overall blood glucose control was good as reflected in near-normal HbA1 fasting plasma glucose values. The mean HbA1 +/- 1 standard deviation was 7.1% +/- 1.2%. The mean fasting plasma glucose concentration was 101.9 mg% +/- 21.5 mg%. Mean FPA for the diabetic women exceeded control values at each gestational period. Significant differences were found in four of the seven intervals. While the highest FPA was noted in a patient with advanced diabetic vasculopathy, exclusion of this patient did not alter the overall findings. The findings were striking and suggest the need for a prospective study designed to account for White's classification of diabetes and the degree of glucose control. Because complications of the diabetic pregnancy include an increased risk of hypertension in the mother and sudden, unexplained fetal loss, two complications associated with abnormal clotting, the increase in fibrin catabolism in patients in tight metabolic control would suggest that events other than glucose regulation impact upon fibrin catabolism and possibly pregnancy outcome in the diabetic mother.
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PMID:Fibrin generation during the diabetic pregnancy. 651 59


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