Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
 277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Ischemic optic neuropathy and retinal arterial occlusion are 2 forms of arterial occlusive disease affecting the eye. Reports in the literature suggest platelet hyperactivity in acute arterial occlusive diseases affecting other organ systems. Therefore, 14 patients with ischemic optic neuropathy and 17 patients with central or branch retinal artery occlusion were studied to determine whether platelets have a role in the pathogenesis of these vascular occlusive disorders. The results of the following investigations were no different in these patients compared with those in 18 control patients with non-vascular eye diseases: prothrombin times, partial thromboplastin times, plasma fibrinogen, factor V, factor VIII, platelet counts and threshold concentrations of ADP, epinephrine and collagen resulting in secondary platelet aggregation and serotonin release. In contrast, platelet coagulant activities concerned with the early stages of intrinsic coagulation were significantly increased in patients with retinal artery occlusion without hypertension or type IV hyperlipoproteinemia, but generally normal in patients with ischemic optic neuropathy and in patients with retinal artery occlusion associated with hypertension, type IV hyperlipoproteinemia, diabetes mellitus and generalized atherosclerosis. These results are consistent with a platelet contribution to retinal arterial occlusive disease in patients without other known contributing factors such as hypertension, serum lipid abnormalities, diabetes mellitus and generalized atherosclerosis and may have implications regarding prophylaxis.
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PMID:Platelet coagulant activities in arterial occlusive disease of the eye. 50 1

Investigations on certain hemocoagulation indices are carried out of 52 diabetics, 32 of them with diabetic nephropathy. The following indices were determined: thrombocyte numer, thrombocyte adhesion and aggregation, recalcification and heparinrecalcification time, partial thromboplastin time (PTT) and prothrombin time, coagulation retraction and thrombelastography. Data for increased blood coagulation are established in diabetics and especially in the presence of nephropathy. Most manifested are the changes in thrombocyte adhesion, in PTT, recalcification and heparin-recalcification time. Changes in thrombelastogram and the rest of the indices are less manifested. In patients with more advanced forms of nephropathy--the increased hemocoagulation is more pronounced. The changes described are considered non diabetes specific and are associated with the accompanying atherosclerosis. Those changes might indicate inclusion of anticoagulants and antiaggregating medicines in the therapeutic program of patients with diabetic nephropathy with the respective indications.
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PMID:[Changes in blood coagulation in diabetic nephropathy]. 122 99

To study factor VII (F VII) hyperactivity in chronic dialysis patients, we measured the plasma levels of F VII activity (F VII c) and antigen (F VII Ag), prothrombin activation fragments 1 + 2 (F1 + 2), thrombin-antithrombin III complexes (TAT), and thrombomodulin in 28 patients on hemodialysis. Marked elevation of F VII c was found in long-term dialysis patients (185 +/- 30%). This hyperactivity was accompanied by both elevation of the F VII Ag level (153 +/- 28%) and enhanced activation of F VII zymogen, expressed as the F VII c/F VII Ag ratio (1.23 +/- 0.23), but pseudocholinesterase activity was decreased. The 6 patients with ischemic heart disease had slightly higher F VII c (200 +/- 25%) than those without ischemic heart disease (181 +/- 30%), although the difference was not significant. Increased F VII c was accompanied by factor Xa hyperactivity (a high plasma F1 + 2 level) in the long-term dialysis patients, but there was no significant elevation of plasma TAT levels when compared with controls matched for age, sex, and the presence or absence of diabetes mellitus. Plasma TAT levels were significantly correlated with plasma thrombomodulin levels, suggesting that thrombin generation in blood as a result of hemodialysis could induce systemic endothelial cell injury.
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PMID:Factor VII hyperactivity in chronic dialysis patients. 133 12

In 45 patients with diabetes mellitus (DM) without cerebro-cardiovascular diseases (CCVD) the modified method of the tissue thromboplastin inhibition test (TTIT) was studied. TTIT is the method of detection of the lupus anticoagulant (LA), LA, first recognized in patients with systemic lupus erythematosus, is presented by a prolonged activated partial thromboplastin time (APTT), a slightly to moderately prolonged prothrombin time (PT), and high incidence of biological false-positive seroreactions for syphilis (BFP). In patients with LA, thrombotic events have been reported. Six of the 45 diabetic patients were TTIT-positive (13.3%). All control subjects were TTIT-negative. In the TTIT-positive diabetics APTT and PT were normal. BFP also were not observed. The difference between LA and these results in TTIT-positive diabetics remains unclear. Clinical profiles except for duration of DM between the TTIT-negative and TTIT-positive diabetics did not differ. Follow-up studies may resolve an association between the results of TTIT and DM.
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PMID:The tissue thromboplastin inhibition test in diabetics without cerebro-cardiovascular diseases. 180 39

Activity of risk factors responsible for experimental diabetes (alloxan and natural diabetogenic factor which is an albumin-like protein) was neutralized in healthy rats simultaneously with an increase of heparin concentration in circulation, which was observed 10 min after the anticoagulation system activation caused by thromboplastin.
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PMID:[The role of endogenous heparin in the protection against risk factors causing experimental diabetes]. 262 44

The procoagulant activity (PCA) of disrupted monocytes was examined in 32 diabetic patients (26 with insulin-dependent and 6 with non-insulin-dependent diabetes) versus 30 control subjects. Diabetes monocytes exhibited a weak PCA before any incubation, associated in 10 cases with a significant amount of factor VII activity. Incubation led to a significant rise in PCA in diabetes cells, when stimulated with lipopolysaccharide or not, and in control cells only after stimulation. In incubated diabetes cells, PCA was prothrombinase-like when factor VII was associated with the freshly isolated cells, and tissue factor-like (as in the controls) when no factor VII was associated with the cells. The characteristics of PCA were not correlated with clinical features or with the type of diabetes. Our study suggests that diabetes monocytes exhibit a higher level of PCA than control ones, possibly corresponding to an in vivo stimulation, or at least a higher responsiveness to stimuli occurring in vitro.
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PMID:Distinctive features of procoagulant response of monocytes from diabetic patients. 273 77

We compared concentrations of antithrombin III (AT-III) in plasma, as determined by an immunological method and by a functional thrombin inhibition method, in the presence of heparin in 160 blood samples from Type I diabetics. Although the correlation was highly significant (P less than 0.001) between the results obtained by the two methods, our data demonstrated that results by the thrombin inhibition assay, 121 (SD 15)%, expressed as percentages of the results for a normal plasma pool, were significantly (P less than 0.001) higher than by the immunoreactive method, 104 (SD 15)%, indicating an overestimation of functionally active AT-III. Concentrations of functionally active AT-III determined by a factor Xa inhibition assay, 105 (SD 13)%, were in the same range as immunoreactive AT-III. Addition of IgG antiserum to normal pooled plasma quenched only about 90% of the AT-III activity determined by the thrombin inhibition assay, but all of the AT-III activity determined by a factor Xa inhibition assay. These results demonstrate that the factor Xa inhibition assay is more specific for the determination of AT-III than the thrombin inhibition assay. We suggest that the high concentrations of heparin cofactor II, 117 (SD 17)%, might have caused an overestimation of AT III in this group of patients with diabetes Type I, and should not be overlooked in other clinical situations.
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PMID:Increased concentrations of heparin cofactor II in diabetic patients, and possible effects on thrombin inhibition assay of antithrombin III. 291 May 81

Patients with diabetes mellitus have higher levels of coagulation factor VIII than the non-diabetic population. This may be a result of poor metabolic control and could contribute to the development of microvascular complications. During ketoacidosis there are acute changes in plasma concentrations of coagulation factors, some of which may be mediated by the rise in vasopressin that occurs. We have investigated the effects of hyperglycaemia without ketosis on some aspects of haemostasis by manipulating blood glucose concentrations using a Biostator. After a 1h run-in period with the blood glucose at 5 mmol/l, the blood glucose was maintained at 5, 15 and 25 mmol/l and maintained for one hour at each level in six male patients with insulin-dependent diabetes. Insulin was infused at 0.25 mu/kg/min. Venous blood samples were taken at the beginning and end of each hour after the run-in period for assays of factor VIII coagulant activity (FVIII:C), von Willebrand factor antigen (vWF:Ag), ristocetin co-factor (FVIIIR:Co), activated partial thromboplastin time (APTT) and vasopressin (aVP). There was a slight, though statistically insignificant fall in median factor VIII:C concentration at each incremental level of increase in blood glucose. Values (at the beginning and end of each hour) were: 1.0 and 1.1 iu/ml at 5 mmol/l; 0.95 and 0.79 iu/ml at 15 mmol/l; and 0.74 and 0.84 iu/ml at 25 mmol. vWF:Ag and FVIIIR:Co were unchanged. Plasma aVP fell slightly from 1.1 to 0.5 pg/ml. The results indicate that high levels of FVIII seen in diabetes are not due to short-term increases in blood glucose and that acute hyperglycaemia does not promote pro-coagulant changes in blood.
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PMID:Effect of controlled hyperglycaemia on factor VIII concentrations in insulin dependent diabetes mellitus. 313 35

In 35 patients with decompensated diabetes mellitus the following hemostatic indices were studied: glycohemoglobin, prothrombin time, partial thromboplastin time, fibrin monomers (determined by protamine sulfate test), fibrinogen and platelet count. A statistically significant decrease of the prothrombin time (p less than 0.001) and of the partial thromboplastin time (p less than 0.001) was found. Glycohemoglobin was significantly increased in all patients. The remaining indices were in the normal ranges. A syndrome of increased latent coagulability emerges which explains the tendency to thromboembolism in diabetes.
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PMID:[Hemostatic studies in decompensated diabetes mellitus]. 321 38

The aim of our study was to evaluate the fibrinolytic system in patients with retinal branch vein occlusion (RVO). The following tests were carried out: prothrombin time, partial thromboplastin time (PTT), fibrinogen degradation products, euglobulin lysis time, fibrinogen, pasminogen, antithrombin III, alpha 2-antiplasmin and alpha 2-macroglobulin. Comparing the results of patients with those of normal controls, only the fibrinogen increase and PTT shortening were significantly different. All other tests taken into account were within normal limits. Only the patients without other associated diseases (diabetes or hypertension) showed a significant activation of fibrinolysis (either with respect to normal or to other RVO patient groups). In conclusion, no important fibrinolytic impairment was seen in our longstanding RVO patients. Fibrinolytic activation seen in patients without verified associated diseases may be related to the presence of a sound endothelium, still able to release plasminogen activators in response to RVO. The fibrinogen and PTT changes in RVO were probably due to other associated diseases.
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PMID:Fibrinolytic behavior in long-standing branch retinal vein occlusion. 369 97


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