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

Antithrombin III activity was moderately but significantly decreased in insulin dependent diabetics (p less than 0.005), while no difference has been found between the diabetic (n = 25) and control groups (n = 22) in antithrombin III plasma concentration. Moreover, antithrombin III activity was inversely correlated with glycosylated plasma proteins (r = 0.57; p less than 0.01). These data show that in diabetes there is a depressed biological activity of antithrombin III and suggest that this reflects nonenzymatic glycosylation of antithrombin III protein.
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PMID:Decreased antithrombin III activity in diabetes may be due to non-enzymatic glycosylation--a preliminary report. 664 86

The effect of nonenzymatic glycosylation on the biologic function of human antithrombin III was evaluated using a chromogenic thrombin substrate assay in the presence of catalytic amounts of heparin. Experimental conditions that increased the rate of nonenzymatic protein glycosylation were associated with decreases in the thrombin-inhibiting activity of antithrombin III. This glycosylation-induced inhibition of heparin-catalyzed antithrombin III activity was completely reversible by preassay incubation with excess sodium heparin. These observations provide a biochemical explanation for the heparin-reversible, accelerated fibrinogen disappearance rate induced by hyperglycemia in diabetic patients. Defective inhibition of the coagulation cascade induced by excessive nonenzymatic glycosylation of antithrombin III in vivo could contribute to accumulation of fibrin in various diabetic tissues.
Diabetes 1984 Jun
PMID:Inhibition of heparin-catalyzed human antithrombin III activity by nonenzymatic glycosylation. Possible role in fibrin deposition in diabetes. 672 50

Thrombus formation depends on adherence of blood-formed elements to the intimal surface through platelet-vessel surface interaction, platelet release phenomena and aggregation, formation of fibrin, and the enmeshing of blood cells. Arterial thrombi involve platelet aggregation, whereas venous thrombi found in low flow or during stasis have greater proportions of erythrocytes and fibrin. It is not known if or how abnormalities of flow resistance, platelet thrombus formation, or endothelial and dynamic parameters affect the microcirculation, largely due to the difficulty of obtaining comprehensive data from these systems. Increases of fibrinogen observed in many disorders may result in minor changes in blood viscosity without known physiologic consequence, but in most disorders in which thrombosis is observed, the pathophysiologic mechanisms are multifactorial and abnormal blood viscosity is presumed to be a significant but not limiting component. Therapeutic approaches in thrombotic disorders should recognize which elements of the thrombotic triad predominate. In arterial disorders focus should be on platelet activity, and the objectives of venous thrombosis treatment include prevention of morbidity and death from pulmonary embolism, reduction of morbidity resulting from the acute thrombotic episode, and prevention of the postphlebitic syndrome. Pathology, mechanism, and treatment for specific thrombogenic disorders are described. Treatments suggested for hyperviscosity involve giving antibiotics during crises. Also discussed are thalassemia, paroxysomal nocturnal hemoglobinuria, polycythemia, cryoglobulinemia, paraproteinemia, diabetes mellitus, and disseminated intravascular coagulation. Studies have established a relationship between thromboembolic disease and oral contraceptives (OCs). The risk is only increased while the patient is taking OCs but is compounded in women undergoing surgery or who have a disorder which predisposes to venous disease. The risk for myocardial infarction or stroke is significantly increased when OCs are taken over age 35 and when there is hypertension, smoking, type-II hyperlipoproteinemia, and diabetes mellitus. The risk appears to be a function of estrogen dosage, causing a 25% mean increase in calf venous volume and 30% decrease in vein velocity of venous blood compared to controls. Low flow rates may contribute to venous thromboembolism. OCs may alter precisely regulated systems of coagulation and fibrinolysis and recent studies confirm abnormalities in the hemostatic system attributed to OCs. 16% of women taking OCs have a 60% or greater reduction in antithrombin III activity. The multiple effects of OCs often result in low-grade activation of the hemostatic system, potentially lowering the threshold to precipitate thrombus formation and possibly explaining the increased incidence of thromboembolic disease. Heparin appears to reverse many of these problems.
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PMID:Blood viscosity and thrombosis: clinical considerations. 676 12

Antithrombin III activity was determined by three techniques in 58 patients with maturity onset diabetes mellitus: a spectrophotometric assay, using the chromogenic substrate Chromozym TH; evaluation of antifactor Xa activity and an immunochemical technique. Although the biological antithrombin III activity was clearly reduced in individual subjects, there was only a slight nonsignificant reduction in the mean anti-thrombin III activity values as compared to normal subjects. No difference was observed between diabetics receiving insulin and subjects taking oral hypoglycemic agents or between diabetics without vascular complications and diabetics with vascular lesions.
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PMID:Determination of antithrombin III activities by different methods in diabetic patients. 676 19

Diabetic coma is frequently associated with thromboembolic complications. A prospective study was undertaken of the haemostatic changes occurring in 15 patients (12 with ketoacidosis, three with the hyperosmolar syndrome) during diabetic coma. When compared with the results after stabilization of the diabetes, ketoacidosis was associated with significantly higher levels of factor VIII coagulant activity, factor VIII-related antigen and fibrin degradation products, a shorter partial thromboplastin time and reduced concentrations of antithrombin III. These results suggest that in uncomplicated ketoacidosis, haematological changes occur which may reflect vascular endothelial damage and intravascular fibrin deposition. Out of three deaths, two patients (both with the hyperosmolar syndrome) had evidence of disseminated intravascular coagulation. To reduce further the mortality and morbidity from diabetic coma, controlled clinical trials of anticoagulant and antiplatelet drugs may be indicated.
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PMID:Haemostatic changes in diabetic coma. 679 75

Both micro and macro-angiopathy involve interaction of blood vessel and plasma factors which may be altered in diabetes. Little is known concerning changes in contact and fibrinolysis factors as prekallikrein, plasminogen and fast antiplasmin in diabetes. We tested also the plasminogen/antiplasmin ratio in 151 diabetics and 64 normal subjects (18 to 74 years old). Our conclusion is:--the absence of correlation between the clinical characteristic of diabetes and prekallikrein level,--the decrease of plasminogen/antiplasmin ratio in complicated diabetes,--in complicated diabetes, correlation between antithrombin III, VIII factor and fibrinogen levels, perhaps, in relation with inflammation signs.
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PMID:[Contact (prekallikrein) and fibrinolytic (plasminogen/antiplasmin value) system in the physiopathology of vascular complications of diabetes]. 681 91

The incidence of thromboses among young women has increased with widespread use of oral contraceptives (OCs) due to the significant thromboembolic risk of estrogen. Estrogens intervene at the vascular, platelet, and plasma levels as a function of hormonal variations in the menstrual cycle, increasing the aggregability of the platelets and thrombocytes, accelerating the formation of clots, and decreasing the amount of antithrombin III. Estrogens are used in medicine to treat breast and prostate cancers and in gynecology to treat dysmenorrhea, during the menopause, and in contraception. Smoking, cardiovascular disease and hypertension, hypercholesterolemia, and diabetes are contraindicators to estrogen use. Thrombosis refers to blockage of a blood vessel by a clot or thrombus. Before estrogens are prescribed, a history of phlebitis, obesity, hyperlipidemia, or significant varicosities should be ruled out. A history of venous thrombosis, hyperlipoproteinemia, breast nodules, serious liver condition, allergies to progesterone, and some ocular diseases of vascular origin definitively rule out treatment with estrogens. A family history of infarct, embolism, diabetes, cancer, or vascular accidents at a young age signals a need for greater patient surveillance. All patients receiving estrogens should be carefully observed for signs of hypertension, hypercholesterolemia, hypercoagulability, or diabetes. Nurses have a role to play in carefully eliciting the patient's history of smoking, personal and family medical problems, and previous and current laboratory results, as well as in informing the patients of the risks and possible side effects of OCs, especially for those who smoke. Nurses should educate patients receiving estrogens, especially those with histories of circulatory problems, to avoid standing in 1 position for prolonged periods, avoid heat which is a vasodilator, avoid obesity, excercise regularly, wear appropriate footgear, and follow other good health practices.
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PMID:[Estrogens and vascular thrombosis]. 692 85

To study the possible role of an increased thrombotic tendency in the vascular complications of diabetes, several tests of hemostatic function were carried out on 91 men and 63 women aged 35-54 years with diabetes and the results compared with findings of 683 men and 393 women of the same age in the Northwick Park Heart Study. Mean values for factor VII, fibrinogen, antithrombin III and platelet adhesiveness were higher in the diabetics, but mean fibrinolytic activity was lower, particularly in the noninsulin-dependent group. 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 thrombotic tendency and microangiopathy in diabetics, but prospective studies are needed to clarify whether the association is a casual one.
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PMID:Hemostatic function tests associated with diabetic microangiopathy. 694 50

Three parameters of coagulability--thrombin generation time (TGT), antithrombin III (AT III), and activated partial thromboplastin time (ATPP)--and two parameters of diabetic control--serial measurements of fasting serum glucose (FG) and hemoglobin A1(HbA1)--were used to study the relationship between diabetic control and hypercoagulability. Four groups of females were studied consisting of 10 young normal, 10 young insulin-dependent diabetic, 10 pregnant nondiabetic, and 8 first-trimester, insulin-dependent, pregnant diabetic subjects. Fasting serum glucose values and HbA1 were higher (P < 0.005) in nonpregnant diabetic subjects (193.1 +/- 29.1 mg/dl, 12.9 +/- 1.1%) and pregnant diabetic subjects (111.0 +/- 13.6 mg/dl, 8.2 +/- 1.7%) than in controls (64.8 +/- 4.4 mg/dl, 5.9 +/- 0.1%) and the nondiabetic pregnant females (71.6 +/- 3.8 mg/dl, 6.1 +/- 0.2%). Young diabetic females, pregnant females, and pregnant diabetic subjects had a shorter (P < 0.01) TGT than did the controls. AT III was greater (P < 0.01) for controls (99.7 +/- 2.7%) than for pregnant nondiabetic (83.2 +/- 3.8%), diabetic (79.5 +/- 2.5%), and pregnant diabetic subjects (76.2 +/- 4.4%). There was a positive correlation (r = 0.88, P < 0.005) between HbA1 and FG in the 10 young diabetic and in the 8 pregnant diabetic subjects (r = 0.74, P < 0.05). In the 10 diabetic females there was a negative correlation between AT III and FG (r = -0.76, P < 0.01) and between AT III and HbA1 (r = -0.79, P < 0.01). Thus, AT III is depressed in both diabetes and pregnancy, with pregnant diabetic subjects displaying the lowest AT III levels. Our observation that depression of AT III levels in young diabetic females was closely correlated with elevations of fasting serum glucose and HbA1 suggests that strict diabetic control may help prevent hypercoagulability in diabetes.
Diabetes Care
PMID:Plasma antithrombin III and thrombin generation time: correlation with hemoglobin A1 and fasting serum glucose in young diabetic women. 744 96

To assess the risk factors for atherosclerosis in Werner's syndrome (WS), coagulation/fibrinolytic system parameters and lipid levels were investigated in 9 non-smoker patients with WS and compared with normal control values (N). The levels of thrombin antithrombin III complex (p < 0.05), D-dimer (p < 0.05), tissue plasminogen activator (p < 0.005) and PA inhibitor 1 (p < 0.01) were significantly increased, while the level of thrombomodulin (p < 0.005) in the fasting plasma was significantly decreased in the WS cases compared with N. Lipid profiles confirmed that 8 of the 9 patients were of hyperlipidemia type IIb, 7 had hyperinsulinemia and 5 fulfilled the criteria for clinical diabetes mellitus. The hypercoagulable condition suggested the existence of multiple risk factors for atherosclerosis in WS in addition to the previously reported hyperinsulinemia and hyperlipidemia.
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PMID:Hypercoagulable state indicates an additional risk factor for atherosclerosis in Werner's syndrome. 749 61


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