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Query: UMLS:C0011860 (
type 2 diabetes
)
57,723
document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)
Basal plasma tissue type plasminogen activator (t-PA) and
plasminogen activator inhibitor
type 1 (PAl-1) antigen levels were studied in 49 non-insulin dependent diabetic patients (23 men, 26 women: ages 51.3 +/- 14.9 years) and 16 age matched non-diabetic subjects (9 men, 7 women: ages 49.8 +/- 12.2 years) as a control group. Compared to a control group, the diabetic patients had a significantly higher mean t-PA antigen (5.15 +/- 3.02 vs 3.20 +/- 2.30 ng/ml) and PAl-1 antigen (35.89 +/- 18.59 vs 17.60 +/- 15.36 ng/ml) levels (p < 0.05). Plasma t-PA antigen level was not influenced by each treatment modality. There was a significant decrease of plasma PAl-1 antigen level after Metformin administration compared to that of before Metformin administration (39.74 +/- 19.39 vs 25.14 +/- 16.18 ng/ml) (p < 0.05), and the insulin-treated group showed a tendency for a decrease of plasma PAl-1 antigen levels after insulin administration but this did not reach statistical significance (29.93 +/- 15.37 vs 17.32 +/- 10.60 ng/ml). Sulfonylurea did not change both plasma t-PA and PAl-1 antigen levels. In conclusion, diabetic patients have high t-PA and PAl-1 antigen levels. Biguanide reduced plasma PAl-1 antigen levels, which might play some helpful role in the improvement of chronic complications in
NIDDM
.
...
PMID:Plasma t-PA and PAl-1 antigen concentrations in non-insulin dependent diabetic patients: effects of treatment modality on fibrinolysis. 130 76
18
type II diabetes mellitus
patients with coronary artery disease (CAD) have been studied. Tissue plasminogen activator (t-PA) antigen and activity,
plasminogen activator inhibitor
(
PAI
) antigen and activity, thrombin-antithrombin III (TAT) complexes were determined in blood samples. Diabetic CAD patients showed higher TAT levels with clearly increased
PAI
levels whereas t-PA levels levels were similar in patients and controls. Long term defibrotide treatment induced marked changes in fibrinolytic parameters of these diabetic patients with CAD with increased t-PA activity, that could be related to an evident reduction of
PAI
antigen and activity. Drugs able to modulate
PAI
activity may be useful in clinical conditions at high risk of thrombotic vascular complications like diabetics with stable angina.
...
PMID:Effects of defibrotide on fibrinolytic activity in diabetic patients with stable angina pectoris. 157 96
The pathogenesis of diabetic vasculopathy has been related to modifications in hemostasis and fibrinolysis. 50
non insulin dependent diabetes
mellitus patients have been studied. Euglobulin clot lysis time, fibrin plate, tissue plasminogen activator (t-PA) antigen,
plasminogen activator inhibitor
(
PAI
) activity, Protein C and S, cholesterol, triglycerides and Hb A1c were determined in blood samples. Diabetic patients showed decreased fibrinolytic activity, as measured by ECLT, with clearly increased
PAI
levels. Fibrinolytic response to venous occlusion was lower than normal. Vascular complications were associated both with an even higher
PAI
activity and with a decreased fibrinolytic response to venous occlusion. Elevated
PAI
activity and decreased fibrinolytic response to stimulus may contribute to vascular disease in diabetes.
...
PMID:Hypofibrinolysis associated with vasculopathy in non insulin dependent diabetes mellitus. 211 76
The activity of free tissue plasminogen activator (f-tPA) and
plasminogen activator inhibitor
(
PAI
) in the plasma of 82 noninsulin-dependent diabetics (
NIDDM
) was measured by bioimmunoassay of the euglobulin fraction obtained from the plasma, and the levels were compared with those of age- and gender-matched normal subjects. Comparison of these levels in both groups revealed that the f-tPA activity tended to be lower in
NIDDM
than in the controls, although the differences were not significant. Normal activity of
PAI
was seen, but f-tPA in
NIDDM
, when accompanied by macroangiopathy such as ischemic heart disease, was significantly depressed. When glycosylated hemoglobin levels were in excess of 10%, the f-tPA activity was significantly decreased, but no reduction was found in
PAI
activity as compared with controls. When
NIDDM
is associated with either macroangiopathy or high glycosylated hemoglobin levels, a decreased f-tPA activity, rather than an increased
PAI
activity, may contribute to the development of a defective fibrinolytic state.
...
PMID:Activity of tissue plasminogen activator and plasminogen activator inhibitor in noninsulin-dependent diabetes mellitus. 214 33
The relative importance and behaviour of plasma and platelet
plasminogen activator inhibitor
(PAI-1) in disease has not hitherto been examined. In this study the concentration of PAI-1 in the plasma and platelets of patients with a variety of disorders was examined using a specific ELISA and a functional assay. Mean plasma PAI-1 was elevated in groups of patients with diabetes mellitus, hypertension, alcoholic cirrhosis, angina and myocardial infarction. Plasma PAI-1 was raised in the post-operative phase and the PAI-1 released after surgery was not derived from platelets. In all groups PAI-1 in the platelet pool reflected the platelet count, except in
type II diabetes mellitus
and chronic renal failure, where a reduced quantity of PAI-1 antigen per platelet was found. In severe chronic renal failure, abnormal platelets and diminished platelet PAI-1 may contribute to the haemorrhagic tendency sometimes seen in this disorder. Plasma PAI-1 represents a larger proportion of total circulating PAI-1 in disease than it does in healthy individuals; PAI-1 per platelet is abnormal only in a minority of disorders. Plasma and platelet pools of PAI-1 vary independently in disease and both merit consideration in evaluating the importance, if any, of PAI-1 in thrombosis or haemorrhage.
...
PMID:The platelet and plasma pools of plasminogen activator inhibitor (PAI-1) vary independently in disease. 220 5
Parameters of fibrinolysis, including euglobulin fibrinolytic activity, tissue-type plasminogen activator (t-PA) antigen,
plasminogen activator inhibitor
(PA-inhibitor) activity, and plasmin-alpha 2-antiplasmin complex (PAP) were studied in 62 patients (35 women and 27 men; ages 53 +/- 16 years) with either insulin-dependent (IDDM) or noninsulin-dependent (
NIDDM
) diabetes mellitus. Compared to a control group of similar age (n = 57), the diabetic patients had a significantly lower mean euglobulin fibrinolytic activity (1.2 +/- 0.7 vs. 1.7 +/- 1.1 ng/ml, p less than 0.01) but significantly higher mean t-PA antigen (15.7 +/- 8.4 vs. 6.6 +/- 2.9 ng/ml, p less than 0.001) and PA-inhibitor activity (2.6 +/- 1.3 vs. 1.5 +/- 0.7 IU/ml, p less than 0.001) levels. Significant univariate correlations were observed between PA-inhibitor activity and age (r = 0.32, p less than 0.05), diastolic blood pressure (r = 0.42, p less than 0.01) and euglobulin fibrinolytic activity (r = -0.40, p less than 0.01). In multivariate analysis, only body mass index (positively) and euglobulin fibrinolytic activity (negatively) remained significantly related to PA-inhibitor activity in the total diabetic population as well as in the
NIDDM
group. The only parameter in the IDDM group significantly related to PA-inhibitor activity was diastolic blood pressure. These results suggest that PA-inhibitor plays a role in the regulation of fibrinolysis in diabetes patients and that factors like obesity and hypertension may be related to reduced fibrinolysis via PA-inhibitor levels.
...
PMID:Tissue-type plasminogen activator antigen and plasminogen activator inhibitor in diabetes mellitus. 244 56
Because of the frequent occurrence of premature cardiovascular disease in patients with non-insulin-dependent,
type II diabetes mellitus
(NIDDM), the attenuated fibrinolytic activity of plasma from type II diabetic patients with increased concentrations of
plasminogen activator inhibitor
type-1 (PAI-1), and the fact that insulin stimulates synthesis of PAI-1 by human hepatic cells in vitro, we and others have hypothesized that accelerated vascular disease in type II diabetes may result in part from impaired fibrinolysis secondary to excessive elaboration of PAI-1 stimulated by insulin. Alternatively, the hyperglycemia associated with type II diabetes could influence the synthesis and secretion of PAI-1 directly. The present study was performed to determine whether PAI-1 secretion is or is not sensitive to the prevailing concentration of glucose in the conditioned medium of endothelial and liver cells, which are thought to be the major sources of circulating PAI-1 in vivo. Confluent cells were exposed to 0, 2.8, 5.6, 11.1, or 22.2 mmol/L (0, 50, 100, 200, or 400 mg/dL) glucose in medium without serum and subsequently to media with or without insulin (7.3 nmol/L). Secretion of PAI-1 by highly differentiated human hepatoma (Hep G2) cells did not increase as a function of increasing concentrations of glucose, whether or not insulin was present. In contrast, with pig aortic endothelial cells, the secretion of PAI-1 increased significantly with extracellular glucose with or without insulin. The increases in PAI-1 were specific (as shown by metabolic labeling experiments) and not attributable to osmotic effects (as shown by replacement of glucose by sorbitol).(ABSTRACT TRUNCATED AT 250 WORDS)
...
PMID:Augmentation of synthesis of plasminogen activator inhibitor type-1 in arterial endothelial cells by glucose and its implications for local fibrinolysis. 824 Nov 3
In this presentation an effort has been made to review the impact of resistance to insulin-mediated glucose uptake and/or hyperinsulinaemia on various metabolic end-points and clinical syndromes. Insulin resistance is present in the great majority of patients with states of glucose intolerance, but frank decompensation of glucose homoeostasis does not occur if individuals can maintain a state of compensatory hyperinsulinaemia. Although compensatory hyperinsulinaemia may prevent the development of
NIDDM
in insulin-resistant individuals, there is substantial evidence that insulin resistance and/or hyperinsulinaemia is associated with higher plasma concentrations of triglyceride, uric acid and
plasminogen activator inhibitor 1
and with lower HDL cholesterol concentrations. Obesity, decreased physical activity and possibly cigarette smoking accentuate the degree of insulin resistance and its manifestations, and a genetic basis is also involved. Resistance to insulin-mediated glucose uptake and/or hyperinsulinaemia have been shown to be associated with high blood pressure, microvascular angina and CHD. Thus, resistance to insulin-mediated glucose uptake is a common phenomenon, which makes a major contribution to the aetiology and clinical course of common and serious diseases. Based on the above considerations, it is difficult to over-emphasize the health-related implication of a defect in insulin-mediated glucose uptake.
...
PMID:Insulin resistance and risk factors for coronary heart disease. 830 13
Plasminogen activator inhibitor 1
(
PAI-1
) levels are elevated in obese insulin-resistant subjects. However the mechanism underlying increased
PAI-1
levels is unknown. To determine the impact of diabetes on
PAI-1
levels and its possible relationship to insulin resistance, hyperinsulinemic euglycemic clamp studies were performed in nine lean control subjects, nine non-diabetic obese subjects and eight obese patients with
NIDDM
. Fasting plasma
PAI-1
levels were 4.0 to 4.7 fold higher in the two obese groups than in the control group. During the 40 mU/m2 x min insulin infusion, suppression of FFA concentration was correlated with fasting plasma
PAI-1
levels in both obese non-diabetic and obese
NIDDM
subjects. It is concluded that (1) obesity rather than diabetes itself plays a major role for the increased
PAI-1
levels in
NIDDM
; (2) resistance to the antilipolytic effect of insulin, resulting in increased FFA concentrations, may participate in producing elevated
PAI-1
levels in android obese subjects.
...
PMID:Are free fatty acids related to plasma plasminogen activator inhibitor 1 in android obesity? 858 88
Determination of various important parameters of coagulation and fibrinolysis, clinical characteristics, and levels of serum lipid were compared in 193 patients with
NIDDM
and 50 control subjects. Levels of fibrinogen, tissue factor pathway inhibitor (TFPI), thrombin-anti-thrombin complex, and
plasminogen activator inhibitor 1
in plasma increased significantly in the diabetic patients. Levels of TFPI correlated significantly with levels of total cholesterol. In the patients with coronary heart disease or cerebral infarction, levels of lipoprotein(a) increased significantly. From these results, we have concluded that there is a thrombotic tendency or at least an imbalance between the hemostatic and thrombosis-protecting system in diabetic patients, especially in patients with angiopathy.
...
PMID:Mechanism on disorders of coagulation and fibrinolysis in diabetes. 867 73
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