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Query: UMLS:C0011860 (type 2 diabetes)
 57,723 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The aim of the study was to test the hypothesis that cerebrovascular reserve capacity and cerebrovascular reactivity are impaired in patients suffering from non insulin-dependent diabetes mellitus. We also intended to investigate factors which may influence resting cerebral blood flow velocity and cerebrovascular reserve capacity. A total of 28 patients suffering from type II diabetes mellitus and 20 healthy control subjects were studied. Based on diabetes duration patients were divided into two groups: subjects with > 10 years and those with < or = 10 years disease duration. Middle cerebral artery mean blood flow velocities were measured at rest and after intravenous administration of 1g acetazolamide. Cerebrovascular reactivity and reserve capacity were calculated. Blood glucose, insulin, glycosylated hemoglobin, hemostatic factors (fibrinogen, alpha-2 macroglobulin and von Willebrand factor antigen) were determined. Cerebrovascular reactivity and reserve capacity values were compared between the two diabetic subgroups and controls. Correlations between laboratory parameters and cerebrovascular reserve were investigated by linear regression analysis. Resting cerebral blood flow velocity was similar in controls and in the two diabetic subgroups. Cerebrovascular reactivity was elevated for a shorter time in patients with > 10 years disease duration than in controls and short-term diabetic patients. Cerebrovascular reserve capacity was lower in the long-term diabetes group (means +/- SD: 39.6 +/- 20.7%) than in patients with < or = 10 years disease duration (63.3 +/- 17.4%, p < 0.02 after Bonferroni correction). Cerebrovascular reserve capacity was inversely related to the duration of the disease (R = 0.53, p < 0.003). None of the determined laboratory factors had any relation with resting cerebral blood flow and cerebrovascular reserve capacity. The vasodilatory ability of cerebral arterioles is diminished in long-standing type II diabetes mellitus.
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PMID:Cerebrovascular reactivity and reserve capacity in type II diabetes mellitus. 1061 58

The purpose of this study was to examine the associations of carotid artery intima-media wall thickness (IMT) with hemostatic proteins and cardiovascular risk factors (CVRFs) in participants with and without non-insulin dependent diabetes mellitus (NIDDM). IMT measurements were determined by high resolution B-mode ultrasound imaging of the carotid arteries in 921 participants with NIDDM and 11,964 non-diabetic participants aged 45-64 years. Fasting glucose, serum lipids and activated partial thromboplastin time, factor VIII fibrinogen, factor VII, antithrombin III, protein C, and von Willebrand factor measurements were made. Compared to non-diabetic participants, participants with NIDDM had a more adverse pattern of CVRFs and a more procoagulatory profile. Participants with NIDDM had 0.06 mm (8.1%) higher mean IMT compared to non-diabetic participants after adjusting for age and gender (P < 0.001). However, only plasma fibrinogen concentrations showed statistically significant positive associations with IMT in both groups. After adjusting for CVRFs and fibrinogen, mean IMT remained 0.04 mm (5.4%) higher in diabetic compared to non-diabetic participants. Despite the more procoagulatory profile in participants with NIDDM, only plasma fibrinogen concentrations were independently associated with mean IMT. The association of NIDDM with mean IMT was only partly explained by CVRFs.
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PMID:Haemostasis and carotid artery wall thickness in non-insulin dependent diabetes mellitus. 1066 Feb 18

We observed the changes of parameters of coagulation and fibrinolytic system in order to understand the clinical implication of these variations in type II diabetic patients. Subjects consisted of 22 patients with type II diabetes mellitus and 25 healthy controls. Compared with the control, activated partial thromboplastin time, prothrombin time were shortened in the patients. The diabetic subjects also displayed higher levels of D-dimer, serum fibrin degradation products, median concentrations of fibrinogen (3.99 vs 2.96 g/L, P < 0.01) and von Willebrand factor (149% vs 87%, P < 0.01). Levels of antithrombin III activity or antigen were not different from control values. Simple linear regression analysis revealed a negative correlation between antithrombin III activity and fast blood glucose. Diabetic patients with vascular complications had significantly higher levels of fibrinogen and D-dimer than those without diabetic angiopathy. Our data demonstrated that patients with type II diabetes mellitus had a hypercoagulable state. We believed the activation of coagulation might contribute to the vascular complications in diabetics.
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PMID:Variations and clinical significance of coagulation and fibrinolysis parameters in patients with diabetes mellitus. 1080 53

Fibrinogen is a strong cardiovascular risk factor in the general population, and increased fibrinogen plasma concentrations have been reported in type 2 diabetic patients. However, the mechanisms leading to hyperfibrinogenemia in type 2 diabetes are not known. It is also not known whether possible alterations of fibrinogen turnover may precede clinical diabetic micro- and macrovascular complications and therefore potentially contribute to their onset. To address these questions, fibrinogen production was determined in six male type 2 diabetic patients without detectable micro- and macrovascular complications (age, 45 +/- 4 yr; body mass index, 27 +/- 0.9 kg/m2) and in seven nondiabetic matched controls using leucine isotope precursor-product relationships. Plasma glucose (P < 0.001), insulin (P < 0.05), and glucagon concentrations (P < 0.01) were increased in the patients. Diabetic patients also had increased plasma fibrinogen concentration (+ approximately 50%; P < 0.01) and pool (+ approximately 40%; P < 0.01) as well as fractional (+ approximately 35%; P = 0.08) and absolute (+ approximately 100%; P < 0.01) synthetic rates. The plasma glucagon concentration was positively related (P < 0.005 or less) to the fibrinogen concentration as well as to fractional and absolute synthetic rates. Thus, fibrinogen production is markedly enhanced, and this alteration is likely to determine the observed hyperfibrinogenemia in type 2 diabetic patients. Hyperglucagonemia may contribute to the increased fibrinogen production. These findings in normoalbuminuric patients without clinical complications support the hypothesis that increased fibrinogen production and plasma concentrations may precede and possibly contribute to the onset of clinical cardiovascular complications in type 2 diabetes.
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PMID:Increased fibrinogen production in type 2 diabetic patients without detectable vascular complications: correlation with plasma glucagon concentrations. 1099 96

Diabetic patients have higher cardiovascular risk than non-diabetic subjects, and fibrinogen has been reported to be one of the independent predictors for diabetic vascular complications. We examined 101 subjects (24 men, 77 women) who were newly diagnosed with type 2 diabetes. Thirty non-diabetic subjects were recruited as controls. The mean (standard deviation, SD) baseline fibrinogen concentrations in men and women were 3.87 (1.17) and 3.42 (1.00) g/L, respectively (not significantly different). Of these 101 subjects, 70 were treated with diet alone and 31 were treated with oral agents. After a mean (SD) follow-up period of 2.38 (0.63) years, there was an 18.5% increase in the fibrinogen concentration from 3.53 (1.06) g/L at baseline to 3.97 (1.07) g/L at follow-up (P < 0.001). The normal subjects had a mean (SD) follow-up period of 1.17 (0.38) years, and showed no significant change in their fibrinogen concentrations from 3.49 (0.90) g/L at baseline to 3.15 (0.61) g/L at follow-up. In the 101 diabetic subjects, only changes in plasma triglyceride correlated with the changes in fibrinogen concentration. Using multivariate analysis with age, sex, duration of diabetes, baseline and changes in body mass index, blood pressure, glycaemic and lipid parameters as independent variables (R2 = 0.106, F= 6.840, P = 0.011), triglyceride (beta = 0.282, P = 0.011) was identified as the only independent variable that predicted the changes in the fibrinogen concentrations. Improved glycaemic control was not accompanied by a reduction in plasma fibrinogen concentration.
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PMID:Hyperfibrinogenaemia did not improve after treating hyperglycaemia in Chinese type 2 diabetic patients. 1102 18

To elucidate the relationship between the recovery of skin temperature in an extremity after exposure to cold water and various factors associated with diabetes, we measured skin temperature in type2 diabetic patients (N=61) and control subjects (N=16). A thermo-tracer was used in thermographic measurements. The right third toe of each subject was immersed in cold water at 0 degrees C for 10 sec. Rt represents the recovery rate of skin temperature at t min after exposure. Rt was significantly reduced in the diabetic patients every 5 min in the 20 min period following exposure compared with control subjects. The diabetic patients group exhibited a significantly positive correlation between R20 and the ankle-brachial index. R20 in the diabetic patients showed a significantly positive correlation with the reduction in systolic blood pressure at the arm observed in Schellong's test. In addition, R20 showed a significantly negative correlation with plasma levels of fibrinogen and plasminogen activator inhibitor-1. However, the severity of diabetic retinopathy and nephropathy was not significantly related to R20 in the diabetic patients. The present data indicate that the recovery of skin temperature after immersion in cold water was markedly reduced in patients with type 2 diabetes mellitus as compared with healthy control subjects. Peripheral arteriosclerosis, impaired sympathetic nerve function and the activation of the blood coagulation system may all contribute to this reduced recovery of skin temperature.
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PMID:Thermographic measurement of skin temperature recovery time of extremities in patients with type 2 diabetes mellitus. 1108 67

Diabetic dyslipoproteinemia characterized by hypertriglyceridemia, low high-density lipoprotein (HDL) cholesterol, and often elevated low-density lipoprotein (LDL) cholesterol with predominance of small, dense LDL is a strong risk factor for atherosclerosis. It is unclear whether fibrate or statin therapy is more effective in these patients. We compared atorvastatin (10 mg/day) with fenofibrate (200 mg/day), each for 6 weeks separated by a 6-week washout period in 13 patients (5 men and 8 women; mean age 60.0+/-6.8 years; body mass index 30.0+/-3.0 kg/m2) with type 2 diabetes mellitus (hemoglobin A1c 7.3+/-1.1%) and mixed hyperlipoproteinemia (LDL cholesterol 164.0+/-37.8 mg/dl, triglycerides 259.7+/-107 mg/dl, HDL cholesterol 48.7+/-11.0 mg/dl) using a randomized, crossover design. Lipid profiles, LDL subfraction distribution, fasting plasma viscosity, red cell aggregation, and fibrinogen concentrations were determined before and after each drug. Atorvastatin decreased all LDL subfractions (LDL cholesterol, -29%; p <0.01) including small, dense LDL. Fenofibrate predominantly decreased triglyceride concentrations (triglycerides, -39%; p <0.005) and induced a shift in LDL subtype distribution from small, dense LDL (-31%) to intermediate-dense LDL (+36%). The concentration of small, dense LDL was comparable during therapy to both drugs (atorvastatin 62.8+/-19.5 mg/dl, fenofibrate 63.0+/-18.1 mg/dl). Both drugs induced an increase in HDL cholesterol (atorvastatin +10%, p <0.05; fenofibrate +11%, p = 0.06). In addition, fenofibrate decreased fibrinogen concentration (-15%, p <0.01) associated with a decrease in plasma viscosity by 3% (p <0.01) and improved red cell aggregation by 15% (p <0.05), whereas atorvastatin did not affect any hemorheologic parameter. We conclude that atorvastatin and fenofibrate can improve lipoprotein metabolism in type 2 diabetes. However, the medications affect different aspects of lipoprotein metabolism.
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PMID:Effects of atorvastatin versus fenofibrate on lipoprotein profiles, low-density lipoprotein subfraction distribution, and hemorheologic parameters in type 2 diabetes mellitus with mixed hyperlipoproteinemia. 1243 54

The present study has been designed to quantify and compare right and left carotid intima-media thicknesses (IMT) in type 2 diabetics and healthy controls. It was also intended to investigate the effects of various risk factors on the carotid IMT in these subjects. A total of 122 subjects; 70 patients with type 2 diabetes and 52 non-diabetic subjects as controls, were recruited for the study. Right and left common carotid artery stiffness indices were assessed with ultrasonography in both groups. Age, body mass index (BMI), duration of diabetes, cigarette smoking, lipid profile including lipoprotein a, Chlamydia pneumonia seropositivity, glycemic indices, fasting insulin levels, serum fibrinogen levels and presence of hypertension, coronary artery disease, degenerative complications of diabetes mellitus were all assessed in order to define their role as determinants of carotid artery IMT. The difference between the groups regarding mean carotid IMT was statistically significant for the left carotid arteries (p = 0.028) and borderline significance was found for the right carotid arteries (p = 0.055). Age has a very strong association with carotid IMT in diabetic patients (p < 0.0001) with univariate analysis. According to the results of multivariate analysis, age and BMI were found to be the most important independent determinants of carotid IMT for both sides. When age was excluded from the model, BMI and coronary artery disease were found to have strong association with IMT on the right (p = 0.0036 and 0.0249) and BMI was the only significant determinant for the left side (p = 0.0025). This study shows that carotid IMT is greater in diabetic subjects compared with healthy controls. For the diabetic subjects, age, BMI and presence of coronary heart disease have a strong influence on the atherosclerotic process of the carotid arteries.
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PMID:Major determinants of the carotid intima-media thickness in type 2 diabetic patients: age and body mass index. 1120 Sep 31

Patients with type 2 diabetes are at high risk for coronary heart disease (CHD); frequently, these patients have abnormal lipid profiles, placing them at even greater risk. A syndrome of insulin resistance, hyperinsulinaemia, hypertension, and high levels of fibrinogen and plasminogen activator inhibitor contributes to cardiovascular risk, which is not sufficiently decreased by glycaemic control alone. In several large interventional trials, CHD risk in patients with diabetes was substantially reduced by aggressive lipid-lowering therapy. In patients with diabetes, CHD, low high-density lipoprotein levels, and normal low-density lipoprotein levels, gemfibrozil reduced fatal and non-fatal CHD events. For lipid-lowering in patients with diabetes and CHD, pravastatin and simvastatin are the only HMG-CoA reductase inhibitors shown to reduce fatal and non-fatal CHD events. Of these, pravastatin has less potential for drug-drug interactions and may be safer to use, particularly for combination therapy with fibric acid derivatives, as may now be important for CHD prevention in mixed dyslipidaemias.
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PMID:Implications of cardiovascular risk in patients with type 2 diabetes who have abnormal lipid profiles: is lower enough? 1122 41

People with type 2 diabetes have a substantially increased risk of coronary heart disease (CHD). Short-term studies with unopposed oral estradiol in women with diabetes have suggested potentially beneficial effects on lipids, thrombotic factors, and insulin sensitivity. However, most (nonhysterectomized) postmenopausal women require combined estrogen-progesterone preparations. We randomized 43 women with type 2 diabetes either to continuous transdermal estradiol (80-microg patches) in combination with oral norethisterone (1 mg daily) or to identical placebos. Blood samples were taken before and after 6 months for measurement of lipoproteins, coagulation factors, and endothelial markers. Total cholesterol and triglyceride concentrations decreased by 8% and 22%, respectively, in those receiving hormone replacement therapy (P < 0.05 relative to change in placebo group after adjustment for baseline concentrations). There was a trend toward a reduction in high density lipoprotein cholesterol concentration (P = 0.06). Factor VII activity decreased by 16% (P < 0.001), and von Willebrand factor antigen decreased by 7% (P = 0.014) with active treatment. Levels of fibrinogen, tissue plasminogen activator, fibrin D dimer, very low density lipoprotein cholesterol, low density lipoprotein cholesterol, lipoprotein(a), and leptin were not significantly altered. No change in glycemic control was detected. Overall, lipid changes may be considered slightly beneficial with respect to CHD risk. The significant decrease in factor VII activity in this study is notable, because elevated factor VII activity has been associated with an increased risk of coronary thrombosis and normally increases with administration of oral estrogen-containing preparations. In addition, a reduction in von Willebrand factor antigen is consistent with an improvement in endothelial function. We suggest that the regimen used in this study may have the potential to reduce CHD risk in women with type 2 diabetes.
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PMID:The effects of transdermal estradiol in combination with oral norethisterone on lipoproteins, coagulation, and endothelial markers in postmenopausal women with type 2 diabetes: a randomized, placebo-controlled study. 1123 98


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